Module 3.pdf

Unit 5: Disorders of Neural Function. Chapters 13-16, 18. There are 12 questions from this unit. 35. Chapter 13. Metabolic Requirements of Nervous Tissue. Consequences of unmet Demand. Nervous tissue has a high rate of metabolism. The brain receives 15% to 20% of the total resting cardiac output...

Unit 5: Disorders of Neural Function. Chapters 13-16, 18. There are 12 questions from this unit. 35. Chapter 13. Metabolic Requirements of Nervous Tissue. Consequences of unmet Demand. Nervous tissue has a high rate of metabolism. The brain receives 15% to 20% of the total resting cardiac output and consumes 20% of its oxygen. Despite its substantial energy requirements, the brain cannot store oxygen or effectively engage in anaerobic metabolism. An interruption in the blood or oxygen supply to the brain rapidly leads to clinically observable signs and symptoms. Inte 36. Chapter 14. Somatosensory Function, Pain, Headache, and Temperature Regulation: Acute pain: elicited by injury to body tissues and activation of nociceptive stimuli at the site of local tissue damage. Generally short duration and tends to resolve when the underlying pathologic process has resolved. Chronic pain: Pain that persists longer than might be reasonably expected after an inciting event. Continues for years. Sustained by factors that are both pathologically and physically remote from the originating cause. Cutaneous and Deep Somatic Pain: cutaneous pain arises from superficial structures. Deep somatic pain originates in deep body structures (muscles, tendons, joints, blood vessels). It is more diffuse than cutaneous pain. Visceral Pain: Origin in the visceral organs and is one of the most common pains produced by disease. The important difference between surface pain and visceral pain is the type of damage that causes pain. Strong contractions, distention, or ischemia affecting the walls of the viscera can cause severe pain. Referred Pain: pain that is perceived at a site different from its point of origin but innervated by the same spinal segment. Example: STEMI pain is referred to left arm, neck, and chest. Types of pain- compare definitions, begins on p. 402-403. 37. Chapter 15. Disorders of the motor unit/Disorders of the Neuromuscular Junction: Myasthenia gravis, neuromuscular junction pathophysiology.p. 443. Myasthenia Gravis is a disorder of transmission at the neuromuscular junction because of antibody-mediated attack on the nicotinic AChR or muscle-specific tyrosine kinase that affects communication between the motor neuron and the innervated muscle. Can occur at any age but peak incidence is young adulthood. The exact mechanism is unclear but it is thought to be caused by sensitized helper T cells and an antibody-directed attack on the acetylcholine receptor in the neuromuscular junction. The antibody attack leads to a shedding of the acetylcholine receptor-rich terminal portions of the folds in the end plate of the muscle fiber, fewer receptors, and a widened synaptic space that impairs signal transmission. The antibodies do not directly block the binding.  The neuromuscular junction serves as a synapse between a motor neuron and a skeletal muscle fiber. The transmission of impulses at the neuromuscular junction is mediated by the release of the neurotransmitter acetylcholine from the axon terminals. Acetylcholine binds to the specific receptors in the end-plate region of the muscle fiber surface to cause muscle contraction. 38. Chapter 15. Disorders of Motor Function: Multiple Sclerosis. Clinical manifestations and Course. Multiple sclerosis is characterized by inflammation and destruction of mostly the white matter of the CNS myelin of the brain, spinal cord, and optic nerve. The peripheral nervous system is spared, and there is usually no evidence of an associated systemic disease. The lesions of MS consist of hard, sharp-edged, demyelinated patches that are visible throughout the white matter as well as sometimes the gray matter of the CNS. Areas commonly affected by MS are the optic nerve, corticobulbar tracts (speech and swallowing), corticospinal tracts (muscle strength), cerebellar tracts (gait and coordination), spinocerebellar tracts (balance), medial longitudinal fasciculus (conjugate gaze function of the extraocular eye muscles), and posterior cell columns of the spinal cord (position and vibratory sensation). Usually presents with an acute or subacute episode of parathesias, optic neuritis, diplopia, or specific types of gaze paralysis. Other common symptoms are abnormal gait, bladder and sexual dysfunction, vertigo, nystagmus, fatigue, and speech disturbance. These symptoms usually last for days to weeks and then completely or partially resolve. Four categories of the disease: Relapsing-remitting, secondary progressive, primary progressive, or progressive relapsing. 39. Chapter 15. Disorders of the cerebellum and basal ganglia: Parkinson’s Disease Degenerative disorder of basal ganglia function that results in variable combinations of tremor, rigidity, akinesia/bradykinesia, and postural changes. Characterized by progressive destruction of the nigrostriatal pathway with subsequent reduction in striatal concentrations of dopamine. Mean onset is 57 years old. Because the basal ganglia also influence the autonomic nervous system, people with Parkinson disease often have excessive sweating, sebaceous gland secretion, and salivation. Cognitive dysfunction may also be present. Treatment must be highly individualized. No treatment will prevent the disease progression, only symptom management. Botulinum toxin injections may be used in the treatment of dystonias such as eyelid spasm and limb dystonias. Antiparkinson drugs act by increasing the functional ability of the underactive dopaminergic system or by reducing the excessive influence of excitatory cholinergic neurons. 40. Chapter 16. Mechanisms of Brain Injury. Primary and Secondary Brain Injuries. Primary brain injuries: Damage is caused by impact. Include focal (contusion, laceration, hemorrhage) or diffuse (concussion, diffuse axonal injury). Secondary brain injuries: damage results from the subsequent brain swelling, infection, or cerebral hypoxia. Most common cause is ischemia. Hematomas. Subdural, acute vs chronic subdural hematomas. Hematomas: Result from vascular injury and bleeding. Epidural Hematoma: usually caused by head injury in which the temporal area of the skull is fractured. Develops between the inner table of the bones of the skull and the dura. Usually results from a tear in an artery associated with a skull fracture. More common in younger people because the dura is less firmly attached to the skull surface than in an older person. Traumatic Intracerebral Hematomas: single or multiple. Occur in any lobe of the brain but are most common in the frontal or temporal lobes, related to the bony prominences on the inner skull surface. Subdural: Develops in the area between the dura and the arachnoid (subdural space) and usually is the result of a tear in the small bridging veins that connect veins on the surface of the cortex to dural sinuses. These veins are snapped in head injury when the brain moves suddenly in relation to the skull. Acute: Acute subdural hematomas progress rapidly and have a high mortality rate because of the severe secondary injuries related to edema and increased ICP. Chronic: Symptoms of chronic subdural hematoma develop weeks after a head injury, so much later that the person may not remember having a head injury. More common in alcoholics and older adults because brain atrophy causes the brain to shrink away from the dura and stretch fragile bridging veins. 41. Chapter 16. Mechanisms of Brain Injury. Stroke. Ischemic vs hemorrhagic. Ischemic: Caused by cerebrovascular obstruction by thrombosis or emboli. Five main mechanisms of stroke subtypes and their frequency: 20% large artery thrombosis (atherosclerotic disease), 25% small penetrating artery thrombosis disease (lacunar stroke), 20% cardiogenic embolism, 30% cryptogenic stroke (undetermined cause), and 5% other. Hemorrhagic: Most frequently fatal stroke results from the spontaneous rupture of a cerebral blood vessel. Common predisposing factors are advancing age and hypertension. Vomiting commonly occurs at onset, and headache occurs after. 42. Chapter 16. Disorders of Brain Function/Cerebrovascular Disease/Stroke. Clinical Manifestations. Specific manifestations are determined by the cerebral artery that is affected, by the area of brain tissue that is supplied by that vessel, and by the adequacy of the collateral circulation. Always sudden in onset and focal and usually are one sided. Most common symptoms are a facial droop, arm weakness, and slurred speech. Other frequent symptoms are unilateral numbness, vision loss in 1 eye or to 1 side, language disturbance, and sudden unexplained imbalance or ataxia. 43. Chapter 18. Neurocognitive Disorders: Alzheimer’s Disease. Diagnosis and treatment. See chap 18 ppt and page 534. A diagnosis of alzheimers can only be confirmed by microscopic examination of tissue obtained from a cerebral biopsy or at autopsy. The diagnosis is based on clinical findings. Neuroimaging and metabolic screening are important steps in excluding other conditions when diagnosing. There is no curative treatment for AD. Medications may slow the progression and improve depression, agitation, or sleep disorders. Cholinesterase inhibitors have been shown to be effective in slowing the progression of the disease by potentiating the action of available acetylcholine and inhibiting acetylcholinesterase. Antipsychotics are not approved for using in treating agitation. Two major goals of care are maintaining socialization and providing support for caregivers. 44. Chapter 15. Disorders of the motor unit/Polyneuropathies: Guillain-Barre Syndrome. Cause, clinical manifestations, and treatment. Guillain-Barre syndrome is an acute immune-mediated polyneuropathy. The syndrome defines a clinical entity that is characterized by rapidly progressive ascending symmetrical limb weakness and loss of tendon reflexes. Most common cause of acute, flaccid nontraumatic paralysis. Manifested by infiltration of mononuclear cells around the capillaries of the peripheral neurons, edema of the endoneurial compartment, and demyelination of ventral spinal roots. Cause probably has an immune component. Most people report an acute, influenza-like illness before the onset of symptoms. Clinical manifestations include progressive ascending muscle weakness of the limbs, producing a flaccid paralysis. Parasthesia and numbness often accompany the loss of motor function. Paralysis will progress to involve the respiratory muscles. Treatment includes support of vital functions and prevention of complications such as skin breakdown and thrombophlebitis. Treatment is most effective if initiated early in the course of the disease. Plasmapheresis and high-dose intravenous immunoglobulin therapy and generally the mainstay of treatment. 45. Chapter 18. Neurocognitive Disorders: Schizophrenia-neurophysiology of symptoms. Page 530. The complete set of pathogenic mechanisms underlying schizophrenia is not clear. Research suggest that changes in the dysregulation of the dopamine and serotonergic system and other neurotransmitter changes such as decreased glutamate activity through dysfunction of its N-methyl- Daspartate receptor play a role. Many of the symptoms of impaired cognition seen in schizophrenia are through to be tied to deficits in GABA. Neuroimaging suggests several functional abnormalities occur which include loss of cortical gray matter, abnormal cortical thinning, reduced numbers of synaptic structures on neurons, reduced dendritic spine density of pyramidal neurons in the prefrontal cortex, and arrested migration of hippocampal neurons. 46. Chapter 18. Neurocognitive Disorders: Mood disorders-neurophysiology of symptoms. Page 531. Epidemiologic and neurobiologic studies suggest interactions between biologic and psychosocial factors over time explain the risk of developing MDD. Multiple possible biologic theories have been identified in the development of depressive disorder including inflammation, HPA axis hyperactivity, low levels of neurotrophic growth factor, and low levels of vitamin D. Growing evidence supports some forms of depression may be linked to ongoing inflammation in the body. Neuroimaging indicates smaller hippocampal volumes and hippocampal hypertrophy in people who have depression and have experienced early abuse. Neurologic disorders of the limbic system and basal ganglia are also involved in the development of mood disorders. Dopamine plays a role in depression. Unit 6. Disorders of Special Sensory Function. Chapters 19, 20. There are 4 questions from this unit. 47. Disorders of Eye Movement. Begins on p. 577. Strabismus vs amblyopia: differences in presentation. Strabismus (squint) refers to any abnormality of eye coordination or alignment that results in loss of binocular vision. When images from the same spots in the visual space do not fall on corresponding points of the two retinas, diplopia (double vision) occurs. May be divided into two forms: nonparalytic forms (concomitant) where there is no primary muscle impairement, and paralytic (nonconcomitant) in which there is weakness or paralysis of one or more of the extraocular muscles. Called intermitted, or periodic, when there are periods in which the eyes are parallel. Amblyopia: Sometimes called lazy eye. Decrease in visual acuity resulting from abnormal visual development in infancy or early childhood. Vision loss ranges from mild (worse than 20/25) to severe (legal blindness, 20/200 or worse). 48. Disorders of the Conjunctiva. Begins on p. 550. Compare the clinical manifestation of allergic, viral, and bacterial conjunctivitis. 1. Allergic: Usually characterized by itching. Bilateral tearing, itching, and redness of the eye. Treatment includes allergen avoidance, use of cold compresses, eye washes with tear substitute, and oral antihistamines. 2. Viral: Common cause is adenovirus. Symptoms include generalized conjunctival hyperemia, copious tearing, and minimal exudate. Usually associated with upper respiratory tract infection. Usually resolves over time with use of cool compresses and artificial tears. Topical antivirals are not recommended. 3. Bacterial: Burning, tearing, mucopurulent or purulent discharge. Normally begins in one eye and within 24 to 48 hours it speards to the unaffected eye. Drainage may be green, white, or yellow. Treatment includes antibiotic drops or ointments. N. gonorrhoeae is the most serious form of conjunctivitis than can lead to corneal ulceration/perforation and permanent blindness if not treated; symptoms include conjunctival redness, chemosis (swelling around the cornea), lid swelling, and tender/swollen periauricular lymph nodes. How can tell one from the other Diagnostically? 49. Disorders of the Retina. Page 581. DISORDERS OF THE RETINAL BLOOD SUPPLY 1. The blood supply for the retina is derived from the central retinal artery, which supplies blood flow for the entire inside of the retina, and from vessels in the choroid, which supply the rods and cones. 2. The retinopathies, which are disorders of the retinal vessels, interrupt blood flow to the visual receptors, leading to visual impairment. 3. Retinal detachment separates the visual receptors from the choroid, which provides their major blood supply. 4. Functioning of the retina, like that of other cellular portions of the CNS, depends on an oxygen supply from the vascular system. One of the earliest signs of decreased perfusion pressure in the head region is a graying-out or blackout of vision, which usually precedes loss of consciousness. This can occur during large increases in intrathoracic pressure, which interfere with the return of venous blood to the heart, as occurs with the Valsalva maneuver, with systemic hypotension, and during sudden postural changes (e.g., postural hypotension) 5. Ischemia of the retina occurs during general circulatory collapse. If a person survives cardiopulmonary arrest, for instance, permanently decreased visual acuity can occur as a result of edema and the ischemic death of retinal neurons. This is followed by primary optic nerve atrophy proportional to the extent of ganglionic cell death. The ophthalmic artery, the source of the central artery of the retina, takes its origin from the internal carotid artery (Capriotti, 2020). Intermittent retinal ischemia can accompany internal carotid or common carotid stenosis. Amaurosis fugax is characterized by transient episodes of monocular visual loss lasting 5 to 10 minutes (Capriotti, 2020). People with the disorder often describe a curtain coming down from Diabetic Retinopathy. Diabetic retinopathy is the most common cause of blindness in the industrialized countries of the world. It ranks first as the cause of newly reported cases of blindness in people between the ages of 20 and 74 years (Wykoff et al., 2021). Advances in treatment have greatly reduced the risk of blindness from diabetes, but because diabetes is so common, retinopathy remains an important cause of visual impairment. 6. Diabetic retinopathy can be divided into two types: nonproliferative (i.e., background) and proliferative (Capriotti, 2020; Drinkwater et al., 2021; Wykoff et al., 2021). Background or nonproliferative retinopathy is confined to the retina. It involves engorgement of the retinal veins, thickening of the capillary endothelial basement membrane, and development of capillary microaneurysms (Fig. 19.18A). Small intraretinal hemorrhages may develop and microinfarcts may cause cotton-wool spots and leakage of exudates. A sensation of glare (because of the scattering of light) is a common complaint. The most common cause of decreased vision in people with background retinopathy is macular edema. The edema is caused primarily by the breakdown of the inner blood–retina barrier at the level of the capillary endothelium, allowing leakage of fluid and plasma constituents into the surrounding retina. 7. Hypertensive Retinopathy.  a. As with other blood vessels in the body, the retinal vessels undergo changes in response to chronically elevated blood pressure. b. In the initial, vasoconstrictor stage, there is vasospasm and an increase in retinal arterial tone because of local autoregulatory mechanisms. i. On ophthalmoscopy, this stage is represented by a general narrowing of the retinal arterioles. ii. Persistently elevated blood pressure results in the compensatory thickening of arteriolar walls, which effectively reduces capillary perfusion pressure. c. These changes are manifested in the retina by i. microaneurysms, ii. intraretinal hemorrhages, iii. hard exudates, and 1. cotton-wool spots. d. Swelling of the optic disc may occur at this stage and usually indicates severely elevated blood pressure (malignant hypertension). e. Older adults often have more rigid vessels that are unable to respond to the same degree as those in younger people. 8. Retinal Detachment a. Retinal detachment involves the separation of the neurosensory retina from the pigment epithelium (Fig. 19.19). It occurs when traction on the inner sensory layer or a tear in this layer allows fluid, usually vitreous, to accumulate between the two layers (Capriotti, 2020). There are four types of retinal detachments: exudative, traction, rhegmatogenous, and combined traction/rhegmatogenous (Capriotti, 2020). 9. Assessing Papilledema and its significance. 1. Funduscopic examination of the eye with an ophthalmoscope provides an opportunity to examine the retinal blood vessels and other aspects of the retina (Fig. 19.16). 2. Because the retina is an embryonic outgrowth of the brain and the blood vessels are to a considerable extent representative of brain blood vessels, the ophthalmoscopic examination of the fundus of the eye permits the study and diagnosis of metabolic and vascular diseases of the brain as well as pathologic processes that are specific to the retina. 50. Disorders of Hearing and Vestibular Function: Otitis Media-Clinical Manifestations 1. Acute onset of otalgia (pulling of the ears in an infant) that may interfere with sleep and/or activity, fever (>39), irritability, otorrhea, hearing loss, evidence of middle ear inflammation, middle ear effusion (decreases mobility of the tympanic membrane). 2. Children older than 3 may have rhinorrhea, vomiting, and diarrhea. 3. Ear pain usually increases as the effusion accumulates behind the tympanic membrane. Perforation of the tympanic membrane may occur acutely, allowing purulent material from the eustachian tube to drain into the external auditory canal.  4. Otitis media with effusion symptoms: Complaint of intermittent ear pain, sensation of fullness in ear, complaint of hearing loss, dizziness, decreased tympanic membrane mobility, visible air- fluid level with or without bubble. 51. Disorders of Hearing and Vestibular Function: Otitis Media-Risk Factors. Page 589. 1. May occur in any age group, but is more frequently diagnosed in children between the ages of 3 months and 3 years. Smoking in the house is a significant risk factor. Other risk factors include prematurity, daycare attendance, having an unimmunized status, bottle-feeding, feeding in the supine position, being overweight or obese, a family history of otitis media, being male, and sharing a bedroom. More frequent in children with craniofacial anomalies or congenital syndromes associated with craniofacial abnormalities. 2. Strucutural immaturity contributes to the increased risk because the eustachian tube is shorter and more horizontal, and it can spread more easily through the eustachian canal of infants who spend most of their day supine. To reduce the risk of contracting otitis media: routine childhood vaccinations against pneumococci and flu, elimination of household smoking, exclusive breast- feeding until 6 months of age, avoiding of feeding while lying down and propping bottles, use of xylitol, and selecting daycare facilities with small staff-to-child ratio.