CBLcards3 Flashcards

1
Q

“Pathways of Sensation to the Brain”

A

Different modalities sensed by specialized receptors, Sensory information transmitted via peripheral nerves to spinal cord or brainstem, Ascends via specific pathways (spinothalamic tract for pain and temperature, dorsal column-medial lemniscal pathway for touch and proprioception), Synapse in thalamus before reaching primary sensory cortex in the brain\

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2
Q

Sensory Loss Patterns and Pathology

A

Dermatomes and peripheral nerve distributions help localize pathology, Patterns of sensory loss (e.g., dermatomal, peripheral nerve distribution) indicate specific nerve or spinal cord involvement\

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3
Q

Symptoms and Signs of Peripheral Neuropathies

A

Paresthesia (tingling or burning sensation), Numbness, Sensory loss (glove-and-stocking distribution), Hypersensitivity to touch or pain, Weakness or muscle atrophy in severe cases\

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4
Q

Management of Pain

A

WHO Pain Ladder: Step 1: Non-opioid analgesics, Step 2: Weak opioids, Step 3: Strong opioids, Non-pharmacological approaches: physical therapy, cognitive-behavioral therapy, acupuncture, TENS\

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5
Q

Nociceptive vs. Pathological Pain

A

Nociceptive pain arises from tissue damage or inflammation, Neuropathic pain results from dysfunction or damage to the nervous system itself\

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6
Q

Mechanisms of Neuropathic Pain Drugs

A

Anticonvulsants (e.g., gabapentin, pregabalin): modulate neuronal excitability, Tricyclic antidepressants (e.g., amitriptyline): enhance descending inhibitory pathways, Local anesthetics (e.g., lidocaine): block sodium channels, reducing nerve excitability\

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7
Q

Effect of Opioids and Local Anaesthetics on Neurotransmission

A

Opioids act on opioid receptors, inhibiting neurotransmitter release and reducing pain transmission, Local anesthetics block sodium channels, preventing action potential propagation and pain signal transmission\

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8
Q

FAST Test

A

Face: facial droop or asymmetry, Arms: arm weakness or drift, Speech: slurred speech or difficulty speaking, Time: Time to call emergency services\

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9
Q

Features and Site of Stroke Pathology

A

Hemiparesis or hemiplegia, Facial droop, Aphasia (expressive or receptive), Visual field deficits, Asymmetrical reflexes\

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10
Q

Types of Dysphasia and Dysarthria

A

Expressive dysphasia: difficulty with speech production,
Receptive dysphasia: difficulty with comprehension,
Dysarthria: difficulty with articulation due to muscle weakness\

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11
Q

Pathological Basis of Strokes

A

Ischemic stroke: blockage of blood flow due to embolism or thrombosis, Hemorrhagic stroke: bleeding into brain tissue due to rupture of blood vessels\

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12
Q

Risk Factors, Investigations, and Management of Stroke

A

Hypertension, diabetes, hyperlipidemia, smoking, atrial fibrillation, Investigations: CT or MRI, carotid ultrasound, ECG, Management: thrombolysis, anticoagulants, antiplatelets, lifestyle modifications\

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13
Q

Role of Drugs in Stroke Management

A

Thrombolytics (e.g., alteplase): dissolve blood clots, Anticoagulants (e.g., warfarin, DOACs): prevent clot formation\

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14
Q

Scoring Systems for Anticoagulation

A

CHA2DS2-VASc Score: Used to assess stroke risk in atrial fibrillation (AF) patients, HASBLED Score: Used to assess bleeding risk in patients on anticoagulation therapy\

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15
Q

Significance of Prompt Recognition in Stroke

A

Time-sensitive treatments like thrombolysis are most effective within a narrow window, Early intervention can prevent or minimize disability and improve outcomes\

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16
Q

Scotoma and Visual Field Examination

A

Scotoma: area of partial or complete visual field loss, Visual field testing (perimetry) maps areas of impairment\

17
Q

Anatomy of Eye and Central Visual Pathways

A

Retina transmits visual information via optic nerve to optic chiasm, Optic tracts carry signals to lateral geniculate nucleus (LGN) in thalamus, Optic radiations project to visual cortex in occipital lobe\

18
Q

Vestibulo-Ocular Reflex Pathways

A

Vestibular signals travel via vestibulocochlear nerve (CN VIII), Synapse in vestibular nuclei in brainstem, Output to oculomotor nuclei coordinates eye movements to maintain gaze stability\

19
Q

Therapeutic Drugs for Vestibular Nausea and Vomiting

A

Antihistamines (e.g., dimenhydrinate), Anticholinergics (e.g., scopolamine), Benzodiazepines (e.g., diazepam)\

20
Q

Questions in Depression History

A

Mood changes, Changes in appetite or sleep, Loss of interest or pleasure, Feelings of guilt or worthlessness, Thoughts of death or suicide, Assess risk factors for suicide\

21
Q

Grief Reaction vs. Depression

A

Grief is typically time-limited and related to a specific loss, Depression persists beyond the expected duration of grief and may lack a clear precipitant\

22
Q

Mechanisms of Antidepressants

A

SSRIs increase serotonin levels by inhibiting reuptake, TCAs block reuptake of serotonin and norepinephrine, among other effects\

23
Q

Signs and Symptoms of Parkinsonism

A

Bradykinesia (slowness of movement), Resting tremor, Rigidity, Postural instability, Parkinson’s disease involves progressive degeneration of dopaminergic neurons in substantia nigra\

24
Q

Diagnosis of Parkinson'92s Disease

A

Based on clinical criteria (e.g., presence of bradykinesia plus at least one other cardinal feature), No specific diagnostic test; imaging may support diagnosis by ruling out other causes\

25
Q

Differentiating Tremor Types

A

Resting tremor: occurs at rest, typically pill-rolling in nature, improves with movement,

Essential tremor: occurs with movement, often familial, may be postural or kinetic\

26
Q

Pathophysiology of Parkinson'92s and Treatments

A

Pharmacological: dopamine replacement therapy (levodopa, dopamine agonists), MAO-B inhibitors, COMT inhibitors, Surgical: deep brain stimulation (DBS) targeting subthalamic nucleus or globus pallidus\

27
Q

Challenges in Parkinson'92s Treatment

A

Motor fluctuations (wearing-off, on-off phenomena), Dyskinesias (involuntary movements), Non-motor symptoms (e.g., autonomic dysfunction, psychiatric symptoms)\

28
Q

Neurocognitive Domains Defined by DSM-V

A

Memory, Attention, Language, Visuospatial skills, Executive function, Social cognition\

29
Q

Scoring Glasgow Coma Scale (GCS)

A

Eye opening, Verbal response, Motor response, Total score ranges from 3 to 15, with lower scores indicating more severe impairment\

30
Q

Definitions of Delirium, MCI, and Dementia

A

Delirium: Acute confusional state characterized by impaired cognition, attention, and awareness, MCI: Intermediate stage between normal aging and dementia, Dementia: Chronic and progressive decline in cognitive function\

31
Q

Investigations for Chronic Cognitive Impairment

A

Mini-Mental State Examination (MMSE) or Montreal Cognitive Assessment (MoCA), Blood tests (e.g., thyroid function, vitamin B12, folate), Neuroimaging (MRI or CT scan), Neuropsychological testing\

32
Q

Features and Natural History of Alzheimer'92s Disease

A

Clinical features: Memory loss, impaired judgment, difficulty with language, personality changes, disorientation, and difficulty in performing familiar tasks, Natural history: Progressive decline in cognitive function\

33
Q

Causes of Delirium and Diagnostic Investigations

A

Causes: Infection (e.g., UTI, pneumonia), medication side effects, metabolic disturbances (e.g., electrolyte abnormalities), hypoxia, substance withdrawal, Investigations: Blood tests (e.g., CBC, electrolytes, renal function), urine analysis, chest X-ray, EEG, toxicology screen\

34
Q

Application of Neuroanatomy and Pathologies in Clinical Scenarios

A

Understanding neuroanatomy helps localize lesions based on clinical presentations, Knowledge of neuro-pathologies aids in interpreting diagnostic tests and selecting appropriate treatment strategies\