Patho Final Review 1.

Neurogenic Shock decreased sympathetic control of blood vessel tone due to a defect in the vasomotor center in the brain stem or the sympathetic outflow to the blood vessels (normovolemic shock) a. Causes: Brain injury, depressant action of drugs, general anesthesia, hypoxia, lack of glucose, spinal anesthesia or spinal cord injury above the midthoracic region b. S/s: Heart rate is slower, skin is dry and warm c. Spinal shock characterized by flaccid paralysis with loss of tendon reflexes below the level of injury, absence of somatic and visceral sensations below the level of the injury, loss of bowel and bladder functions. i. Is an immediate response to acute spinal cord injury ii. Can result in vasodilation, increased venous capacity, hypotension Seizures an abrupt and temporary alteration in cerebral activity resulting in changes in electrical discharge from neurons in the cerebral cortex; Classified as partial or generalized seizures a. Partial seizures Seizures begin in a specific or focal area of one cerebral hemisphere i. Simple partial involve only one hemisphere and no loss of consciousness or responsiveness 1. S/s depends on area of brain affected motor, sensory, or autonomic signs 2. Motor movement can spread to other cortical areas, with sequential involvement of body parts in an epileptic-type march called Jacksonian seizure 3. Auras may be a warning sign; represents a simple partial seizure ii. Complex Partial involves impairment of consciousness and often arise in temporal lobe; known as psychomotor seizures 1. S/s automatisms (repetitive nonpurposeful activities like lip smacking, grimacing, patting) 2. Postictal state confusion, hallucinations, illusional experiences (dj vu, jamais vu), overwhelming fear, uncontrolled forced thinking, detachment, depersonalization iii. Secondarily Generalized partial seizures focal at onsent but then become generalized as neuronal discharge spreads, involves deeper structures like thalamus 1. Can result in tonic clonic seizures b. Generalized seizures begin simultaneously in both hemispheres i. Absence (petit mal) seizures generalized, nonconvulsive epileptic events 1. S/s- Blank stare, motionlessness, unresponsiveness, automatisms (lip smacking, increased/decreased postural tone, clonic motion in eyelids) 2. Occur mostly in children, and stop in adulthood or progress to generalized motor seizures 3. Atypical absence seizures greater alterations in muscle tone and less abrupt onset and cessation 4. May resemble complex partial seizures ii. Atonic seizures sudden, split-second loss of muscle tone leading to slackening of the jaw, drooping of the limbs, falling to the ground (drop attacks) iii. Myoclonic seizures brief involuntary muscle contractions induced by stimuli of cerebral origin 1. S/s bilateral jerking of muscles that generalized or confined to the face, trunk or one or more extremities iv. Tonic seizures rigid, violent contraction of muscles, fixing the limbs in a strained position v. Clonic seizures repeated contractions and relaxations of the major muscles vi. Tonic-Clonic (grand mal) seizures 1. S/s of Tonic phase- sharp tonic contraction of muscles with extension of extremities, immediate loss of consciousness, bowel/bladder incontinence, possible cyanosis from contraction of airway and respiratory muscles 2. S/s Clonic rhythmic bilateral contraction and relaxation of extremities 3. Postictal phase person remains unconscious until RAS begins to function again c. Diagnosis - H&P, MRI, EEG d. Treatment individualized; usually with antiepileptic drugs that either suppress repetitive firing of isolated neurons or by inhibiting transmission of electrical impulses i. Ethosuximide DOC for absence seizures ii. Surgery removing anygdala and anterior part of hippocampus and entorhinal cortex iii. Precautions in child bearing women interaction with oral contraceptives, affect on fertility, congenital abnormalities e. Status Epilepticus seizures that do not stop spontaneously or occur in succession w/o recovery i. Tonic-clonic status epilepticus is a medical emergency ii. IV Diazepam or lorazepam is first-line therapy Multiple Sclerosis - demyelinating disorder characterized by inflammation and selective destruction of CNS myelin; upper motor neuron disease a. Patho Possibly immune-mediated; Demyelination of nerve fibers in white matter of brain, spinal cord, optic nerve. Myelin is formed by oligodendrocytes. Demyelinated fibers have conduction abnormalities such as decreased conduction speed or conduction block i. Plaques lesions of MS that are hard, sharp-edged, usually on the optic nerves, brain stem, cerebellu, spinal cord ii. Two stages of plaque formation: 1) Development of small inflammatory lesions, 2) Lesions extend, consolidate and demyelination and and gliosis occur iii. Usually affects those 20-40 yrs, more women than men b. S/s paresthesias, optic neuritis, diplopia, abnormal gait, bladder and sexual dysfunction, vertigo, nystagmus, fatigue, speech disturbance, depression, euphoria, inattentiveness, apathy, forgetfulness, loss of memory i. Lhermitte sign electric shock-like tingling down the back and onto legs that is produced by flexion of the neck c. Classifications:

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Relapsing-remitting episodes of acute worsening with recovery and a stable course between relapses Secondary progressive disease gradual neurologic deterioration with or without superimposed acute relapses in a person w/previous relapsing-remitting disease iii. Primary progressive nearly continuous neurologic deterioration from onset iv. Progressive relapsing gradual neurologic deterioration from onset of symptoms but with subsequent superimposed relapses d. Diagnosis Evidence of CNS lesions that are occur in diff parts of the CND at least 3 months apart; MRI, examination of CSF that show elevated IgG levels (not specific) e. Treatment aimed at modifying the course and managing symptoms of the disease i. Good nutrition and adequate rest and relaxation ii. Physical therapy to maintain muscle tone iii. Pharmacologic treatment Drugs that: 1. Treat acute attack or initial demyelinating episodes corticosteroids, ACTH, plasmapheresis 2. Modify course of disease Interferon Beta (immune enhancer), Glatiramer acetate (blocks myelin damaging T cells by acting as myelin decoy), Metoxantrone 3. Treat symptoms of disease Dantrolene, baclofen or diazepam for spacticity; cholinergic drugs for bladder problems; antidepressant drugs for depression Guillain-Barre Syndrome an acute life-threatening polyneuropathy characterized by rapidly progressive limb weakness, symmetric flaccid paralysis and loss of tendon reflexes (a disease of peripheral nerves) a. Patho - Possibly immune-mediated; most have had an acute influenza-like illness before onset of symptoms; also liked to Campylobacter jejuni, cytomegalovirus, Epstein-Barr virus, myocplasma pneumonia, vaccinations b. Classifications: Pure motor axonal degeneration, axonal degeration of both motor and sensory nerves, Variant (has ophtamlmoplegia, ataxia, areflexia) c. S/s Paresthesias, numbness, loss of function, postural hypotension, arrhythmias, facial flushing, abnormalities of sweating, urinary retention i. Pain in shoulder girdle, back, posterior thighs d. Treatment support of vital functions, prevention of complications such as skin breakdown and thrombophlebitis, plasmapheresis, high-dose IV immunglobulins Myasthenia Gravis disorder of the neuromuscular junction that affects impulse transmission between the motor neuron and the innervated muscle cell a. Patho autoimmune disease caused by antibody-mediated loss of acetylcholine receptors in neuromuscular junction due to: i. Complement-mediated injury to the postsynaptic muscle membrane ii. Accelerated acetylcholine receptor degradation by receptor specific antibodies iii. Blockade of receptors by antibodies attached to the acetylcholine binding sites b. S/s Muscle weakness, fatigability with sustained effort, initial weakness in eye muscles - ptosis due to eyelid weakness or diplopia; respiratory muscle weakness, difficulty chewing or swallowing, weakness in proximal limb movements, speech impairment i. Myasthenic crisis respiratory muscles are so weak and compromise ventilation so ventilator support and airway protection is needed. Usually occurs during periods of stress c. Diagnosis H&P, confirmed by response to a short-acting anticholinesterase test (Edrophonium), immunoassay d. Treatment i. Pharmacological reversible anticholinesterase drugs (neostigmine, pyridostigmine), corticosteroids, immunosuppressants ( azathioprine, cyclosporine) ii. Plasmapheresis usually for crisis or short-term treatment iii. IV immunoglobulin iv. Surgery to remove thymus Epidural hematoma - A hematoma that develops between the inner bones of the skull and dura a. Usually results from a tear in an artery, most often the middle meningeal, usually in associated with a head injury in which the skull is fractured b. Rapid expansion of hematoma compresses the brain c. More common in young person because the dura is less firmly attached to skull surface than that of older person d. S/s - Brief period of unconsciousness followed by lucid period, then rapid unconsciousness; ipsilateral pupil dilation, contralateral hemiparesis; increased ICP, tentorial herniation, death Subdural hematoma a. Develops between the dura and arachnoid and is usually the result of a tear in the small bridging veins that connect veins on the surface of cortex to dural sinuses; veins are readily snapped in head injury when brain moves suddenly in relation to cranium b. Venous source of bleeding develops more slowly c. Classification i. Acute: symptoms appear within 24 hours of injury 1. S/s decerebrate posturing, loss of consciousness ii. Subacute 2-10 days after injury iii. Chronic symptoms appear several weeks after injury 1. S/s drowsiness, confusion, headache, apathy Cerebrovascular accidents (stroke) acute focal neurologic deficit from a vascular disorder that injures brain tissue. Two categories Ischemic or hemorrhagic a. Ischemic caused by an interruption of blood flow in a cerebral vessel due to thrombosis or emboli i. Penumbra the area of minimally perfused cells surrounding the necrotic core; the metabolic activities of the cells are impaired, but cells can survive depending on return of adequate circulation, amt of toxic products, degree of edema, etc

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Transient Ischemic attacks brief episodes of neurologic dysfunction resulting from focal cerebral ischemia not associated with infarction; disturbed blood flow is reversed before infarction occurs (ie a zone of penumbra w/o central infarction) iii. Thrombotic (Large vessel) stroke 1. Due to thrombi that occur in atherosclerotic blood vessels 2. Plaques usually occur at areas of bifurcations (origins of internal carotid and vertebral arteries) 3. S/s Aphasia, neglect, visual fied defects, transient monocular blindness 4. Not associated with activity, can occur at rest; usually accompanied by atherosclerotic heart or pheripheral arterial disease iv. Cardiogenic Emoblic stroke 1. Caused by a moving blood clot that travels from its origin to the brain 2. Most frequent site middle cerebral artery; most common origin left heart or from atherosclerotic plaque in the carotid arteries 3. Risk factors rheumatic heart disase, atrial fibrillation, recent MI, ventricular aneurysm, bacterial endocarditis b. Hemorrhagic caused by bleeding into brain tissue due to a blood vessel rupture caused by hypertension, aneurysm, arteriovenous malformation, head injury or blood dyscrasias i. Patho rupture results in a focal hematoma and sometimes intraventricular hemorrhage, edema, compression of the brain contents or spasm of the adjacent blood veseels ii. Predisposing factors advancing age, hypertension, aneurysm, trauma, erosion of the vessels by tumors, blood coagulation disorders, vasculitis, drugs iii. S/s Vomiting at onset, headache, contralateral hemiplegia with initial flaccidity progressing to spasticity c. Risk factors i. Modifiable Hypertension, hyperlipidemia, smoking, diabetes, heart disease, carotid artery disease, coagulation disorders, obesity/inactivity, heavy alcohol use, cocaine use ii. Non-modifiable age, gender, race, heredity d. S/s depends on artery affected; usually weakness of face and arm, unilateral numbness, vision loss in one eyes or to one side, language disturbance, slurred speech, sudden unexplained imbalance or ataxia e. Diagnosis H&P, with throrough neurologic exam; CT scans for rapid identification of hemorrhage, MRI for imaging ischemic lesions f. Treatment Thrombolytic therapy, mechanical clot disruption, tissue plasminogen activator to treat acute ischemic stroke; must have CT scan first and must be given within 3 hours of onset of symptoms 9. Spinal cord injuries (p. 916-24) - usually involve damage to the vertebral column or supporting ligaments as well as the spinal cord a. Injury to vertebral column due to fractures, dislocations, subluxations. Result from combo of compressive force or bending movements. Flexion vs. extension injuries (most common in cervical spine C4-C6). Compression injuries occurs when there is spinal loading from a highvelocity blow to top of head or when landing forcefully on feet or buttocks, causing verterbral bones to shatter, squash, burst. b. Acute spinal cord injury damage to neuronal elements, due to direct trauma to the cord, fracture-dislocations or sublaxation of spine. Can be complicated by loss of blood flow to the cord, resulting in ischemia. i. Primary neurologic injury- occurs at time of injury and is irreversible. Characterized by small hemorrhages in gray matter of cord, followed by edematous changes in white matter that lead to necrosis of neural tissue 1. Cause: Force of compression, stretch and shear associated with fracture or compression of spinal vertebrae, dislocation of vertebrae, penetrating injuries that produce laceration of spinal cord ii. Secondary injuries tissue destruction that occurs and ends in progressive neurologic damage following primary injury. Vascular damage, neuronal injury leading to loss of reflex below injury, release of vasoactive substances that cause vasospasm and impedes blood flow, produces necrosis c. Central cord syndrome injury is predominantly in central gray or white matter of cord. Motor function of upper extremities affected, lower extremities may not be affected or affected to a lesser degree, with some sparing of sacral sensation. Bowel, bladder, and sexual function are affected to various degrees. Seen in elderly persons mostly. d. Anterior cord syndrome infarction of anterior spinal artery, damaging anterior 2/3 of cord. Loss of motor function of corticospinal tract, loss of pain, temp sensations e. Brown-Sequard syndrome due to damage to a hemisection of anterior and posterior cord. Loss of voluntary motor function from corticospinal tract, proprioception loss from ipsilateral side of body, contralateral loss of pain and temp sensation below lesion f. Conus Medullaris syndrome due to damage of conus medullaris or sacaral cord and lumbar nerve roots in neuronal canal. Results in flaccid bowel, bladder, altered sexual function. Motor function in feet, legs may be impaired w/o sensory impairment. i. Cauda equina syndrome damage to lumbosacral nerve roots asymmetric nerve paralysis, sensory impairment, pain g. Disruption of motor, somatosensory function, reflex activity, ANS system, temperature, bladder, bowel sexual dysfunction (p.921-923) 10. Type I Diabetes destruction of the pancreatic beta cells. Absolute lack of insulin requires exogenous insulin replacement to reverse catabolic state, control blood glucose levels and prevent ketosis a. Type 1a Immune mediated due to a combination of genetic predisposition, an environmental triggering event (such as infection) and a Tlymphocyte-mediated hypersensitivity reaction against some beta cell antigen i. Two types of autoantibodies, insulin autoantibodies (IAAs) and islet cell autoantibodies ii. Usually in younger kids b. Type 1b idiopathic no evidence of autoimmunity; strongly inherited; episodes of ketoacidosis with periods of absolute insulin deficiency i. Not common; usually affects Africans or Asians c. S/s Polyuria, polydipsia, polyphagia, weight loss, recurrent blurred vision, fatigue, paresthesias, skin infections 11. Type 2 Diabetes a condition of hyperglycemia due a relative insulin deficiency a. Metabolic abnormalities due to:

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Insulin resistance failure of target tissues to respond to insulin, leading to decreased uptake of glucose in skeletal muscle and impaired suppression of glucose production in the liver ii. Increased glucose production by the liver iii. Deranged secretion of insulin by the pancreatic beta cells b. Pathogenesis involves both genetic and acquired environmental factors (obesity, physical inactivity, waist circumference) c. Visceral obesity is accompanied by an incrase in fat storage and postprandial FFA concentrations, leading to: i. Excessive and chronic elevation of FFA can cause beta cell dysfunction (lipotoxicity) ii. FFAs act at level of peripheral tissues to cause insulin resistance and glucose underutilization by inhibiting glucose uptake and glycogen storage iii. Accumulation of FFAs and triglycerides reduces hepatic insulin insensitivity d. Metabolic syndrome In people with type 2 diabetes, hyperglycemia is also associated with intra-abdominal obesity, high levels of plasma triglycerides and low levels of high-density lipoproteins (HDLs), hypertension, systemic inflammation, abnormal fibrinolysis, abnormal function of the vascular endothelium and macrovascular disease (coronary artery, cerebrovascular and peripheral arterial disease) e. S/s Polyuria, polydipsia, polyphagia (usually not common in type 2); recurrent blurred vision (due to exposure of lens and retina to hyperosmolar fluids), weakness and fatigue (due to lowered plasma volume); parasthesias (due to temporary dysfunction of the peripheral sensory nerves); chronic skin infections (hyperglycemia and glycosuria favor growth of yeast organisms) Hypothyroidism - Deficiency in thyroid hormone a. Congenital hypothyroidism i. Cause: Due to a congential lack of thyroid gland or from abnormal biogynthesis of thyroid hormone or deficient TSH secretion; Can result in mental retardation and impaired physical growth ii. S/s prolongation of physiologic jaundice, respiratory difficulties, hoarse cry, enlarged tongue, feeding difficulties, lack of interest, somnolence, choking during nursing, enlarged abdomen, umbilical hernia iii. Treatment T4 supplementation b. Acquired hypothyroidism causes a general slowing down of metabolic processes and myxedema i. Causes Destruction or dysfunction of the thyroid gland (primary hypothyroidism), Impaired pituitary function (secondary) or hypothalamic dysfunction (tertiary); Hashimoto thyroiditis (autoimmune disorder) 1. Primary due to thyroidectomy, ablation of gland with radiation, certain goitrogenic drugs such as lithium carbonate, proylthiuracil, and methamiazole; large amounts of iodine or iodine deficiency ii. S/s gradual onset of weakness and fatigue, weight gain despite loss of appetite, cold intolerance, dry rough skin, coarse brittle hair, puffy face with edematous eyelids, thinning of the outer third of the eyebrows, conductive deafness, decreased GI motility (constipation, flatulence, abdominal distention), mental dullness, lethargy, impaired memory, enlarged tongue, hoarse husky voice, carpal tunnel, slow pulse, enlarged heart iii. Diagnosis H&P, low T4 and elevated TSH levels, test for antithyroid antibodies for Hashimoto thyroiditis iv. Treatment replacement therapy with synthetic preparations of T3 or T4 Goiter an increase in the size of the thyroid gland that can occur in hypothyroid, euthyroid and hyperthyroid states a. Can be diffuse (involving entire gland) w/o nodularity or can contain nodules Diffuse goiters usually become nodular b. Can be toxic produces signs of extreme hyperthyroidism c. Diffuse nontoxic and multinodular goiters are result of compensatory hypertrophy and hyperplasia of follicular epithelium from some derangement that impairs thyroid hormone output d. Multinodular goiters produce largest thyroid enlargement i. Can compress the esophagus and trachea, leading to diffuclty in swallowing , a choking sensation and inspiratory stridor ii. Can also compress superior cava, leading to distention of the veins of the neck and upper extremities, edema of eyelids and conjunctiva and syncope with coughing Hashimoto thyroiditis an autoimmune disorder in which the thyroid gland may be totally destroyed by an immunologic process; is the most common cause of hypothyroidism and goiter a. Affects mostly women b. Pathogenesis goiter at onset, hypothyroidism will follow; transient hyperthyroid state can occur due to leakage of preformed thryroid hormone from danaged cells of the gland Myxedema nonpitting mucous type of edema caused by an accumulation of a hydrophilic mucopolysaccharide substance in the connective tissues throughout the body a. Usually observed in the face, but can also be elsewhere leads to enlarged tongue, carpal tunnel, impairment of muscle function with stiffness, cramps, pain, pericardial or pleural effusion, mucopolysaccharide deposits in the heart can cause generalized cardiac dilation, bradycardia and altered cardiac function Parkinsons Disease a progressive degenerative disorder of basal ganglia function that results in variable combinations of tremor, rigidity and bradykinesia; usually beings after 50 yrs old a. Patho- dopamine depletion results from degeneration of the dopamine nigrostriatal system; also develops as a postencephalitic syndrome, side effect of therapy with antipsychotic drugs that block dopamine receptors, toxic reactions to chemical agents or due to severe carbon monoxide poisoning b. Cause interaction b/t environmental genetic factors i. Oxidative stress, apoptosis, mitochrondrial disorders ii. Genetic mutation in the gene encoding alpha-synuclein, which is one of the major components of the Lewy bodies that are found in the brain tissue of persons with Parkinson disease iii. Mutation in gene that encodes protein parkin c. S/s

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vi. Treatment i. Nonpharmacologic group support, education, daily exercise, adequate nutrition ii. Pharmacologic antiparkinsonian drugs act by increasing functional ability of the underactive dopaminergic system or by reducing the excessive influence of the excitatory cholinergic neurons 1. Levodopa that increase dopamine levels, carbidopa a. AE: on-off phenomenon, in which frequent, abrupt and unpredictable fluctuations in motor performance occur during the day 2. Rotigotine for initial treatment, apomorphine for rescue medication 3. Bromocriptine, pramipexole, ropinirole dopamine agonists to stimulate receptors iii. Surgery 1. Old method destroying part of the thalamus or globus pallidus in basal ganglia with an electrical stimulator or supercooled tip of a metal probe 2. Current deep brain stimulation involves implant of electrodes into subthalamic nuclei or pars interna of globus pallidus a. Electrodes delivers electrical simulation to block abnormal nerve activity that causes tremor and abnormal motor activity 17. Meningitis - inammation of the pia mater, the arachnoid, and the CSF-lled subarachnoid space a. Inammation spreads rapidly because of CSF circulation around the brain and spinal cord. The inammation usually is caused by an infection, but chemical meningitis can occur. There are two types of acute infectious meningitis: acute purulent meningitis (usually bacterial) and acute lymphocytic (usually viral) meningitis. Factors responsible for the severity of meningitis include virulence factors of the pathogen, host factors, brain edema, and the presence of permanent neurologic sequelae. b. Bacterial Meningitis caused by Streptococcus pneumonia (the pneumococcus) or Neisseria meningitis (the meningococcus),except in neonates (infected most by group B streptococci). Haemophilus inuenza infection was a leading cause of meningitis in decades past, but its incidence has declined dramatically during recent years because of vaccination against H. inuenza. Epidemics of meningococcal meningitis occur in settings such as colleges and the military, where young people reside in close contact. Other pathogens in adults are gram-negative bacilli and Listeria mono cytogenes. c. Risk factors: i. The very young and the very old are at highest risk for pneumococcal meningitis. ii. Risk factors associated with contracting meningitis include head trauma with basilar skull fractures, otitismedia, sinusitis or mastoiditis, neurosurgery, dermal sinus tracts, systemic sepsis, or immune compromise. d. Pathophysiology of bacterial meningitis, the bacterial organisms replicate and undergo lysis in the CSF, releasing endotoxins or cell wall fragments. These substances initiate the release of inammatory mediators, which set off a complex sequence of events permitting pathogens, neutrophils, and albumin to move across the capillary wall into the CSF. As the pathogen senter the subarachnoid space, they cause inammation, characterized by a cloudy, purulent exudate. Thrombophlebitis of the bridging veins and dural sinuses or obliteration of arterioles by inammation may develop, causing vascular congestion and infarction in the surrounding tissues. Ultimately, the meninges thicken and adhesions form. These adhesions may impinge on thecranial nerves, giving rise to cranial nerve palsies, or mayimpair the outow of CSF, causing hydrocephalus. e. S/s: The most common symptoms of acute bacterial meningitis are sudden onset of headache, fever, and stiff-ness of the neck (nuchal rigidity), sometimes accompanied by nausea, vomiting, photophobia, and alteredmental status. Other signs include seizures, cranialnerve palsies, and focal cerebral signs. i. Meningococcal meningitis is characterized by a petechial rash with palpable purpura in most people. These petechiae vary in size from pinhead to large ecchymoses or even areas ofskin gangrene, often associated with rapid onset ofhypotension, acute adrenal hemorrhage (the Waterhouse-Friderichsen syndrome), and multiple organ failure. ii. Persons infected with H. inuenzaeor S. pneumonia maypresent with difculty in arousal and seizures, whereas those with N. meningitis infection may present with delirium or coma. Cranial nerve damage (especially CNVIII, with resulting deafness) and hydrocephalus may occur as complications of pyogenic meningitis. f. Diagnosis of bacterial meningitis is based on the history and physical examination, along with laboratory data. Two assessment techniques can help determinewhether meningeal irritation is present. The Kernig signis resistance to extension of the knee while the person islying with the d.

Tremor of the hands, feet, head, neck, face, lips, tongue jaw 1. Characterized by rhythmic, alternation flexion and contraction movements (4-6 beats /min) that resembles the motion of rolling a pill b/t thumb and forefinger 2. Unilateral; occurs when the limb is supported and at rest; disappears with movement and sleep; eventually becomes bilateral Rigiditiy resistance to movement of both flexors and extensors throughout the full range of motion 1. Seen in passive joint movement and involves jerky, cogwheel-type movement that takes a lot of energy to perform Bradykinesia slowness in initiating and performing movements and difficulty with sudden, unexpected stopping of voluntary movements 1. Difficulty initiating walking, difficulty turning, may freeze in place in doorways or when preparing to turn 2. Leans forward to maintain center of gravity, small shuffling steps, no arm swing Advanced s/s loss of postural reflexes that predisposes to falling backward, stiff, masklike facial expression, loss of blinking reflex, rigid tongue, palate and throat that leads to drool; slow monotonous speech that is poorly articulated Autonomic s/s excessive and uncontrolled sweating, sebaceous gland secretion and salivation. Lacrimation, dysphagia, orthostatic hypotension, thermal regulation, constipation, impotence, urinary incontinence Cognitive dysfunction Dementia

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hip exed at a right angle. The Brudzinskisign is elicited when exion of the neck induces exion ofthe hip and knee. These postures reect resistance to thepainful stretching of the inamed meninges from thelumbar level to the head. Lumbar puncture ndings,which are necessary for accurate diagnosis, include acloudy and purulent CSF under increased pressure. Bacteria can be seen on smears and can easily be culturedwith appropriate media. g. Treatment includes urgent antibiotics while diagnostic testing ensues..Initial choice of antibiotics includes broad-spectrum coverage with a third-generation cephalosporin, vancomycin, and sometimes ampicillin. Further adjustment of antibiotics is driven by results of CSF cultures. Effective antibiotics produce rapid lysis of the pathogen,which produces inammatory mediators that have the potential for exacerbating the abnormalities of the blood-brain barrier. To suppress this pathologic inammation, adjunctive corticosteroid therapy is increasingly administered with or just before the rst dose of antibiotics inpatients of all ages. h. Persons who have been exposed to someone with meningococcal meningitis should be treated prophylactically with antibiotics. A quadrivalent polysaccharideprotein conjugate vaccine is now available to protect against meningococcal meningitis. The vaccine is recommended for all persons aged 11 to 18 years and for per-sons 19 to 55 years who are at increased risk for meningococcal disease (e.g., military recruits, college students living in dormitories, microbiologists who are routinely exposed to N. meningitides and persons with complement deficiencies or anatomic or functionalasplenia). i. Viral Meningitis manifests in much the same way as bacterial meningitis, but the course is less severe and the CSF ndings are markedly different. There are lymphocytes in the uid rather than polymorphonuclear cells, the protein content is only moderately elevated, and the sugar content usually is normal. The acute viral meningitides are self-limited and usually require only symptomatic treatment, except for herpes simplex virus(HSV) type 2, which responds to intravenous acyclovir. i. Causes: Most often enteroviruses, including coxsackievirus, poliovirus, and echovirus. Others include Epstein-Barr virus, mumps virus, HSV, and West Nile virus. Although often the virus cannot be identied, newer assays are emerging that allow in some circumstances for rapid identication of viral ribonucleic acid (RNA) in CSF Skull fractures/head injury Encephalitis generalized infection of the parenchyma of brain or spinal cord a. Cause: Usually virus (Herpes Simplex Virus, West Nile), but can also be due to bacteria, fungi, other organisms i. Mode of transmission: mosquito bite, rabid animal bite, ingestion b. Patho local necrotizing hemorrhage that ultimately becomes generalized, with prominent edema. Progressive degeneration of nerve cell bodies. c. S/s fever, nuchal rigidity, neurologic disturbances lethargy, disorientation, seizures, focal paralysis, delirium, coma d. Diagnosis H&P, CSF studies Increased intracranial pressure Cranial cavity has three components: Blood (10%), brain tissue (80%) and CSF (10%). Each of these three contributes to the Intracranial pressure, which is normally maintained within a range of 0-15 mm HG. a. Abnormal increases are caused by volume changes: i. Increase blood volume from vasodilation of cerebral vessels, obstruction of venous outflow ii. Increased tissue due to brain tumor, brain edema, bleeding into brain tissue iii. Increased CSF due to excess production, decreased absorption or obstructed circulation b. Monro-Kellie Hypothesis: A change in volume of one component can be compensated by a decrease in the volume of one or both of the other two components i. CSF and blood volume are best able to compensate for change in ICP; tissue volume is relatively restricted from undergoing change ii. Initial increases in ICP are buffered by a translocation of CSF to spinal subarachnoid space and increased reabsorption of CSF iii. Cerebral blood vessels ability to buffer volume can become exhausted quickly, leading to venous pressure and ICP increase c. Hypoventilation can be used for ICP, as it will cause decrease PCO2 leading to vasodilation d. Compliance ratio of change in volume to the resulting change in pressure; so if intracranial volume increases and compliance is high, there is little to no effect on ICP i. Factors affecting compliance amt of volume increase, time frame for accommodations, size of the intracranial compartments e. Cerebral Perfusion Pressure the difference between Mean Arterial Blood Pressure (MABP) and ICP (CPP=MABP-ICP); is determined by the pressure gradient between the internal carotid artery and subarachnoid veins i. Normal: 70-100 mm HG, ischemia not seen until CPP is below 40 mm hg ii. Monitored frequently in persons with brain conditions that increase ICP and impair brain perfusion iii. When ICP approaches of exceeds MABP, tissue perfusion is inadequate, cellular hypoxia results, neuronal death may occur 1. 1st s/s Decreased level of consciousness f. Late reflex seen in marked increase of ICP CNS ischemic response, where neurons in the vasomotor center respond to ischemia by producing marked increase in MABP to try to increase CPP, along with widened pulse pressure and reflex bradycardia i. Also known as Cushing reflex ( 3 signs- hypertension, bradycardia, widened pulse pressure as late signs of increased ICP) Acromegaly Growth Hormone excess in adults, which represents an exaggerated growth of the ends of the extremities (fingers, hands, toes) a. Causes: GH-secreting adenomas (usually benign). b. Patho: Insidious onset, symptoms often present for a while before diagnosis made. Excessive GH occurs after epiphyses of long bones have closed, so person cant grow taller, but the soft tissues continue to grow. Enlargement of small bones of hands, feet, of membranous bones of face, skull, splayed teeth, enlarged cartilaginous structures of larynx and vocal tract (deep voice). i. Additionally disorders of fat and carbohydrate metabolism, leading to increased free fatty acids in body fluids, decreased glucose uptake by muscles, increased glucose production in the liver, increased insulin secretion Diabetes mellitus c. S/s enlarged hands, feet, broad bulbous nose, protruding jaw, slanting forehead, splayed teeth w/ disturbed bite and difficulty chewing, deepening voice, tendency to develop bronchitis, kyphosis, arthralgias, degenerative arthritis of spine, hips, knees, enlargement of organs, esp heart which can lead to death

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Other excessive sweating with unpleasant odor, oily skin, heat intolerance, moderate weight gain, muscle weakness, fatigue, menstrual irregulatites, decreased libido, hypertension, sleep apnea, paresthesias (nerve entrapment, compression), headaches d. Treatment Somatostatin analongs to inhibit GH, dopamine agonists, GH analongs, removal of any tumors, radiation therapy (may take several years for remission) Adrenal insufficiency two forms: Primary (Addisons disease) and Secondary adrenal insufficiency due to a disorder of the HPA system a. Secondary occurs as the result of hypopituitarism or because the pituitary gland has been surgically removed b. Tertiary due to a hypothalamic defect c. Can also be due to rapid withdrawal of glucocorticoids that have been administered therapeutically i. Glucocorticoids cause adrenal cortical atrophy and loss of cortisol production 1. Adrenal suppression can be critical during periods of stress and surgery d. Acute adrenal crisis life threatening condition that can be sudden or that can progress over several days i. If Addison disease is underlying problem, exposure to minor illness can result in nausea, vomiting, muscular weakness, hypotension, dehydration, vascular collapse ii. Massive bilateral adrenal hemorrhage can cause this; hemorrhage can be caused by meningoccoal septicemia, adrenal trauma, anticoagulant therapy, adrenal vein thrombosis, adrenal metastases iii. Treatment: extracellular fluid restoration and glucocorticosteroid replacement therapy (several liters of 0.9% saline, 5% dextrose); Oral hydrocortisone replacement therapy can be resumed once saline infusion is d/c and person is taking food and fluids by mouth. Possibly use broad-spectrum antibiotic as well Addisons disease adrenal insufficiency in which all layers of adrenal cortex are destroyed, resulting in lack of adrenal cortical hormones and elevated ACTH levels (due to lack of feedback inhibition) a. Cause: Autoimmune destruction, tuberculosis, metastatic carcinoma, fungal infection, cytomegalovirus infection, amyloid disease, hemochromatosis, AIDS, certain drugs b. Manifestations arent apparent until about 90% of adrenal cortex has been destroyed; related to mineralocorticoid deficiency (urinary losses of sodium, glucocorticoid deficiency, hyperpigmentation due to elevated ACTH levels c. S/s Bronzed skin, hyperpigmentation of body creases, nipples, mucus membranes, urinary losses of sodium, water and retention of potassium (hyperkalemia), orthostatic hypotension, dehydration, weakness, fatigue cardiovascular collapse, shock, poor tolerance to stress hypoglycemia, lethargy, fever, anorexia, n/v, weight loss d. Treatment: Lifetime oral replacement therapy; Hydrocortisone is Drug of choice, can also use fludrocortisones, regular schedule for meals, exercise Cushing syndrome excess glucocorticoid hormone. Three forms: 1) Pituitary form, due to excessive production of ACTH by a tumor of pituitary gland and is called Cushing disease; 2) Adrenal form, due to benign or malignant adrenal tumor; 3) Ectopic Cushing syndrome due to a nonpituitary ACTH-secreting tumor a. Iatrogenic Cushing syndrome - Results from long-term therapy with a potent pharmacologic preparations of clugocorticoids b. S/s altered fat metabolism causes protruding abdomen, buffalo hump on back, round, plethoric moon face; muscle weakness, thin extremities (due to protein breakdown, muscle wasting); thin parched skin over forearms, legs, purple striae on breast, thighs, abdomen; osteoporosis ( due to destruction of bone proteins) that leads to back pain, compression fractures of vertebrae, rib fractures; development of renal calculi i. Other Derangements in glucose metabolism (some have Diabetes mellitus), hypokalemia, increased susceptibility to infection, increased gastric acid secretion leading to gastric ulcers or bleeding, hirsutism, mild acne, menstrual irregularities, emotional disturbances c. Diagnosis: Urine analysis looking for 24-hr excretion of cortisol; late night serum or salivary cortisol levels, overnight dexamethasone suppression test, test for plasma levels of ACTH d. Treatment: Surgery, irradiation, drugs i. Preferred method: transsphenoidal removal of pituitary adenoma or hemihypophysectomy; followed by cortisol replacement therapy for 6-12 months Pheochromocytoma a tumor of chromaffin tissue, which contains sympathetic nerve cells that stain with chromium salts; usually located in adrenal medulla a. Tumor secretes massive amounts of epinephrine and norepinephrine, resulting in hypertension. Some have sustained HTN; others have intermittent high levels of HTN b. Secretion is paryoxysmal rather than continuous, causing periodic episodes of severe headache, excessive sweating, and palpitations. Less often, nervousness, tremor, facial pallor, weakness, fatigue and weight loss can occur. c. Diagnosis urinary and blood assays for catecholamins and their metabolites; CT and MRI to locate tumors and possible metastases d. Treatment Surgery or drugs to block action or synthesis of catecholamines

i.

Labs Hemoglobin A1C marker for chronic hyperglycemia, reflecting average blood glucose levels over a 2- to 3-month period. Glucose entry into red blood cells is not insulin dependent, so the rate at which glucose becomes attached to the hemoglobin molecule depends on blood glucose levels. Goal is to keep diabetics under 7%.

Definitions

1. Decerebrate posturing - extensor posturing rigidity of arms with palms of the hands turned away from body, stiffly extended legs and plantor flexion of the feets a. Occurs with rostral-to-caudal deterioration, when lesions extend to involve the midbrain and upper brain stem; more ominous than decorticate 2. Decorticate posturing - flexion of arms, wrists and fingers, with abduction of upper extremities, internal rotation and plantar flexion of lower extremities a. Due to lesions of cerebral hemisphere or internal capsule (ie cerebral cortex) 3. Somogyi effect Normal or elevated blood glucose levels are present at bedtime; hypoglycemia occurs at about 2-3 am; which causes an increase in the production of counter-regulatory hormones. By about 7am, in response to counter-regulatory hormones, the blood glucose rebounds significantly to the hyperglycemic range. Treatment includes decreasing the evening (predinner or bedime) dose of intermediate-acting insulin or increasing the bedtime snack. 4. Bruzinkski sign With one hand under the neck and the other on the persons chest, sharply flex chin on chest, watch hips and knees. Abnormal response is resistance and pain in neck with flexion of hips and knees. Indicates meningeal irritation (meningitis, infections). 5. Kernigs sign In flat-lying supine position, raise leg straight or flex thigh on abdomen, then extend knee. Abrnormal response is resistance to straightening because of hamstring spasm and pain down posterior high. Indicates meningeal irritation. Pathophysiology Processes To Know: 5 cardinal signs of inflammation, vitamin D homone (remember it's role with calcium and the parathyroid hormone), need to know the levels of the spinal cord and what they correspond to as it relates to function - sacral S2,34 innervates bowel, bladder and sexual organs for example, review the stress response (remember there is a lot of endocrine in the stress response - remember what the adrenals due, glucocorticoid, mineralcorticois) - reveiw the stress response if you are not remembering hormones and proteins involved, remember that hydrocortisone is used to Addison's disease because there is a lack o mineral corticoids and glucocorticoids - so if I ask you what mineral and glucocorticoids do - you can tell me.