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Study Guide Cranial Nerves and Para/Sympathetic Nervous System
Cranial nerves Functions CN I Olfactory Nerve Sense Of Smell (Sensory) CN II Optic Nerve Ability to see; signals from the retina to the brain (Sensory) CN III Oculomotor Nerve Ability to move and blink the eye, constriction of pupils, accommodation of the lens responsible for close vision, eyelid opening (Motor) CN IV Trochlear Nerve Ability of the superior oblique muscle of the eye to move the eyes up, down, back and forth (Motor) CN V Trigeminal Nerve Sensation in the face and cheeks and jaw movements for chewing (Both Sensory and Motor) “Tri”= 3 parts: ophthalmic, maxillary and mandibular CN VI Abducens Nerve Ability of lateral rectus muscle of the eye which controls outward eye movement (Motor) CN VII Facial Nerve Facial muscle movement, taste, production of tears (lacrimation), salivation, ability to close the eyelid (Both Sensory and Motor) CN VIII Vestibulocochoclear Ability of hearing and balance (Sensory) CN IX Glossopharyngeal Ability to taste and swallow, gag reflex, salivation, monitoring carotid bodies/sinuses (Both Sensory and Motor) CN X Vagus Ability to digest and regualate the heart rate, taste, swallowing, palate elevation, talking (Both Sensory and Motor) CN XI Accessory Ability to turn hear, shrug shoulders and neck muscle movement (Motor) CN XII Hypoglossal Ability to move the tongue (Motor)
- Differentiate between clinical manifestations of upper motor neuron and lower motor neuron lesions.
Upper motor neurons lesions manifestations include increase muscle tone, spastic paralysis, increased deep tendon reflexes and a positive Babinski’s sign which occurs when the bottom of The foot is stimulated and the toes curl upwards. Lower motor neuron lesions manifestations include flaccid paralysis, muscle atrophy, or muscle wasting, decreased reflexes and a negative Babinski sign, when the bottom of the foot is stimulated and the toes curl downward, plantar flexion.
- How the action potential is generated? What is depolarization and Repolarization? Action potential is the sudden change in electrical activity across a cell membrane. This is caused by ions crossing the cell membrane, causing a shift of ions. When an impulse is sent down an axon, a sudden influx of sodium ions crosses the cell membrane, causing rapid depolarization where the inside of the cell becomes less negative. This change can be seen on a graph with a upstroke indicated by the depolarization. This action is followed by repolarization showed on the graph as a downstroke, and occurs when there is an outward movement of potassium ions.
- Describe pathophysiology, clinical manifestation, diagnosis and treatment of Parkinson disease. The pathophysiology of Parkinson's disease is a progressive disease that occurs due to the loss of dopaminergic neurons in the substantia nigra. It causes degeneration of the motor fibers, increased release of neurotransmitters in the central nervous system and a decreased level of dopamine in the basal ganglia. Some clinical manifestations include tremors, slow movement, stiffness and issues with balance. Diagnosis is done by a neurologist based on physical exam of movement and mental tasks. There is no definitive test that is used, it is based on symptoms the patient is experiencing. There is no cure of this disease, medication for symptom management to improve the patient’s quality of life. Levadopa is prescribed to counteract the symptoms caused by the dopaminergic deficit. Dopamine agonists are used in conjunction with Levadopa. One combination drug commonly used for Parkinson's treatment is Carbadopa/Levodopa, known as Sinemet. Anticholinergics such as Benztropine and trihexyphenidyl are effective for controlling Parkinson's symptoms.
- Write down 6 events occurring during synaptic transmission. Synaptic transmission, or neurotransmission, refers to the mechanism through which a nerve signal, or action potential, moves from one neuron to another across a synapse. The first step is the action potential arrives at the axon terminal of the motor neuron. The second step occurs when the calcium channels open and calcium enters the axon terminal. The third step occurs when the entered calcium causes the synaptic vessels to release acetylcholine through exocytosis.
Autonomic dysreflexia is a life-threatening medical condition caused by a spinal cord injury at or above the T6 level. It is characterized by an increased response of the involuntary nervous system to stimuli. It can be triggered by various factors such as bladder and bowel complications and urinary tract infections. Below the level of the lesion, it can cause hypertensive crisis, headache, skin pallor and vasoconstriction. Above the level of the injury, it can cause profuse sweating, vasodilation, bradycardia, flushed skin and distended neck veins. These occur due to an unopposed sympathetic outflow. Management includes removing the stimuli, prevention of spinal cord damage, head stabilization and high dose steroids.
- Draw a table to show actions of sympathetic vs. parasympathetic nervous stimulation on various organs. Organ Sympathetic NS “Fight or Flight” Parasympathetic NS “Rest & Digest” Vascular Smooth Muscles Constricts blood vessels in skin Dilates blood vessels in skeletal muscles
N/A
Pupils Dilate Constrict GI Tract Decreases stomach movement and secretions Sphincters constrict Increased stomach movement and secretions Sphincters relax Salivary Glands Heart Increased rate Increased Contractility Increased AV Node conduction Decreased rate Decreased Contractility Decreased AV Node Conduction Bronchioles Dilates bronchial smooth muscles Constrict bronchial smooth muscles Bladder Relax bladder wall Constricts sphincter Contracts bladder wall Relax sphincter Urinary Relaxation, Decreased UO Contraction, Increased UO Male Sex Organs Ejaculation Erection
- Describe signs/symptoms and prevention of deep venous thrombosis?
Signs and symptoms of deep venous thrombosis include: pain or tenderness in the leg, typically the calf or thigh, swelling of the leg or along a vein, warmth in the area of swelling or pain, reddened or discolored skin on the leg. Other symptoms include, shortness of breath, pain with deep inhalation or bloody emesis. Prevention of a DVT includes early mobilization; living a sedentary lifestyle will increase the risk of forming a DVT. Elevation and the use of anticoagulants can also be therapies for prevention. Another way to prevent DVT's is to wear compression socks, especially for those who are on their feet for long periods of time, or sedentary for long periods of time. In hospitals, many times physicians will order pneumatic compression devices that help to apply intermittent pressure on the lower extremities for bed bound patients for the prevention of DVT's.
