Exam 5 Study Guide - PDF

DeM/S  Define differences between bone cells Osteoblast: bone forming cells  “bone makers”  Derived from mesenchymal cells  Produce osteocalcin when stimulated by vitamin D  Form new bone o Synthesize osteoid  Which brings on the formation of new bone  Non-mineralized bone matrix  Follow Wol...

DeM/S  Define differences between bone cells Osteoblast: bone forming cells  “bone makers”  Derived from mesenchymal cells  Produce osteocalcin when stimulated by vitamin D  Form new bone o Synthesize osteoid  Which brings on the formation of new bone  Non-mineralized bone matrix  Follow Wolfe’s law  bone is shaped according to its function  Become osteocytes that are imbedded in bone Osteocytes: bone maintaining  Develop dendritic processes that extend to either the bone surface or the bone’s vascular space  Help maintain bone by signaling osteoblasts and osteoclasts to form and reabsorb  Coordinate osteoblast and osteoclast functions  Respond to parathyroid hormone Osteoclasts: bone resorbing  “bone breakers”  Large multinucleated cells.  Attached to integrins by podosomes (help bind to bone)  Cause resorption of bone by secretion of hydrochloric acid (HCl) and a protease enzyme which help dissolve bone minerals and collagenase.  Cells are “resting” when not resorbing o Once resorption is complete then disappears by degeneration reverting back to its parent cell or leaving the site = “resting osteoclast”  Understand difference between compact and spongy bone Compact Bone:  Also called cortical bone.  85% of the skeleton  Solid and extremely strong  Haversian system o Basic structural unit in compact bone Spongy Bone:  Also called cancellous bone  15% of the skeleton  Filled with red bone marrow  Lacks Haversian system  Trabeculae: plates or bars o Instead of Haversian system  Understand basics of bone remodeling and bone repair Bone Repair: bone heals itself  Hematoma formation  clot forms  Procallus formation  produces granulation tissue  Callus formation  replaces the callus with lamellar bone or trabecular bone  Remodeling  periosteal and endosteal surfaces are remodeled to the size and shape of the bone before the injury   Remodeling:  Bone-remodeling units  Repair of microscopic injuries and maintenance of bone integrity  Phaseso Activation of the remodeling cycle o Resorption o Formation of new bone (secondary bone)  Takes 3-4 months Describe different joint classifications Joints: are the sites where two or more bones meet  Promote stability and mobility of the skeleton  Help move bones and muscles  Classifications based on movement: o Synarthrosis- immovable o Amphiarthrosis- slightly movable o Diarthrosis- freely movable  Classifications based on structure: o Fibrous Joints- directly united to bone by dense fibrous connective tissue  Usually synarthroses (immovable)  However, many fibrous joints allow some movement  Degree of movement depends on the distance between the bones and the flexibility of the fibrous connective tissue  Ex: sutures o Cartilaginous Joints- connected by fibrocartilage or hyaline cartilage  Symphysis  bones are united by a pad or disk of fibrocartilage  Examples: symphysis pubis and intervertebral disks  Synchondrosis  bones are united by hyaline cartilage (costal cartilage)  Examples: joints between the ribs and the sternum o Synovial Joints- most movable, most complex, diarthrosis  Fibrous joint capsule  articular capsule  Synovial membrane  lines the inner surface of the joint capsule  Articular cartilage covers and pads the articulating bony surfaces. o Articular Cartilage Hyaline cartilage covers the end of each bone  Reduces friction in the joint and distributes forces of weight bearing  Has no blood vessels, lymph vessels, or nerves  Is insensitive to pain and regenerates slowly after injury o Proteoglycans Act as a pump  Permit enough fluid to be pressed out to ensure that a fluid film is always present on the surface of the cartilage, even after hours of weight bearing Define muscle fiber differences and types Muscle Fiber o Each muscle fiber is a single muscle cell  Surrounded by a membrane capable of excitation and impulse propagation o White Muscle (Type II fibers): Fast o Red Muscle (Type I fibers): Slow o Myofibrilsfunctional units of contractions o Muscle Membrane Sarcolemma: propagates impulse  Basement membrane: maintains cell’s shape Understand basics of muscle contraction Muscle Contraction  Function of muscle : to accomplish work  Ryanodine receptors (RyRs): primary ion channels that control calcium release in muscles o RyR1: skeletal muscle o RyR2: cardiac muscle o RyR3: diaphragm smooth muscle, and brain  Phases: o Excitation The spread of action potential from the nerve terminal to the neuromuscular junction  Initiates an electrical impulse; muscle fiber action potential  Triggers voltage-sensitive receptors in the t-tubule wall, opening RyR channels and releasing calcium o Coupling Release of calcium leaves actin free to bind with myosin o Contraction Thin filament, actin, then slides toward the thick filament, myosin, forming a cross-bridge that causes muscle to shorten (cross-bridge theory)  “all or nothing” principle applies o Relaxation Cross-bridge detaches, and a sarcomere lengthens as calcium is pumped back into the sarcoplasmic reticulum Understand basics of types of muscle contraction and muscle movement Types of Muscle Contraction Isometric Contraction: o Static or holding contraction o Muscle maintains a constant length as tension is increased o Muscle contracts, but the limb does not move Isotonic Contraction: o Lengthening (eccentric) or shortening (concentric) contraction o Muscle maintains a constant tension as it moves o Muscle contracts and the limb moves        Movement of Muscle Groups  Agonist: o Prime mover o Contracts  Antagonist: o Reciprocal muscle o relaxes Describe what happens with aging of the m/s system Aging of the Musculoskeletal System  Bones: o Loss of bone o Stiff, brittle, decreased strength o Lengthened bone remodel time o Slow mineralization o Evidence of osteoporosis o Increased bone resorption  Joints: o Cartilage- more rigid, fragile, stiff o Range of motion- decreased  Muscles: o Apoptosis of muscle cells o Sarcopenia- age related loss of muscles from loss of satellite cells o Decreased muscle strength and bulk o Reduced oxygen intake, basal metabolic rate, and lean body mass  Exercise in older adults: o Improves muscle strength o Helps increase bone mineral density o Improves balance, coordination, and mobility o Improves lean body mass o Decreases the risk for falls Define types of fractures and in which populations they are most prevalent Types of Fractures  Complete: bone is broken all the way through  Incomplete: bone is damaged but still is one piece o Closed or simple (complete or incomplete) skin is intact o Open or compound (complete or incomplete) skin is broken  Comminuted: bone breaks into more than two fragments  Linear: fracture runs parallel to the long axis of the bone  Oblique: fracture of the shaft of the bone is slanted  Spiral: encircles the bone  Transverse: occurs straight across the bone  Greenstick: perforates one cortex and splinters the spongy bone  Torus: cortex buckles but does not break  Bowing: longitudinal force is applied to a bone  Pathologic: break occurs at the site of pre-existing abnormality    Stress: fatigue and insufficiency; transchondral Understand basic patho of bone fracture Bone Fracture  Broken bone can damage the surrounding tissue, periosteum, and blood vessels in the cortex and marrow  Bone is unique: after a fracture it will heal with normal tissue, not scar tissue  Healing occurs in phases: o Inflammatory phase Lasts 3-4 days  Bone tissue destruction  Triggers and inflammatory response  Hematoma formation o Repair phase Lasts several days  Capillary ingrowth, mononuclear cells, and fibroblasts transforms hematoma into granulation tissue  Osteoblasts within the pro-callus synthesize collagen and matrix to form callus o Remodeling phase Lasts months to years  Unnecessary callus is resorbed, and trabeculae are formed  At the end, bone can withstand normal stresses  Improper reduction or immobilization o Nonunion  Failure of the bone ends to grow together  Gap between ends of the bone fills with dense fibrous and fibrocartilaginous tissue  Occasionally, fibrous tissue contains a fluid-filled space that resembles a joint: referred to as false joint or a pseudarthrosis o Delayed union  Does not occur until approximately 8-9 months after a fracture o Malunion  Healing of the bone in a nonanatomic position Describe Support structure injuries, subluxation, and dislocation Support Structure Injuries  Strain: tear or injury to a tendon (fibrous connective tissue that attaches skeletal muscle to bone.  Sprain: tear or injury to a ligament (fibrous connective tissue that connects bones)  Avulsion: complete separation of a tendon or ligament from its bony attachment site Dislocation  Temporary displacement of bone from its joint Subluxation  Contract between the bones in the joint only partially lost Associated with fractures, muscle imbalance, rheumatoid arthritis, other joint instability     Clinical manifestations: pain, swelling, limitation of motion, joint deformity Describe Epicondylitis, tendinopathy, bursitis Epicondylitis  Inflammation of a tendon where it attaches to a bone o Tennis elbow lateral epicondylitis o Golfer’s elbow medial epicondylitis Tendinopathy  Tendinitis inflammation of a tendon  Tendinosis painful degradation of collagen fibers Bursitis  Inflammation of a bursa o Sacs lined with synovial membrane and filled with synovial fluid; sacs (bursa) are located among the tendons, muscles, and bony prominences Define Myositis ossificans –patho and manifestations Myositis Ossificans (heterotopic ossification)  Complication of local muscle injury  A reaction to a bruise in muscle that has been injured. During the healing process of the bruise, calcium can become deposited in the bruise causing a hard bone like structure within the muscle o It is known to happen more often in athletes with repetitive trauma to the same area before the bruise muscle has appropriate time to heal.  “Rider’s bone” in equestrians  “Drill bone” in infantry soldiers  Thigh muscles in football players  clinical manifestations: o unusually slow recovery from a contusion injury o pain and range of movement often improve in the first few weeks after an injury, however, as bone is gradually formed in the muscle, the pain and muscle stiffness worsen. Define Rhabdomyolysis – patho, manifestations Rhabdomyolysis  Life threatening complication of severe muscle trauma with muscle cell loss o Crush syndrome (most severe) vs. crush injuries o Compartment syndromes  Rapid breakdown of muscle that causes the release of intracellular contents o Protein pigment myoglobin into extracellular space and bloodstream  Classic Triad o Muscle pain o Weakness o Dark urine (from myoglobin) Define Compartment syndrome patho and manifestations Compartment Syndrome  Complication of fractures o Blood flow to affected area is compromised because of increased venous pressure, leading to decreased arterial inflow, ischemia, and edema  Clinical manifestations (5Ps)   o Pain: out of proportion to the injury o Paresthesia (a burning or prickling sensation) o Pallor o Pulselessness o Paralysis (late sign) Describe Osteoporosis – Basic opg/rankl/rank system, patho and manifestations, be able to describe risk factors and different causes Osteoporosis  Reduced bone mass or density and an imbalance of bone resorption and formation  40.5 C (104.9 F)  cardiovascular and thermoregulatory centers may cease functioning with higher temperatures  heat loss through the evaporation of sweat creases, core temperature increases rapidly  high core temperatures and vascular collapse produce o cerebral edema o degeneration of the CNS o swollen dendrites o renal tubular necrosis o death results unless immediate, effective treatment is initiated rapid peripheral cooling will cause peripheral vasoconstriction and limit core cooling  clinical manifestations: o confusion, altered mental status, slurred speech o loss of consciousness (coma) o hot, dry skin or profuse sweating o seizures o very high body temperature 20. Sleep; phases basics, sleep cycle, OSAS, patho and manifestations Sleep  Active, multiphase process  Hypothalamus is the major sleep center o Suprachiasmatic nucleus (SCN)  Controls the timing of the sleep-wake cycle o Hypocreatins (ovexins)  Promote wakefulness and REM sleep  Two phases: o Rapid eye movement (REM) sleep  REM is 20% to 25% of sleep time  Also known as paradoxic sleep  Vivid dreaming occurs during REM  Controlled by mechanisms in the hypothalamus and pontine reticular formation  occurs every 90 minutes, beginning after 1-2 hours of sleep o Non-rapid eye movement (NREM) sleep—slow wave  NREM is 75% to 80% of sleep time  Initiated by the withdrawal of neurotransmitters from the reticular formation and by the inhibition of arousal mechanisms in the cerebral cortex  Stages: evaluated by electroencephalography (EEG)  N1- light sleep, 3% to 8% of sleep time  N2- longest sleep, 45% to 55% of sleep time  N3- slow-wave sleep, 15% to 20% of sleep time  Is restorative and reparative; growth processes occur during slowwave sleep o Each of which has its own series of stages o While asleep individuals progress through the four stages of NREM sleep and REM sleep in predictable cycle Sleep Cycle  Predictable cycle while asleep, individual progresses through REM and NREM sleep  First cycle of the night begins with stage N1  Individual progress through N2, N3, and REM sleep  A new cycle begins with stage N2, follows each REM sleep  With each successive cycle the amount of time spent in stage N3 sleep decreases and time spent in REM sleep increases   Awakened individual begins the next cycle at stage N1 Obstructive Sleep Apnea (OSAS)  Disorder of breathing during sleep, related to upper airway obstruction and is associated with reduced blood oxygen saturation and hypercapnia o Risk factors obesity, male gender, and age o Characterized by repetitive increases in resistance to airflow within the upper airway with loud snoring, gasping, intervals of apnea lasting 10-30 seconds, fragmented sleep, and chronic daytime sleepiness o Obstruction caused by soft palate or base of tongue or both collapsing against the pharyngeal walls because of decreased muscle tone especially during REM sleep o Level of negative intrathoracic pressure is most likely stimulus for arousal o Potentially fatal systemic illnesses are associated  Hypertension, pulmonary hypotension, heart failure, nocturnal cardiac dysrhythmias, myocardial infarction, and ischemic stroke o Combination of intermittent hypoxia and hypercapnia, arousals, increased sympathetic tone, altered baroreflex control during sleep, CV changes induced by negative intrathoracic pressure contribute to these complications o Commonly associated with fatigue, decline in cognitive functions, car accidents, and poor work performance 21. Describe basic patho and clinical manifestations of Age Related Macular degeneration Age Related Macular Degeneration (AMD)  Drusen or retinal waste products accumulate in the deep retinal layers  An eye disease that can blur your central vision  Happens when aging causes damage to the macula (the part of the eye that controls sharp, straight-ahead vision)  Two types: o Dry AMD (atrophic AMD)- involves loss of retinal pigment epithelium photoreceptors with overall atrophy of cells  Happens in 3 stages early, intermediate, and late  Usually progresses slowly over years  There’s no treatment for late dry AMD, but you can find ways to make the most of your remaining vision  If you have late dry AMD only in 1 eye, you can take steps to protect your other eye o Wet AMD (neovascular AMD)- when abnormal blood vessels grow in the back of the eye and damage the macula; vessels leak and bleed causing retinal detachment  Less common type of late AMD  Usually causes faster vision loss  Any stage of dry AMD can turn to wet AMD, but wet AMD is always late stage  Treatment options available  Clinical manifestations: o Early dry AMD no symptoms o Intermediate dry AMD some have no symptoms; others may notice mild symptoms like mild blurriness in their central vision or trouble seeing in low lighting o Late AMD (wet or dry) straight lines start to look wavy or crooked; blurry area near the center of vision, over time this blurry area may get bigger or may see blank spots; colors may seem less bright than before and may have more trouble seeing in low lighting. 22. Define Glaucoma; basic patho and clinical manifestations Glaucoma  Intraocular pressures above the normal pressures of 12 to 20 mmHg are maintained by the aqueous fluid  Increased pressure that compresses and damages the optic nerve  Clinical manifestations: o Eye pain, pressures o Headaches o Rainbow-colored halos around lights o Low vision, blurred vision, narrowed vision (tunnel vision), or blind spots o Nausea and vomiting 23. Differentiate between Types of hearing loss Types of Hearing Loss  Conductive hearing loss: o Impaired sound conduction from the outer to inner ear  Sensorineural hearing loss: o Impairment of the organ of corti or its central connections o Presbycusis age related hearing loss  Usually in high frequencies  Mixed hearing loss: o Caused by combo of conductive and sensorineural losses  Functional hearing loss: o Occurs for no organic reason o Thought to be caused by emotional or psychologic factors  Tinnitus ringing of the ears 24. Describe Vertigo; basic patho Vertigo  Sensation of spinning that occurs with inflammation of the ear’s semicircular canals 25. Differentiate between Arousal vs awareness Arousal  State of being awake  Mediated by the reticular-activating system Awareness  Cognitive functions that embody awareness of self, environment, and affective states (moods)  Content of thought 26. Define Coma Coma  No verbal response to the external environment or to any stimuli; noxious stimuli such as deep pain or suctioning yields motor movement  Coma is produced by either: o bilateral hemisphere damage or suppression  by means of metabolic derangement; hypoxia, hypoglycemia, uremia, or toxins (ammonia from liver failure o brainstem lesions or metabolic derangement that damages or suppresses the reticular activating system 27. Differentiate between Brain and cerebral death Brain Death  Brain has no potential for recovery and can no longer maintain the body’s internal homeostasis  State laws: o Entire brain, brainstem, and cerebellum stops functioning o Brain is autolyzing (self digesting) or has already autolyzed on postmortem examination Cerebral Death  Death of the cerebral hemisphere is exclusive of the brainstem and cerebellum  Brainstem may continue to maintain homeostasis (normal respiratory and cardiovascular functions, temperature control, and gastrointestinal function) 28. Describe Seizure; types, patho, manifestations Seizure Disorders  Resting potential instability  Seizure initiation o Bursts of action potentials  Produced by long-lasting depolarization of neuron caused by influx of extracellular calcium that opens then voltage-dependent sodium channels o Hypersynchronization  Clinical manifestations: o Depends on type of seizure o Aura  Partial seizure experienced as a peculiar sensation preceding the onset of a generalize seizure or complex partial seizure that may take the form of gustatory, visual, or auditory experience o Prodromal  Early clinical manifestations malaise, headache, or a sense of depression, may occur hours to few days before onset of seizure o Tonic phasecontraction o Clonic phase relaxation o Postictal phase period immediately following the cessation of seizure activity  Types :  Generalized Seizures : neurons bilaterally o eg. Absent, myoclonic, clonic, tonic-clonic, atonic  Partial (focal) Seizures: neurons unilaterally o Begins in specific region of the cortex o Eg. Simple, complete  Status Epilepticus: o A medical emergency o A state of continuous seizures lasting more than 5 minutes or second seizure is experienced before the person has fully regained consciousness from the preceding seizure, or a single seizure lasts longer than 30 minutes Seizure: a sudden, transient alteration of brain function caused by an abrupt explosive, disorderly discharge of cerebral neurons Epilepsy: a recurrence of seizures and a disorder for which no cause can be found Convulsion: tonic-clonic (jerky, contract-relax) movements associated with some seizures. Causes:  Epilepsy, metabolic disorders, infection, fever  Acute alcohol withdrawal, brain trauma, congenital defects  Electrolyte disturbances, brain tumor, vascular problems 29. Differentiate between Broca vs. Wernicke Wernicke Dysphagia  Disturbance in understanding all language; verbal and reading comprehension Broca Aphasia  Expressive dysphagia of speech and writing, but with retention of comprehension 30. Describe each and differentiate between Delirium and dementia Delirium (hyperkinetic confusional state)  Associated with right middle temporal gyrus or left temporo-occipital junction disruption  Acute state of brain dysfunction  Onset is usually abrupt  Autonomic nervous system is overactive  Common in critical care units, postsurgical, or during withdrawal of CNS depressants (eg. Alcohol, narcotics, etc)  Clinical manifestations: o Early difficulty in concentrating, restlessness, irritability, insomnia, tremulousness (trembling), poor appetite o Typically resolves suddenly or gradually in 2-3 day Dementia  Progressive failure of cerebral functions that is not caused by impaired level of consciousness  Onset is usually gradual  Progressive dementias produce nerve cell degeneration and brain atrophy  Age is the greatest risk factor  Losses: o Orientation o Memory (most commonly lost) o Language o Judgement o Decision making 31. Discuss Alzheimer disease patho and manifestations Alzheimer  One of the most common causes of severe cognitive dysfunction in older adults  Familial, early and late onset  Nonhereditary (sporadic, late onset)  Exact cause of Alzheimer disease is unknown  Clinical manifestations: o Forgetfulness o Emotional upset o Disorientation o Confusion o Lack of concentration o Decline in abstraction, problem solving, and judgement  Diagnosis is made by ruling out other causes of dementia; definitive diagnosis only postmortem exam 32. Discuss Basics of herniation syndromes Herniation Syndromes  33. Describe Types of cerebral edema Cerebral Edema  Increase in the fluid (intracellular or extracellular) within the brain  Harmful effects are cause by distortion of blood vessels, displacement of brain tissues, and eventual herniation of brain tissue from one compartment to another  Results from infection, hemorrhage, tumor, ischemia, infarct, or hypoxia  Types of Cerebral Edema o Vasogenic: most clinically important  Caused by increased permeability of the capillary endothelium of the brain after injury to the vascular structure  Results in disruption of blood-brain barrier o Cytotoxic: metabolic  Toxic factors directly affect the cellular elements of the brain parenchyma causing failure of the active transport system  Blood brain barrier not disrupted  Cells swell by loss of potassium and gain of sodium with water following sodium o Interstitial: seen most commonly with non-communicating hydrocephalus  Caused by transependymal movement of CSF from the ventricles into the extracellular spaces of brain tissues 34. Understand Basics of hydrocephalus, communicating and noncommunicating Hydrocephalus Excess fluid within the cranial vault, subarachnoid space, or both Caused by interference in CSF flow o Decreased reabsorption  blockage of arachnoid villi (absorption) from SAH or infection o Increased fluid production  Choroid plexus tumor o Obstruction within the ventricular system  Tumor or congenital malformation Arnold-Chiari  S/S of ICP o cushing triad = HTN, bradycardia, irregular respirations  Communicating (extraventricular) Hydrocephalus o From impaired absorption o CSF can flow through ventricles o Blockage can occur once CSF leaves the ventricles, most commonly at the arachnoid villi therefore affecting absorption  Most common cause subarachnoid hemorrhage, developmental malformation, head injury, neoplasm o Normal pressure hydrocephalus  Occurs mostly in middle aged people  Long term presentation: memory decline, gait disturbance, and incontinence  Noncommunicating Hydrocephalus o Internal o Intraventricular  Blockage occurs along narrow pathways that connect the ventricular system o Common causes:  Congenital abnormality or mass lesions compress one of the structures of the ventricular system  Most common narrowing of the aqueduct of Sylvius “aqueductal stenosis” (between 3rd and 4th ventricle) 35. Differentiate Paresis vs paralysis Paresis  Person can still move the affected muscle or muscles, however, these movements are weaker than normal Paralysis  Person is unable to move affected muscle or muscle group at all.   36. Differentiate Upper vs lower motor neuron syndromes Upper Motor Neuron Syndromes (spastic paresis or paralysis)  Hemiparesis or hemiplegia upper and lower extremities on one side  Paraparesis or paraplegia affects lower extremities  Quadriparesis or quadriplegia all 4 extremities  Upper motor neuron syndromes usually associated with hyperreflexia  spinal shock- complete cessation of spinal cord functions below the lesion o complete flaccid paralysis, absence of reflexes, and marked disturbances of bowel and bladder function  associated with pyramidal motor syndrome o series of dysfunctions that result from interruption of the pyramidal system Lower Motor Neuron Syndromes  lower motor neurons are large motor neurons in the anterior (ventral) horn of the spinal cord and motor nuclei of the brainstem  axons from these nerve cell bodies bring nerve impulses from upper motor neurons to the skeletal muscles via anterior spinal roots or cranial nerves  dysfunction impairs voluntary and involuntary movement  degree of paralysis or paresis proportional to number of lower motor neurons affected  flaccid paresis or flaccid paralysis- muscle has reduced or absent tone o accompanied by hyperreflexia or areflexia o denervated muscles undergo atrophy over weeks to months mostly from disuse o denervated muscles demonstrate fasciculations (quivering or rippling of muscle under skin): fibrillation (isolated contraction of single muscle fiber) is not clinically visible 37. Describe Huntington disease patho and manifestations Huntington Disease (chorea)  Autosomal dominant hereditary degenerative disorder; short arm chromosome 4  Severe degeneration of the basal ganglia (caudate nucleus) and frontal cerebral atrophy o Depletion of GABA, excess dopaminergic activity, loss of glutamate  Clinical manifestations: o abnormal movement o progressive dysfunction of intellectual processes (dementia) o thought processes which marks onset of the disease o chorea most common type of abnormal movement o choreiform movements begin in the face and arms and progresses to the rest of the body o symptoms of frontal lobe dysfunction = executive attention deficits; short term memory loss; reduced capacity to plan, organize, and sequence; bradyphrenia; and apathy o euphoria and depression may be present 38. Describe Parkinson disease patho and manifestations Parkinson Disease  Degeneration of the dopaminergic pathway to the basal ganglia causes in under activity of the direct motor pathway (normally facilitates movement) and over activity of the indirect motor loop (normally inhibits movement) o Results in inhibition of the motor cortex manifested with bradykinesia and rigidity o Subthalamic nucleus overactivity influences the limbic system which results in emotional signs and symptoms Hallmark pathologic features of PD are loss of dopaminergic pigmented neurons in the substantia nigra pard compacta with dopaminergic deficiency in the putamen portion of the striatum  Clinical manifestations: o Onset of symptoms is insidious o Classic motor manifestations of PD  Bradykinesia (slow movement of limbs), tremor at rest, muscle rigidity (cogwheel), hypokinesia (abnormally diminished motor activity), stooped posture o Nonmotor symptoms  Hyponosmia, fatigue, pain, autonomic dysfunction, sleep fragmentation, depression, and dementia with or without pyschosis 39. Differentiate Decorticate vs. decerebrate posturing Decorticate Posture  Characterized by upper extremities flexed at the elbows and held close to the body and lower extremities that are externally rotated and extended  Occurs when the brainstem is not inhibited by the motor function of the cerebral cortex Decerebrate Posture  Increased tone in extensor muscles and trunk muscles, with active tonic neck reflexes  All four limbs are rigidly extended with head is in neutral position  Caused by severe injury to the brain and brainstem; resulting in overstimulation of postural righting and vestibular reflexes. 40. Describe Focal brain injuries Focal Brain Injuries  Contusion: bruising of the brain o Coup-contrecoup (coup = directly below point of impact, contrecoup = on the pole opposite the site of impact)  Laceration: tearing of brain tissue  Extradural (epidural) hematoma: accumulation of blood above the dura mater  Subdural hematoma: blood between dura mater and arachnoid membrane  Intracerebral hematoma: bleeding in the brain  Open: head trauma o Skull fracture with exposure of the cranial vault to the environment o Linear, comminuted, compound, and basilar skull fractures in the cranial vault or skull base. 41. Describe Diffuse brain injuries Diffuse Brain Injuries  Results from the effect of head rotation (primary) or shaking effect  Brain experiences shearing stresses resulting in axonal damage ranging from concussion to severe diffuse axonal injuries (DAI) state o Shearing, tearing, or stretching of nerve fibers  Pathophysiology can only be seen with microscope  Oxygen free radicals contributed to secondary injury 42. Define Mild concussion: I, II, III  Mild Concussion  Temporary axonal disturbance causing attention and memory deficits  Grade I: confusion, disorientation, and momentary amnesia  Grade II: momentary confusion and retrograde amnesia o No loss of consciousness in Grade I or II  Grade III: confusion with retrograde and anterograde amnesia o Loss of consciousness for seconds to minutes  Characterized by immediate onset of clinical manifestation at the time of injury 43. Define Grade IV concussion Grade IV  Disconnection of cerebral systems from the brain stem and reticular activating system  Physiologic and neurologic dysfunction without substantial anatomic disruption  Loss of consciousness ( 24 hours o Involves widespread physiologic impairment throughout the cerebral cortex and diencephalon o Actual tearing of some axons in both hemispheres o Recovery often incomplete o Decerebrate and decorticate posturing  Severe: o Involves disruption of many axons in both hemispheres and those extending to the diencephalon and brainstem o Associated with brainstem signs that disappear in a few weeks o Higher mortality and morbidity 45. Describe Spinal cord trauma; patho and manifestations Spinal Cord Trauma  Most commonly occurs due to vertebral injuries o Simple fracture o Compressed fracture o Comminuted fracture and dislocation  Traumatic injury of vertebral and neural tissues as a results of compressing, pulling, exerting tension on tissue, or shearing tissues so that they slide into one another  Occur most often in young men and older adults  Often causes spinal shock with cessation of all motor, sensory, reflex, and autonomic functions below the transected area  Loss of motor and sensory function depends on level of injury  Paraplegia- paralysis of lower half of the body  Quadriplegia- paralysis involving all 4 extremities  Autonomic hyperreflexia (dysreflexia) o Massive, uncompensated cardiovascular response to stimulation of the sympathetic nervous system o Syndrome of a sudden and dangerous increase in blood pressure that may occur at any time after spinal shock resolves o Condition is life-threatening o Mostly affects individual with lesions at T6 or above o Stimulation of the sensory receptors below the level of the cord lesion 46. Define Spinal shock Spinal shock: applies to all phenomena surrounding physiologic or anatomic transection of the spinal cord that results in temporary loss or depression of all or most spinal reflex activity below the level of injury 47. Differentiate between different syndrome associated with Spinal cord injury Spinal Cord Injuries  Complete Spinal Cord Transection: o Loss of motor function, muscle flaccidity, loss of all reflexes loss of pain, temperature, touch, and proprioception (body’s ability to sense movement, action, and location), atonic b/b, respiratory impairment  Partial Cord Transection: o Asymmetric flaccid motor paralysis, asymmetric reflex loss, preservation of some sensation, b/b impairment less severe, can perspire in some area below lesion o Brown-Sequard Syndrome- ipsilateral paralysis/paresis; ipsilateral loss of touch, vibration, and position sense; contralateral loss of pain and temperature o Central Cord Syndrome- motor deficits in upper extremities > lower extremities o Anterior Cord Syndrome- loss of motor; loss of pain and temperature; touch, pressure, position, and vibration intact (posterior columns intact) o Posterior Cord Syndrome- impaired light touch and proprioception o Cauda Equina Syndrome- lower extremity motor deficits; sensorimotor dysfunction; b/b, and sexual dysfunction 48. Describe Autonomic hyperreflexia Autonomic Hyperreflexia (Dysreflexia) A condition in which your involuntary nervous system overreacts to external or bodily stimuli.  Clinical manifestations: o Hypertension (up to 300mm Hg systolic) o Bradycardia ((30 to 40 beats/min) o Pounding headache, blurred vision, sweating above the lesion with flushing of skin, piloeretion (erection or bristling of hairs due to the involuntary contraction of small muscles at the base of hair follicles) 49. Describe CVA patho and manifestations Cerebrovascular Accident  Thrombotic Stroke: o arterial occlusions caused by thrombi formed in arteries supplying the brain or in the intracranial vessels o Development of cerebral thrombosis most frequently is attributed to atherosclerosis and inflammatory disease processes that damage arterial walls  Embolic Stroke: o Fragments that break from a thrombus formed outside the brain o Typically involves small vessels or bifurcation points o Associated with Afib o High recurrence rate  Hemorrhagic Stroke: o HTN, ruptured aneurysm, AV malformations, cavernous angioma o Can occur secondary to TBI  Lacunar Stroke: o Microinfarct small than 1cm in diameter and involves the small perforating arteries, predominantly in the basal ganglia, internal capsules, and pons o Caused by lipohyalinosis, subintimal lipid-loading foam cells, and fibrinoid materials that thicken the arterial walls and are associated with smoking, HTN, DM. 50. Discuss TIA Transient Ischemic Attacks (TIA)  Brief episode of neurologic dysfunction caused by focal disturbance or brain or retinal ischemia with clinical symptom lasting less than 1 hour and without evidence of infarction  Results of thrombotic particles causing an intermittent blockage of circulation or spasm. 51. Describe SAH patho and manifestations Subarachnoid Hemorrhage  Blood escapes from defective or injured vasculature into the subarachnoid space  Clinical manifestations: o Thunderclap headache, nausea/vomiting, loss of consciousness, neuro deficits due to rise in ICP  o Kernig sign-straightening of knee with the hip and knee in a flexed position produces pain in the back and neck regions o Brudzinski sign- passive flexion of the neck produces neck pain and increased rigidity o Vasospasm major complication after rupture between days 5-14  As a results of presence of blood and its breakdown; along with oxy-hemoglobin which scavenges nitric oxide and its breakdown triggers a free radical cascade that disrupts multiple blood vessel layers and initiates release of inflammatory factors o Leads to delayed cerebral ischemia 52. Describe Basics of vascular manifestations Intracranial Aneurysm  Result from defects in the vascular wall and are classified on the basis of form and shape o Result from atherosclerosis, congenital abnormality, trauma, inflammation or infection  Commonly asymptomatic; but signs vary according to the location and size of aneurysm  CN III, IV, V, and VI are affected  Most common first indication is acute subarachnoid hemorrhage, intracerebral hemorrhage, or combined subarachnoid-intracerebral hemorrhage or combined subarachnoid-intracerebral hemorrhage  No single pathologic mechanism exists  Combination of genetic, congenital, and acquired factors are present 53. Differentiate Headaches; types and patho/clinical manifestations Headaches  Migraine: familial, episodic disorder whose marker is headache and is defined as repeated, episodic headache lasting 4-72 hours o Caused by a combination of multiple genetic and environmental factors o Usually women 25-55 years old o Clinical manifestations:  Unilateral, throbbing, worsened by movement, moderate or severe headache  Nausea  Vomiting  Accompanied by photophobia or phonophobia o Triggers:  Altered sleep patterns, skipping meals, overexertion, weather change, stress or relaxation from stress, hormonal changes (menstrual periods), excess afferent stimulation (bright lights, strong smells), chemicals (alcohol or nitrates)  Cluster: occur in clusters for a period of days followed by a long period of spontaneous remission o Usually men between 20-50 years old o Trigeminal activation o Autonomic dysfunction characterized by: Sympathetic nervous system under-activity and parasympathetic over-activity o Unilateral trigeminal distribution of severe pain with ipsilateral autonomic manifestations (tearing on affected side, ptosis (upper eyelid droops over eye) of the ipsilateral eye, and stuffy nose) o Either acute or chronic type o Chronic paroxysmal hermicrania is a cluster headache with more frequent daily attacks; primarily in women  Tension-type o Most common o Has both central and peripheral mechanism associated with etiology o Mild to moderate bilateral headache with a sensation of a tight band or pressure around the head with gradual onset of pain o Occurs in episodes and may last for several hours or several days o Occurs at least 15 days per month for at least 3 months o Can be acute or chronic 54. Describe CNS infections; pathogens, patho, clinical manifestations Infection and Inflammation of the CNS  Can occur by bacteria, viruses, fungi, parasites, and mycobacteria  Meningitis : o Bacterial primarily infection of the pia mater and arachnoid and of the fluid of the subarachnoid space.  Infection by bacteria is pus producing (pyogenic)  Meningeal vessels become hyperemic and neutrophils migrate into the subarachnoid space; inflammatory reaction occurs, and exudate ensues and increases rapidly o Aseptic (viral, nonpurulent, lymphocytic) meningitis limited to meninges o Fungal meningitis chronic less common type o Clinical manifestations :  Depend on type and range from throbbing headache to neck stiffness and rigidity and decreasing responsiveness; specific CN dysfunction is common  Kernig positive, Brudzinski sign +  Encephalitis : o Acute febrile illness, usually of viral origin with nervous system involvement o Most common forms of encephalitis are caused by arthropod-prone viruses and herpes simplex virus o Meningeal involvement appears in all encephalitides o Clinical manifestations :  Fever, delirium, confusion, seizures, abnormal and involuntary movement, and increased ICP 55. Describe MS patho and manifestations Multiple Sclerosis  Acquired autoimmune MS is a progressive, inflammatory, demyelinating disorder of the CNS; with scarring or formation of plaque and loss of axons  Demyelination results from an immunogenetic-viral cause  Syndromes o Mixed (general) type  Optic signs  Brainstem signs diplopia, vertigo, nystagmus, dysarthria o Spinal type  Involves spinal tracts and dorsal column  Weakness, numbness, or both in one or more limbs  Spastic ataxia  Bladder and bowel symptoms o Cerebellar  Motor ataxia  Hypotonia  asthenia 56. Describe ALS patho and manifestations Amyotrophic Lateral Sclerosis (ALS)  Diffusely affects upper and lower motor neurons of the cerebral cortex, brainstem, and spinal cord (corticospinal tracts and anterior roots)  Pathogenesis not clear o Lower and upper motor neuron degeneration occurs as well as degeneration of non-motor neurons in the cortices and spinal cord  Disease leads to progressive weakness leading to respiratory failure and death  Patient has normal intellectual and sensory function until death 57. Describe Myasthenia gravis; patho and manifestations Myasthenia Gravis  Acquired chronic autoimmune disease  Results from defect in nerve impulse transmission at the NMJ o An IgG antibody is produced against acetylcholine receptors (antiacetylcholine receptor antibodies)  Weakness and fatigue of muscles of the eyes and the throat causing diplopia and difficulty chewing, talking, swallowing  Foremost complaint is muscular fatigue and progressive weakness  Complaints of fatigue after exercise and has recent history of recurring upper respiratory infections  Eye manifestations diplopia, ptosis, ocular palsies  Myasthenia Crisis: o Occurs when severe muscle weakness causes extreme quadriparesis or quadriplegia, respiratory insufficiency with SOB and markedly decreased tidal volume and vital capacity, and extreme difficulty swallowing  Cholinergic Crisis: o may arise secondary to drug overdose o clinical picture resembles that of myasthenic crisis but weakness occurs 30-60 minutes after taking anticholinesterase medication   o associated with episodes of diarrhea and complaints of cramping, fasciculation, bradycardia, pupillary constriction, increased salivation, and increased sweating are present