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30 Cards in this Set

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Case 1
TZ is 23yob professional basketball player. While waiting to play in a championship game, he collapsed on the sidelines. His pulse could not be palpated, his BP was 60/45 mmHg, breathing was almost imperceptible, his pupils were dilated, and his face was pale. He was nonconcious for about 15 seconds; then color began to return to his face, and his breathing and pulse quickly returned to normal. TZ regained his awareness of the environment on regaining conciousness. He reported feeling fine, although he felt weak; no headache or confusion followed the attack.
Question:
What is the most likely diagnosis?
TZ fainted. The most likely cause was excitement, so the diagnosis was vasodepressor syncope.
Case 2
BG a 47 yom, had a myocardial infarction 3 wks ago. He has been referred to physical therapy for cardiac rehab. He is taking propanolol, a b-blocker
Question:
1. What effect does blocking b-adrenergic receptors have on cardiovasular function?
2. Given the aerobic exercises perscriptions are based on a percentage of predicted age-related maximal heart rate, how will the b-blocker effects impact your exercise Rx?
1. Activation of b-adrenergic receptors accelerates heart rate, increases heart contractability, an vasodilates arteries in the heart and in skeletal muscle. Blocking b-adrenergic receptors benifits the heart by decreasing myocardial O2 demand, allowing LZ to accomplish more physiologic work w/o compromising cardiac function.
2. B/c b-blockers decrease heart rate, age-adjusted normal values for heart rate cannot bee used as guidelines for exercise Rx. The following guidelines can be used to establish target heart rate. An exercise stress test, monitoring heart rate and BP during treadmill or stationary bicycle excercise, must be administered to determine the heart rate at which symptoms occur, and a % (60%-90%) of that heart rate can be used as a guideline for aerobic exercise. If an exercise stress test cannot be performed, a Rx of an exercise heart rate 20 beats/min above resting heart rate, w/ instructions to decrease or stop exercise if symptoms occur, is appropriate.
1. As a cardiac rehabilitation client begins treadmill exercise, which of his visceral and vascular sensory receptors would register changes? To what stimuli would the receptor respond?
Receptor(s):
Pressure Receptors
Response to:
Increased BP, 2nd to increased heart rate, stroke volume, and the increased venous return by the musle pump

Receptor(s)
stretch receptors in the lungs
Response to:
Dilation of the bronchi and bronchioles

Receptor:
Chemoreceptors in the carotid and aortic bodies
Response to:
Concentration of blood O2

Receptor(s)
Chemoreceptors in the medulla
Response to:
Blood levels of H and CO2

Receptor(s)
Chemoreceptors in the hypothalamus
Response to:
Blood glucose levels and blood osmolarity

Receptor(s):
Hypothalamic thermoreceptors
Response to:
Increased blood temp. 2nd to an increase in metabolic rate
2. What is the function of visceral afferents?
visceral afferents convey information from the internal organs and blood vessels into the CNS
3. What areas of the brain directly control autonomic function? What areas modulate activity in the autonomic control centers?
Neurons in the medulla and pons, and hormones from the pituitary gland directly control autonomic functions. Parts of the hypothalamus, thalamus, and limbic system modulate the brainstem control
4. What are the differences b/t the autonomic and somatic efferent systems?
Autonomic regulation is primarily unconscious and can be orchestrated by hormones, functions of the organs regulated can be adjusted by local factors independent of the CNS, an dthe autonomic efferent pathways typically use two neurons as opposed to the single neuron of the somatic efferent pathway.
5. What are the sympathetic trunks? How do sympathetic fibers that leave the paravetebral ganglia reach effectors in the periphery, for example, blood vessels in skeletal muscle and in the skin?
Sympathetic trunks are a series of interconnected paravertebral ganglia. Postganglionic neurons leaving the paravetrebral ganglia join either the ventral or dorsal ramus and travfel in a peripheral nerve to reach the vascularture in skeletal muscles or skin .
6. What are splanchnic nerves?
Splanchnic nerves are composed of preganglionic axons that innervate abdominal and pelvic viscera
7. What is the primary function of the sympathetic nervous system? How can sympathetic activation elicit vasodilation in skeletal muscles under certain conditions and vasoconstriction in the same vessels when conditions change?
The sympathetic system optimizes blood supply according to the requirements of various organs. Sympathetic activation can elicit vasodilation and, at other times, vasoconstriction b/t different effects are elicited by activation of subtypes of receptors on the postsyaptic membrane
8. What are capacitance vessels, and what is their significance? How is the blood flow in skeletal muscle arterioles controlled?
Capacitance vessels are veins and venules that can hold large quantities of blood when their walls are relaxed. Vasoconstriction of their walls prevents fainting when a person is standing. Blood flow in skeletal muscle arterioles is controlled by a- and b2-adrenergic receptors, muscarinic cholinergic receptors, and local blood chemistry
9. What would happen if the sympathetic fibers to the levator palpebrae superioris muscle and the pupil of the eye did not function?
Interference w/ the sympathetic innervation to the muscle that elevates the eyelid and to the pupil of the eye would result in a drooping eyelid and a constricted pupil
10. What functions does the sympathetic nervous system regulate?
The sympathetic system regulates body temp., blood flow in internal organs, skeletal muscle, and skin, and metabolism
11. What functions are controlled by the parasympathetic nervous system?
Parasympathetic activity tends to promote energy conservation and storage. In addition, parasymp. neurons innervate the lacrimal gland, the pupil and lens of the eye, and the bowels, bladder, and external genitalia
12. A pt. w/ CRPS (complex regional pain syndrome - ch 7) arrives for an appointment w/ the following signs affecting the left side of the face: bright red dry skin, drooping of the eyelid, and a constricted pupil. What is your interpretation of these signs?
The pt. w/ CRPS has very recently had a successful injection of a drug to block the stellate ganglion, producing the signs of decreased sympathetic activity ipsilateral to the block. The purpose of the block is to reduce pain so that the pt.'s ability to tolerate active exercise improves temporarily
Case 1
DT is a 35 yom who was brought to the emergency room by a friend 2 days ago. At that time, DT complained of aching, burning pain in his thighs and a feeling of weakness that began 2 days prior to admission. He has no history of trauma. His current condition is as follows:
-he is unable to communicate, so sensation and cognitive functions cannot be tested.
-he is subject to abnormal variations in BP and HR
-he is completely paralyzed. his breathing is maintained by a respirator
-nerve condition velocity is markedly slowed bilaterally in the tested nerves, the median an tibial nerves. Amplitude of recorded potentials is normal.

Question:
What is the location of the lesion(s) and probable etiology?
Rapid onset, motor system more involved than sensory, cranial nerve involvement, and respiratory paresis indicate Guillian-Barrre syndrome. Nerve conduction velocities results indicate that the lesions affect the peripheral nervfes, specifically the myelin. See ch 2 for a revfiew of this disorder
Case 2:
A 16-yow was injured 2 days ago when a load of lumber fell from a shelf, pinning her left forearm. The following signs and symptoms are noted on her left side:
-she does not feel pinprick, touch, temp. differences, or vibration on the medial hand, little finger, and medial half of the ring finger
-sweating is absent in the same distribution as the sensory loss.
-radial writs extension and flexation and finger extension are normal strength on manual muscle tests.
-she is unable to flex the middle and distal phalanges of the forth and fifth digits, abduct or adduct her fingers, or adduct the hand

Question:
1. What is the location of the lesion(s)?
2. How could the probable rate of recovery be predicted?
1. Sensory and motor signs w/ the specific history of trauma indicate crushing injury (axonopathy) of the ulnar nerve.
2. Nerve conduction velocity tests can isolate the localization of the lesion prior to Wallerian degeneration of the axons distal to the injury, and the probable rate of recovery of function can be calculated by assuming regrowth of the distal axon of about 1 mm/day
Case 3:
a 7-yob has progressive proximal muscle weakness. Clinical examination and electrodiagnostic tests reveal the following
-sensation and coordination are w/i normal limits
-he falls 2x when walking 100 ft
-he has difficulty coming to standing and climbing stairs.
-lumbar lordosis is increased
-manual muscle tests indicate that shoulder girdle and hip muscle are approx. 50% of normal strength, knee and elbow muscle are about 75% or normal strength, and distal muscles have near normal strength
-velocity of nerve conduction is normal
-electromyographic potentials recorded from hip girdle muscle are of small amplitude

Question:
What is the location of the lesion(s) an probable etiology?
Lack of sensory and coordination deficits, combined w/ weakness and normal nerve conduction velocity, indicates a primary disease of muscle. The small amplitude potentials recorded from muscle confirm the diagnosis of myopathy
1. What mechanism allows peripheral nerves to lengthen and shorten w/o injury?
peripheral nerves are able to be stretched and shortened w/o injury due to the following mechanisms: axons wrinkle w/i the endoneurium when the nerve is not stretched, the endoneurium, perineurium, and external epineurium act as extensible tubes, the fascicles glide relativfe to each other, fascicular plexuses share the loading, and the entire nerve slides relative to surrounding tissues
2. what signs are produced by complete severance of a peripheral nerve?
Complete severence of a peripheral nerve causes loss of sensation, abnormal sensations, lack of sweating, inability to control smooth muscle in arterial walls, and paralysis of muscles in the area supplied by the portion of the nerve distal to the lesion
3. List the trophic changes that occur in denervated tissue
The tropic changes that occur in denervated tissues include muscle atrophy, shininess of the skin, brittle nails, and thickening of subcutaneous tissue.
4. Give an ex. of a myelinopathy. What part of the nerve is damaged in a myelinopathy? Describe the sequence of events that produce a compression mononeuropathy.
Carpal tunnel syndrome is an ex of a myelinopathy. The myelin is damaged by repeated mechanical stimuli: focal compression due to pressure, excessive stretch, vibration, and/or friction. Compression of a peripheral nerve decreases epineurial blood flow and axonal transport, causing edema of the endoneurium and epineurium. The edema further restricts blood and axonal transport, causing edema of the endoneurium an epineurium. The edema further restricts blood and axoplasmic flow. The external epineurium and perineurium thickens, causing myelin damage, leading to the development of ectopic foci and decreased nerve conduction velocity. Mechanical or chemical stimulation of ectopic foci generates neuropathic pain in the peripheral nerve distribution. The decreased nerve conduction velocity results ini impaired d\discriminating touch, proprioception, and movements.
5. Describe an axonopathy.
Axonopathy is typically the result of crushing a nerve, which disrupts all sizes of axons. Reflexes are decreased or absent. Following the injury, Wallerian degeneration and then muscle atrophy occurs. Prognosis is good b/c regenerating axons are confined to intact CT and myelin sheaths and are able to reinnervate appropriate targets
6. Why is the prognosis for a severed nerve poor?
B/c the axon and CT are completely severed, regenerating axons are not guided by intact sheaths to the appropriate target organ. The lack of guidance and the presence of tissues that physically interfere w/ the optimal direction of regrowth lead to inappropriate innervation and neuroma formation.
7. What is multiple mononeuropathy?
Multiple mononeuropathy is focal damage randomly affectging more than one peripheral nerve. The presentation of signs and symptoms is asymmetrical.
8. What are the most common causes of polyneuropathy?
polyneuropathy is most frequently the result of diabetes, nutritional deficiencies 2nd to alcohol abuse, and autoimmune disorders
9. Why do the signs and symptoms of polyneuropoathy usually appear distally first?
Polyneuropathy usually presents w/ distal involvement first b/c the longest axons are most susceptible to inadequate axonal transport and to the random process of demylenation
10. How can myelinopathy be distinguished from axonopathy?
myelinopathy can be distinguished from axonopathy by nerve conduction velocity studies. Myelinopathies produce severe slowing of the NCV, and axonopathies primarily produce decreased amplitude of the evokeded potential.
How can neuropathy be distinguished from myopathy?
Electromyography can be used to distinguish neuropathy from myopathy. Myopathy will have small-amplitude compound muscle action potentials (ch 10)
Classify each of the following signs as resulting from neuronal hyperactivity or hypoactivity: absent reflexes, muscle spasm, lack of sweating, paralysis, muscle fasciculations, and cyanosis of the skin,.
Neuronal hyperactivities produce muscle spasms, muscle fasciculations, and cyanosis of the skin. Neuronal hypoactivity produces absent reflexes, lack of sweating, and muscle paralysis
Sensory loss in a dermatoma pattern, normal NCS, muscle hypertonia, and slowly progressive muscle atrophy that includes the paraspinal muscles are indicative of lision in what region of the nervous system?
The signs and symptoms listed are characteristic of CNS lesion.