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Comprehensive Textbook Of Medical Physiology. Review of Pathology. Robbins Pathologic Basis of Disease 9th Edition. Ramdas Nayak Pathology. Concise Pathology for Exam Preparation. Robbins Basic Pathology Student Edition. Color Atlas of Forensic Medicine and Pathology. AK Khurana Opthalmology. Diseases of Ear, Nose and Throat. Mahajan and Gupta Textbook of Community Medicine. Park Textbook of Preventive and Social Medicine. Exam Preparatory Manual for Undergraduates Medicine.
Mathew Medicine Prep Manual for Undergraduates. Bedside Clinics in Medicine. Long Cases in General Surgery. L Saha Bedside Clinics in Surgery. Das Manual on Clinical Surgery 13th Edition. Sabiston Textbook of Surgery. Manipal Manual Of Surgery 4th Edition. Williams Obstetrics 25th Edition. Williams Gynaecology. Sakshi Arora Gynecology. Latest developments, experimental medicines and future geriatrics, immunology, and clinical pharmacology pages are included.
Usage of various colour codes to define all disorders in terms of aetiology, management and care. Every disease's pathogenesis is portrayed in the form of vibrant flowcharts. Malarial parasite life cycle diagrams are provided along with a summary. It has applied to and collected more than 20 recent versions of traditional textbooks.
The appendices have reference values for common laboratory study and widely used formulas, and format for neurological analysis.
Unknown 3 April at Subscribe to: Post Comments Atom. Students Benefitted. Exacerbations are usually unpredictable and unprovoked.
Onset of action is rapid 30 seconds and lasts for short duration 5 minutes. It reverses of muscular weakness dramatically in myasthenia. Test dose 2 mg intravenous is given to check for reactions. If there is definite improvement drop further test.
If negative further 8 mg IV is given. When the test is positive, it produces substantial improvement in weakness, ptosis, diplopia, nasal voice, etc. Adverse effect include nausea, diarrhea, salivation, bradycardia, syncope, abdominal cramps, fasciculation treated with atropine The response is positive when there is increase in at least 2 mm of the palpebral fissure from before to after the test.
In normal individuals the amplitude of the evoked muscle action potentials does not change at these rates of stimulation. It is most commonly associated with small cell carcinoma of lung and the treatment is with aminopyridines. Write a short note on drugs used in myasthenia gravis. Treatment ee br ot Goals: To increase the activity of acetylcholine on the remaining receptors at the NMJ. Stop the antibody mediated damage at the NMJ.
Oral anticholinesterases: Help weakness but do not change the natural history of myasthenia. Onset of action is within minutes and lasts for hours. Cholinergic crisis characterized by pallor, perspiration, pupillary constriction, paralysis, fasciculation and excessive salivation can be seen with drug over dosage.
Muscarinic effects e. Choice is guided by benefit, risk and urgency. These are used in patients who do not respond to pyridostigmine or who develop relapse on treatment. Write a short note on muscular dystrophies or hereditary myopathies. Muscular dystrophy is subdivided by their mode of inheritance, age at onset, distribution of involved muscles, rate of progression, and prognosis Table Cardiac disturbances occur in most patients with myotonic dystrophy.
Disturbances in conduction system are common. Complete heart block and sudden death may occur. Mitral valve prolapse also occurs commonly in myotonic dystrophy patients. Myotonia may improve with phenytoin, mexiletine, and quinidine.
Write a short note on causes of endocrine myopathies. Causes of High Creatinine Phosphokinase Box List the causes of high creatinine phosphokinase.
The cerebellum is made up of two hemispheres separated by a midline vermis. There are three lobes anterior, posterior, and flocculo nodular lobe.
Ataxia Ataxia may be the result of cerebellar lesion or due to a combination of cerebellar and extracerebellar lesions.
Write a short note on cerebellar signs. Cerebellar Ataxia Q. Write a short note on cerebellar ataxia. Column involvement is known as sensory ataxia. When there is proprioceptive or vestibular deficit, balance is impaired only when eyes are closed, and the patient may fall if not caught. Minimal lesions can be demonstrated by asking the patient to stand on his toes with eyes closed.
This results in breaking of an act into its components. This is demonstrated by getting the patient to tap back of their own hand repeatedly with the other hand, or to tap their foot on the floor. This produces apendular jerk at the knee. It produces three on more swings at the knee when the knee reflex is elicited with patient in sitting posture and the legs hanging from bedside. Most common form degenerative ataxia caused by unstable trinucleotide GAA expansion in chromosome located on 9q.
The protein involved is frataxin. There IA also loss of dorsal root ganglion cells with depletion of large myelinated fibers in peripheral nerves.
It is due to involvement of dorsal column. Treatment: No definite treatment, physiotherapy and occupational therapy, spasticity is treated with baclofen, orthopedic advice and surgery. Write a short note on CNS disorders characterized by involuntary movements. It is a negative myoclonus. Ballismus is often unilateral hemiballisums. Chorea can be defined as involuntary movements that are abrupt, unpredictable and nonrhythmic, resulting from a continuous random flow of muscle contractions.
Write a short note on myoclonus and its causes. Repetitive, stereotypic movements or sounds that are suppressible and that relieve a feeling of inner tension. Tremor is characterized by involuntary, rhythmic and sinusoidal alternating movements of one or more body parts. Write a short note on hemiballismus.
It is usually unilateral, and hence called hemiballismus Table Cause of some important movement disorders are listed in Table Haloperidol 0. What is parkinsonism? How would you classify parkinsonism?
Discuss the management of idiopathic parkinsonism. Prevalence is higher in men than women M:F 1. It leads to progressive disability with time.
Probably multiple interacting environmental risk factors and genetic susceptibility plays a role. It causes severe Parkinsonism in young drug users of MPTP by producing oxidative stress leading to death of neuronal cell. They are rare but cause early onset and familial PD. This leads to formation of Lewy body within the nigral cells. Lewy bodies are also seen in the basal ganglia, brainstem and cortex. They become gradually more widespread and increase as the disease progresses.
Ja yp Clinical Manifestations A. Motor symptoms: Always asymmetrical in onset and become bilateral within a year. It often begins with rhythmic flexion- extension of the fingers, hand, or foot, or with rhythmic pronation- supination of the forearm. Initially, it may be confined to one limb or to the two limbs on one side before becoming more generalized. It also affects jaw and chin, but not the head.
Increased resistance to passive movement is characteristic clinical feature that accounts for the flexed posture of many patients. Rigidity causes stiffness and a flexed posture.
Unlike spasticity, it is not dependent on speed of movement. Frequency of spontaneous blinking decreases producing a serpentine stare. It results in difficulty in activities such as tying shoelaces or buttoning, and difficulty rolling over in bed.
Feet may be glued to floor. Postural instability and freezing may result in fall forward. Reduced eye blink. Nonmotor features Table However; it is not specific for PD. It may be rarely required to distinguish PD from other causes of tremor, or drug induced Parkinsonism. Stages of Parkinson's disease Table What are the stages of Parkinson's disease? Secondary Parkinsonism Table Trauma: Pugilistic encephalopathy. Parkinson-plus syndromes Table Frequently experience hyperextension of the neck with early gait disturbance and falls.
Corticobasal ganglionic degeneration Rebeitz-KolodnyRichardson syndrome Asymmetric dystonic contractions and clumsiness of one hand coupled with cortical sensory disturbances manifest as apraxia, agnosia, focal myoclonus, or alien limb phenomenon. Symptomatic pharmacologic treatment: Drug treatment in PD is symptomatic rather than curative. None of the currently available drugs are neuroprotective. For example, trihexyphenidyl, benztropine, and orphenadrine. Hence, rarely used as first-line drugs unless patient has severe tremors.
They should be avoided in patient above 65 years of age. It is the single most effective drug available for the treatment. It provides symptomatic benefit in most patients with Parkinsonism and is often particularly helpful in relieving bradykinesia. Resolve hypokinesia and rigidity first and tremor later. Its plasma half life is around two hours. Early use lowers mortality rate. Combined with a dopa decarboxylase inhibitor—benserazide cobeneldopa or carbidopa cocareldopa to reduce the adverse effects e.
It is like a light switch; without warning, all of a sudden, person goes from full control to complete reversion back to bradykinesia, tremor, etc.
It lasts from 30 minutes to several hours and then get control again. The on-off phenomenon can be controlled in part by reducing dosing, intervals, administering levodopa 1 hour before meals and restricting dietary protein intake or treatment with dopamine agonists. They produce asymptomatic motor benefit when used as a monotherapy and enhance the efficacy of carbidopa levodopa formulations when used as adjuncts voided.
Example selegiline, rasagiline. Dopamine agonists are contraindicated in patients with psychotic disorders and are best avoided in those with recent myocardial infarction, severe peripheral vascular disease, or active peptic ulceration. They are used as an alternative or an addition to levodopa therapy. Entacapone prolongs the duration of levodopa by decreasing its peripheral metabolism.
The more potent tolcapone is less preferred because of rare but serious hepatotoxicity. It has a mild antiparkinsonian effect and short-lived effect on bradykinesia.
Hence, it is rarely used and are reserved for patients who are unable to tolerate other drugs. Amantadine-either alone or combined with an anticholinergic agent, helpful for mild Parkinsonism. It acts by potentiating the release of endogenous dopamine. For example, carbidopa, benseraside. Best site is subthalamic nucleus. DBS in these areas alleviates Parkinsonian motor signs particularly during the off periods and reduces troublesome dyskinesias, dystonia and motor fluctuations that result from drug administration.
DBS is usually reserved for patients with medically refractory tremor or motor fluctuations. Characteristic Features of Extrapyramidal Lesion Table Write short note on characteristic features of extrapyramidal lesion. Write a short note on chorea and mention the disease which causes chorea. These movements disappear during sleep. Causes of Chorea Table Japanese encephalitis, measles, mumps Vascular, e.
Immunologic, e. Drugs, e. L-dopa, oral contraceptive, phenytoin Degenerative disorders of the brain Benign hereditary Pregnancy Chorea gravidorum Endocrine-metabolic dysfunction: e. It follows acute rheumatic fever by months. Severity varies and disorder may continue for a few months. These antibodies disrupt the basal ganglia function. Inflammation is seen in caudate nucleus. Clinical features include both neurological abnormalities chorea, weakness and hypotonia and psychiatric disorders such as emotional lability, hyperactivity, distractibility, obsessions and compulsions.
It can be demonstrated by an inability to sustain eye closure or tongue protrusion. The dose is 1—2 mg BID. HD is a progressive, fatal, highly penetrant autosomal dominant disorder characterized by motor, behavioral, and cognitive dysfunction.
Onset is typically between the ages of 25 and 45 years. This is called as anticipation. Dysarthria, gait disturbance, and oculomotor abnormalities are common features. Depression with suicidal tendencies, aggressive behavior, and psychosis can be prominent features.
Treatment ot he Multidisciplinary approach, with medical, neuropsychiatric, social, and genetic counseling for patients and their families.
Depression and anxiety is treated with appropriate antidepressant and antianxiety drugs. Write a short note on definition of tremor and mention its types with examples. Tremor is an unintentional, rhythmic muscle movement involving to-and-fro movements oscillations of one or more parts of the body produced by alternating or synchronous contractions of antagonist muscles. It is the most common of all involuntary movements and can affect the hands, arms, head, face, voice, trunk, and legs.
For example tremor occuring when the hands are lying on the lap or hanging next to the trunk while standing or walking. It may be shaking of the limb, even when the individual is at rest. There are several subtypes of action tremor. For example holding the arms outstretched. For example moving the wrists up and down. For example as handwriting or speaking. Classification Tremor is most commonly classified by its appearance and cause or origin. Most commonly observed in the hands but may involve the head, voice, tongue, legs, and trunk.
Tremor of the hands is typically present as an action tremor. It decreases on alcohol consumption. It may affect any muscle. Dystonic tremors occur irregularly and often relieved by complete rest. Cerebellar tremor may be associated with dysarthria speech problems , nystagmus rapid involuntary movements of the eyes , gait problems, and postural tremor of the trunk and neck. The characteristics may vary but generally include sudden onset and remission, increased incidence with stress.
Many individuals have a conversion disorder or psychiatric disease. It may be exaggerated by strong emotion such as anxiety or fear , physical exhaustion, etc. It is generally not caused by a neurological disease. Write a short essay on differences between extramedullary and intramedullary lesions of the spinal cord. Write short note on common causes of compressive myelopathies. The reflexes will be brisk below the involved segment.
Deformity or any swelling in the vertebra Tenderness in the vertebra The area of sweating may help lack of sweating below the level in localizing the level of lesion.
Rectus abdominis is innervated by the terminal branches lower six or seven thoracic spinal nerves via the lower intercostal and subcostal nerves. If a lesion lies above T6, entire rectus abdominis is weak so there is no contraction of muscle.
If it is at or below T10, the upper abdominal muscular function is preserved, whereas the lower abdominal muscles are weak. Therefore, when the head is flexed against resistance patient supine , the intact upper abdominal muscles pull the umbilicus upward and shift of umbilicus 3 cm when head flexed is considered significant. Write a short note on paraplegia in flexion, paraplegia in extension. Occurs in late stage of paraplegia or progressive lesion and spinal arc is dominant.
It is attributed to increased hyperexcitability of spinal cord circuitry and lead to flexor spasms. Write a short note on causes of extramedullary spinal cord compression. Edema due to venous obstruction impairs neuronal function, and ischemia due to arterial obstruction may causes necrosis of the spinal cord. Hence, it is important to diagnose and treat early. Localized over the spine or in a root distribution. Maybe aggravated by coughing, sneezing or straining.
Sensory: Occurs early. Paresthesia, numbness or cold sensations especially in the lower limbs , spread proximally to a level on the trunk Motor: Occurs late. Weakness, heaviness or stiffness of the limbs commonly legs Sphincters: Occurs late. Urgency or hesitancy of micturition, and retention of urine br Signs of spinal cord compression: Vary according to the level of the cord compression and the structures involved.
MRI can define the extent of compression and associated abnormality in the soft-tissue. Useful function can be regained if treatment e. It refers to findings seen when the damage is confined to one side lateral half of the spinal cord. With compressive lesions, there is a band of pain at the level of the lesion in the distribution of the nerve roots involved by compression.
Causes: Due to extramedullary lesions, usually caused by penetrating Gun shot or tumor. Write a short essay on the pathogenesis of syringomyelia. Syringomyelia is a cavitary expansion of the spinal cord. Syrinxes commonly develop in the lower cervical and high thoracic regions or in the high cervical region.
They may extend proximally to the medulla or pons syringobulbia. This abnormality at the foramen magnum probably allows normal pulsatile CSF pressure waves to be transmitted to fragile tissues of the cervical cord and brainstem. This results in secondary cavity formation. There is gradually destruction of spinothalamic neurons, anterior horn cells and lateral corticospinal tracts.
It leads to progressive myelopathy. Write a short essay on etiology, clinical features and management of subacute combined degeneration. It is myelopathy that develops due to nutritional deficiency of vitamin B12 deficiency, including pernicious anemia. Treatment is by replacement therapy, beginning with mg of intramuscular vitamin B12 repeated at regular intervals or by subsequent oral treatment. Explain clinical features of any one of them.
Paraplegia Q. Write a short note on causes and differential diagnosis of spastic paraplegia. Causes: It can occur in disorders of cerebrum, spinal cord, spinal roots, peripheral nerves or muscles. It is usually due to disorders of spinal cord.
It is usually produced to subacute or chronic lesion. Acute lesions usually cause flaccid paralysis. Gradual onset B. The most distal bulbous part of the spinal cord L1-L2 is called the conus medullaris. The conus medullaris consists of the cord segment between S2 and S5 as well as coccygeal segments.
Distal to this end of the spinal cord is a collection of nerve roots L onwards to cocxygeal , which are horsetail-like in appearance called the cauda equina Table Write a short note on differences between conus medullaris lesions and cauda equina lesions. They develop due to loss of sensation and reduced blood supply. Following measures will be helpful. Needs aspetic care and may require skin grafting. Indwelling catheter is not advisable as it predisposes to infection, reduces bladder capacity and promotes calculus formation.
If fecal matter becomes hard, manual evacuation is done. Hence, regular passive movements of the limbs should be encouraged. In severe spasticity, intrathecal baclofen via a pump or sectioning of the anterior roots rhizotomy. Write a short note on different types of spinal pain.
Discuss hemiplegia in an elderly male. Give the differential diagnosis, investigations and its treatment. Hemiplegia is paralysis of one side of the body.
Hemiparesis is the weakness of one side of body. Cerebral metastasis, subdural hematoma, granulomas tuberculosis-younger age, fungal , pyogenic abscesses metastatic infection, post-traumatic , rapidly growing malignant neoplasms e.
Write a short note on wasting of small muscles of hand. Causes Table Motor neuron disease MND is a devastating, progressive, heterogeneous group of neurodegenerative condition caused by loss of upper and lower motor neurons in the spinal cord, cranial nerve nuclei and motor cortex.
There is no involvement of sensory or other nonmotor tracts. It causes progressive weakness and eventually death usually as a result of respiratory failure or aspiration. Various types of motor neuron disease are listed in Table There is no involvement of sensory system. Hence, sensory symptoms e. Amyotrophic Lateral Sclerosis Q. Epidemiology: Incidence is 1 to 2. Peak onset-sixth to seventh decade one to two decades earlier in India.
Complex genetic and environmental interaction for neuronal degeneration. This indicates that protein aggregation may be involved in its pathogenesis similar to other neurodegenerative disorders.
Other mechanism involved in pathogenesis may be oxidative neuronal damage, glutamate mediated excitotoxicity, mitochondrial dysfunction and impaired axonal transport. They present with simultaneous involvement of upper and lower motor neurons. Usually in one limb, spreading gradually.
Often present with focal motor weakness of distal or proximal upper or lower limbs. The focal motor weakness spreads to contiguous muscles in the same region before involvement of another region. Then involves other limbs and trunk muscles. These movements disappear as coma deepens. If it is bilateral it is due to raised ICT.
It is diagnostic of lesions in midbrain and pons. It indicates diffuse cortical anoxic damage and drug intoxication. It can be also due to profound overdose of sedatives or anticonvulsants. The eyes are tonically deflected to side irrigated with cold water and this position may be held for minutes. Lumbar puncture: should be performed in coma only after careful risk assessment.
It should not be performed when there is a suspicion of an intracranial mass lesion. CSF examination may help in the diagnosis of meningoencephalitis or other infection, or in subarachnoid hemorrhage. Patients can open their eyes or have random limb and head movements but there is complete absence of response to commands or to communicate. It is usually due to extensive cortical damage.
Brainstem function is intact. Hence, breathing is normal without the need for mechanical ventilation. Patients may remain in this vegetative state for years. Even after 12 months if there is no recovery, it is called permanent vegetative state PVS.
These include nonreflexive response to sensory stimulation, awareness of the self or the environment, or language comprehension or expression. It may be seen in bilateral frontal lobe lesions, hydrocephalus and a mass in the region of third ventricle.
There is complete paralysis except vertical eye movements and intact lid movements blinking in ventral. This syndrome is due to extensive transverse lesions in the pontine and midbrain infarction. These patients may keep their eyes firmly closed and resist the opening of the eye by examiners.
Their eyes roll up when the lids are raised. It may be due to feigned or hysterical state. For example —— Diabetic with hypoglycemic coma: Administer hypertonic glucose without waiting for reports. Have a secure IV line. Write a short note on brain death. Brain death occurs from irreversible brain injury which is sufficient to permanently eliminate all cortical and brain stem function i.
Diagnosis of Brain Death Brain death is a clinical diagnosis. No other tests are necessary and complete clinical examination including independent brain death determinations by two licensed physicians is conclusive.
Documentation Time of death is the time the arterial PaCO2 reached the target value OR when ancillary test officially interpreted. Symmetric compression of the optic chiasm by a pituitary adenoma, meningioma, craniopharyngioma, glioma, or aneurysm results in a bitemporal hemianopia.
They have macular sparing, because collaterals from the middle cerebral artery supply the macular representation at the tip of the occipital lobe. This condition can be distinguished from bilateral prechiasmal visual loss by noting that the pupil responses and optic fundi remain normal. Patterns of visual field loss are shown in Fig.
It is usually due to vascular disease and may be difficult to identify whether the visual loss was monocular carotid circulation or binocular vertebrobasilar circulation.
This term has been used only for passive swelling of the optic disc secondary to raised intracranial pressure. Causes of papilledema Table It also develops due to any cause that produces edema in the head of the optic nerve e. Write a short note on the causes of papilledema.
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