Patho Exam 2

  1. Cancer
    Defined as Diseases in which abnormal cells divide without control and are able to invade other tissues
  2. Tumor
    • -Referred to any swelling that is caused by inflammation
    • -New growth, or neoplasm
  3. Benign tumors
    • -Encapsulated
    • -Well differentiated cells
    • -Well organized stroma
    • -Do not invade beyond their capsule nor to regional lymph nodes or distant locations
  4. Malignant tumors
    • Tumors that are initially benign can progress to cancer
    • -More rapid growth rates and specific microscopic alterations
    • -Loss of differentiation and absence of normal tissue function
    • -Lack a capsule and grow to invade nearby blood vessels, lymphatics and surrounding tissues
    • -Can spread beyond the tissue of origin (metastasis)
  5. Metastasis
    The most deadly characteristic of cancer is their ability to spread far beyond the tissue of origin
  6. Cancer naming
    Cancers are named according to the cell type from which they originate
  7. Carcinomas
    Cancers arising in epithelial tissues
  8. Adenocarcinomas
    Cancers arising from ductual or glandular structures
  9. Suffix sarcoma
    Cancers arising from the mesenchymal tissue (include connective tissue, muscle and bone)
  10. Lymphomas
    Cancers of the lymphatic tissue
  11. Leukemias
    Cancers of blood forming cells
  12. Anaplasia
    Loss of cellular differentiation
  13. Carcinoma in situ (CIS)
    • -Preinvasive epithelial tumors of glandular or squamous cell origin
    • -Localized to epithelium
    • -Have not penetrated the local basement membrane or invaded the surrounding stroma
    • -Not malignant
    • -Includes in number of sites including cervix, skin, oral cavity, esophagus and bronchus
  14. CIS (carcinoma in situ) can have one of the following three fates
    • 1. Remain stable for a long time
    • 2. Progress to invasive and metastatic cancers
    • 3. Regress and disappear
    • -Can vary from low grade to high grade dysplasia
    • -Removal is called "watchful waiting"
  15. Tumor Initiation
    • -Process that produces the initial cancer cells
    • -Dependent on specific mutations and characteristics of the microenvironment
  16. Tumor promotion
    • -Population of cancer cells expands with diversity of cancer cell phenotypes
    • -Dependent on additional mutations and a changing tumor microenvironment
  17. Tumor progression
    • -Process leading to spread of the tumor to adjacent and distal sites
    • -Further mutations and changing microenvironments at the primary tumor
  18. Genetic changes
    • -May occur by both mutational and epigenetic mechanisms
    • -Mutations include small scale changes in DNA such as point mutations.
    • -Chromosome translocations
  19. Chromosome translocation
    Large changes in chromosome structure in which a piece of one chromosome is translocated to another chromosome
  20. Gene amplification
    • -Repeated duplication of a region of a chromosome
    • -Tens or even hundreds of copies are present instead of the normal two copies of a gene
  21. Gene expression
    • May be altered by epigenetic effects including -DNA methylation
    • -histone acetylation
    • -altered expression of non-coding RNA
  22. Clone proliferation or clonal expansion
    Cancer cell has a selective advantage over its neighbors; its progeny can accumulate faster than its nonmutant neighbors
  23. Transformation
    • Process by which a normal cell becomes a cancer cell
    • -Directed by progressive accumulation of genetic chance that alter the basic nature of the cell and drive it to malignancy
  24. Cancer development in many ways is analogous to wound healing
    • -mediators recruit inflammatory/immune cells (primarily T lymphocytes and macrophages, but also B cells and neutrophiles) and cells normally associated with tissue repair (fibroblasts, adipocytes, mesenchymal stem cells) These cells form the stroma (make up 90% of tumor mass)
    • -Cancer cells in different regions of the tumor are genetically diverse
    • -Hallmarks of cancer are consequences of cancer-stromal interactions
  25. First hallmark of cancer
    Uncontrolled cellular proliferation
  26. Proto-oncogenes
    genes that encode components of receptor-mediated pathways designed to regulate normal cellular proliferation
  27. Oncogenes
    • -A cancer cell that characteristically expresses mutated or overexpressed proto-oncogenes
    • -Cell is driven into a state of unregulated expression of proliferation signals and uncontrolled cell growth
    • -May be activated by gene amplification
  28. Autocrine stimulation
    Process where some cancers can acquire the ability to secrete growth factors that stimulate their own growth
  29. Imatinbid
    • -A drug that specifically targets tyrosine kinase
    • -Represents the first successful chemotherapy target against the product of a specific oncogenic mutation
  30. Tumor-suppressor genes
    • -Uncontrolled cancer cell proliferation is related to inactivation of tumor-suppressor genes.
    • -AKA anti-oncogenes
    • -We have two copies of the tumor-suppressor gene-one from each parent
    • -Both copies must be inactivated; therefore two mutations are necessary
  31. Retinoblastoma (RB) gene
    • Prototypical tumor-suppressor gene
    • -Monitors anti-grwoth cellular signals
    • -Blocks activation of the growth/division phase in cell cycle
    • -Mutations in RB lead to persistent cell growth
  32. Tumor protein p53 (TP53)
    • -Tumor-suppressor gene
    • -Called the guardian of the genome
    • -Activates caretaker genes (maintain genomic integrity)
    • -Stress activates kinases that phosphorylate p53 into an active suppressor of cell division and activator of caretaker genes
    • -Controls initiation of cellular senescence or apoptosis
    • -Loss of function of these genes leads to increased mutation rates and cancer
  33. Caretaker genes
    Encode proteins that are involved in repairing damaged DNA
  34. Genomic instability
    • Increased tendency of alterations-mutability in the genome during the life cycle of cells
    • -May also result from increased epigenetic silencing or modulation of gene function
    • -Many cancers have increased methylation of DNA in the promoter region of tumor-suppressing genes
  35. Oncomirs
    microRNAs that stimulate cancer development and progression
  36. Senescence
    Cease dividing
  37. Hayflick limit
    Most normal cells are not immortal and can divide only a limited number of times
  38. Telomeres
    • Protective ends, or caps, of repeated hexanucleotides on each chromosome and are placed and maintained by a specialized enzyme called telomerase
    • -When cancer cells reach a critical stage, they activate telomerase to rebuild their telomeres
  39. Angiogenesis or neovascularization
    • Process of establishing new blood vessels within the tissue undergoing repair
    • -Angiogenetic factors normally control development of new vessels
    • -Hypoxia-inducible-factor 1a, is a major regulator of angiogenesis in normal tissue
  40. Hypoxia-inducible-factor 1a
    • Increased expression of HIF 1a is related to:
    • -increased resistance to chemotherapy
    • -increased tumor cell glycolysis
    • -increased metastasis and a poor prognosis
  41. Warburg effect
    • Even in the presence of oxygen, cancer cells may not use mitochondrial oxidative phosphorylation
    • -reprogrammed to use glycolysis-Warburg effect
    • -The shift from OXPHOS to glycolysis allows lactace and other products of glycolysis to be used for more efficient production of lipids, nucleotides, amino acids, and other molecular building blocks needed for rapid cell growth
    • -Promoters of aerobic glycolysis are activated by oncogenes and mutate tumor-suppressor molecules.
    • -FDG is missing a key hydroxyl group so it cannot be broken down by glycolysis and thus FDG accumulates in cells
    • -This can be detected with an imaging machine
  42. Apoptosis
    • Programmed cell death
    • -Mechanism by which individual cells can self-destruct under conditions of tissue remodeling or as a protection against aberrant cell growth that may lead to malignancy
    • -Apoptotic pathways are dysregulated in most cancers
    • -Excess expression of anti-apoptotic members of the Bcl-2 family may also provide increased resistance to chemotherapeutic drugs
    • -Successful cancers suppress apoptotic pathways and increase resistance to cell death
  43. Two pathways that can trigger apoptosis
    • Intrinsic: mitochondrial pathway.
    • Extrinsic: activated through a plasma membrane receptor complex. Known as death receptor
  44. Chronic Inflammation
    • Recognized for close to 150 years as being an important factor in the development of cancer
    • -Some organs are more susceptible to the oncogenic effects of chronic inflammation (GI tract, prostate, thyroid gland)
  45. Chronic infection with helicobacter pylori
    • -Important cause of peptic ulcer disease
    • -Associated with gastric carcinoma
    • -Increased gastric acid secretion, atrophic gastritis and duodenal ulcers can progress to dysplastic changes and finally gastric adenocarcinoma
  46. Inflammation and tumors
    • Successful tumors appear capable of manipulating cells of the inflammatory response from a rejection response towards wound healing and tissue regneration
    • The process includes:
    • -Induction in the damaged tissue of cellular proliferation
    • -Neovascularization
    • -Local immune suppression
    • These activities benefit cancer progression as well as increase resistance to chemotherapeutic agents.
  47. Tumor associated macrophages (TAM)
    • -Key cells that promote tumor survival
    • -Related to the degree of macrophage infiltration and progression of tumor
    • -Most tumors have large numbers of TAMS which correlates with a worse prognosis
    • Monocytes (can differentiate) are attracted from the blood into the tumor.
    • -Develop the capacity to block T cytotoxic cell and NK cell functions and produce cytokines that are advantageous for tumor growth and spread
    • -Secrete cellular growth factor and fibroblasts growth factor
    • -Overall effect is increased tumor growth, invasion of the blood vessels, increased oxygen to the tumor and invasion through the degraded matrix into the local tissue
  48. Treg cells
    • Role of treg cells during wound healing is to control or limit the immune response to protect the host's own tissues against autoimmune reactions
    • -Their role in tumors is manipulated to prevent a destructive anti-tumor immune response and provide cytokines that facilitate tumor cell proliferation and spread
  49. Metastasis
    The spread of cancer cells from the site of the original tumor to distant tissues and organs through the body
  50. Epithelial-mesenchymal transition (EMT)
    • Model for transition to metastatic cancer
    • -Process that occurs normally in embryonic development as well as wound healing and tissue repair
    • -EMT that includes diminished cell-to-cell adhesion, digestion of the surrounding ECM and increased motility of individual cancer cells
    • -Process of EMT increases resistance to apoptosis
    • -After release from local to distant metastasis, cancer cells must be able to invade local blood and lymphatic vessels
    • -After release from ECM and digestion of basement membrane, mobile cancer cells gain access to circulation
    • -Tumor cells will bind to blood platelets that shields the tumor cells and creates a small tumor embolus or cancer clot, that can promote cancer survival in distant locations
  51. Neovascularization
    • In cancer, offers malignant cells direct access into venous blood and draining lymphatic vessels.
    • Most often spread first to regional lymph nodes through the lymphatics and then to distant organs through the bloodstream
  52. Dormancy
    • Cellular quiescence
    • A stable nonproliferative state that is reversible
  53. Paraneoplastic syndromes
    • Syndrome complexes that are triggered by a cancer but are not caused by direct local effects of the tumor mass
    • -For example: a small fraction of carcinoid tumors release substances including serotonin into the bloodstream that cause flushing, diarrhea, wheezing and rapid heartbeat.
    • -A number of cancers can trigger an antibody response that attacks the nervous system causing a variety of neurologic disorders
    • -Are the earliest symptoms of an unknown cancer
  54. Pain and cancer
    • Caused by indirect or direct mechanisms
    • Specific sites prone to cancer-associated pain:
    • -Bone metastases
    • -Brain tumors
    • -Pain in the abdomen may be caused by bowel obstruction
    • -Inflammation and infection
    • -Hepatic malignancies
    • -Mucosal surfaces can develop ulcerative lesions
  55. Fatigue
    • -Most frequently reported symptoms of cancer and cancer treatment
    • -Physiologic understanding includes mechanisms for decreased muscle contractility
  56. Cachexia
    • Multiorgan syndrome includes a constellation of clinical manifestations including:
    • -Anorexia
    • -Wasting
    • -Thermogenesis
    • -Altered heart and liver function
    • -Gut malabsorption
    • -Early satiety
    • -Taste alterations
    • -Altered protein, lipid and carbohydrate metabolism
    • -Changes in metabolic pathways
    • -Contributing further to muscle wasting is an increase in apoptosis and an impaired capacity for regeneration
  57. Anemia
    • Commonly associated with malignancy
    • -mechanisms that cause anemia include chronic bleeding, severe malnutrition, cytotoxic chemotherapy, malignancy in blood-forming organs
    • -Defects in erythropoietin production and shortened duration of red cell survival
    • -Administration of erythropoietin has been effective in correcting anemia
  58. Leukopenia and Thrombocytopenia
    • Direct tumor invasion of the bone marrow causes both leukopenia (decreased total white blood cell count) and thrombocytopenia (a decreased number of platelets)
    • -Many chemotherapeutic drugs affect rapidly dividing cells and are toxic to the bone marrow
  59. Infection
    • Most significant cause of complication and death in persons with malignant disease
    • -Advanced malignancies are highly immunosuppressive, as well as radiotherapy and chemo used to treat it
  60. Gastrointestinal tract
    • The GI tract relies on rapidly growing cells to produce and effective barrier.
    • Both chemo and radiation therapy may cause a decreased cell turnover leading to oral ulcers, malabsoprtion, and diarrhea.
    • -Increases the risk for infection
  61. Alopecia
    • Hair loss
    • -results from chemo effects on hair follicles
  62. Histologic Staging
    • Classification of cancer can be facilitated by a variety of clinical tests including:
    • -Immunohistochemical stains
    • -Flow cytometry
    • -Electron microscopy
    • -chromosome analysis
    • -Genetic studies
    • Critical to determine if cancer has spread, known as stage of cancer
  63. Stage of cancer
    Involves determining the size of the tumor, the degree to which is has locally invaded and the extent to which it has spread
  64. Stage 1 Cancer
    Cancer confined to the organ of origin
  65. Stage 2 Cancer
    Cancer that is locally invasive
  66. Stage 3 cancer
    Cancer that has spread to regional structure such as lymph nodes
  67. Stage 4 cancer
    Cancer that has spread to distant sites
  68. TNM System
    • One common scheme for standardizing staging
    • T: indicates tumor spread
    • N: indicates node involvement
    • M: indicates the presence of distant metastasis
  69. Tumor markers
    • Substances produced by both benign and malignant cells that are either present in or on tumor cells or found in the blood, spinal cord or urine.
    • Tumor markers include hormones, enzymes, genes, antigens and antibodies
  70. Uses of tumor markers
    • 1. To screen and identify individuals at high risk for cancer
    • 2. To help diagnose the specific type of tumor in individuals with clinical manifestations relating to their tumor
    • 3. To follow the clinical course of a tumor
    • Some nonmalignant conditions can produce tumor markers
  71. Classification of tumors
    • -Originally based on gross and light microscopic appearance
    • -Now commonly accompanied by immunohistochemical analysis of protein expression
  72. Surgery with cancer
    surgery is often the definitive treatment of cancers that do not spread beyond the limits of surgical excision
  73. Radiation therapy
    • Ionizing radiation damages cells by impairing enough energy to cause molecular damage, especially to DNA
    • -Cellular compartments with rapidly renewing cells are in general more radiosensitive
    • -Radiation is good for localized cancers and resgions that cannot be reached through surgery like the brain and pelivis
    • -Sources such as small I-labeled capsules can also be temporarily placed into body cavities
  74. Brachytherapy
    • Radiation source that temporarily places a capsule into the specific body cavity
    • -This method is useful in the treatment of cervical, prostate and head and neck cancers
  75. Chemotherapy
    • Antimetabolites block normal growth pathways in all cells
    • -Some cancer cells are highly sensitive to DNA damaging agents
    • -Single chemotherapeutic agents often shrink cancers but these drugs give alone rarely, if ever provide a cure
    • -Usually given in combination
    • -Cancers are more likely to develop drug resistance if there are significant delays between planned courses of chemo.
  76. Induction chemotherapy
    seeks to cause shrinkage or disappearance of tumors
  77. Adjuvant chemotherapy
    Given after surgical excision of a cancer with the goal of eliminating micrometastases
  78. Neonadjuvant chemotherapy
    Given before localized (surgical or radiation) treatment of cancer. This can shrink a cancer so that surgery may spare more normal tissue
  79. Sipuleucel-T (Provenge)
    • An immunization that has been approved
    • -Dendritic cells are obtained from an individual with prostate cancer and after modifications, injected back into the patient.
    • -Has extended patient's lives by 4.1 months
  80. A characteristic of a malignant tumor includes that it
    can spread far from the tissue of origin.
  81. Cancer of the connective tissue is referred to as a
  82. A cancerous tumor that is very poorly differentiated is referred to as being
  83. The serum marker used to evaluate a tumor of the adrenal gland is
  84. Which gene in its normal state negatively regulates cell proliferation?
    Tumor-suppressor genes
  85. A mutation that occurs due to changes in nucleotide base-pairs is described as a
    point mutation
  86. The process whereby tumor cells generate their own blood supply is referred to as
    • angiogenesis
    • Angiogenesis is the generation of new blood vessels. Thrombospondin is a protein that inhibits the growth of new blood cells. Carcinogenesis is the development of cancerous cells. Transforming growth factor is a proangiogenic factor (aids in the development of blood vessels).
  87. Genomic instability refers to
    • increased tendency for genome alterations and mutability during cell life cycles
    • Genomic instability refers to an increased tendency of alterations—mutability—in the genome during the life cycle of cells. Inherited and acquired mutations in caretaker genes that protect the integrity of the genome and DNA repair increase the level of genomic instability and risk for developing cancer.
  88. When a patient is diagnosed with a benign tumor, it can be assumed that the tumor is:
    • well differentiated and well encapsulated
    • Benign tumors are well encapsulated and well differentiated, but actually do retain some normal tissue. They do not spread to regional lymph nodes, nor are they generally resistant to treatment.
  89. Research has shown a connection between the development of cancer and the: (select all that apply)
    • Epstein barr virus, Hep B, Hep C, Human papilloma virus.
    • Hepatitis B and hepatitis C have been linked to the development of liver cancer, usually due to chronic inflammation. Epstein-Barr virus can lead to B-cell lymphomas in those patients who are immunosuppressed. Human papillomavirus has been linked to cervical, anogenital, and penile cancers. Research has not shown a link between cancer and the hepatitis A virus.
  90. Neural systems essential to cognitive function
    • 1. attentional systems
    • 2. memory and language systems
    • 3. Affective or emotive sysmtems
  91. Consciousness
    • State of awareness both of oneself and of te environment
    • Has two distinct components: arousal and awareness
  92. Arousal
    • -State of awakeness
    • -Mediated by the reticular activating system
    • -regulates attention, and information processing, maintains consciousness
  93. Awareness
    • -Content of thought
    • -Encompasses all cognitive functions
    • -Mediated by attentional systems, memory, language and executive systems
  94. Alterations in arousal
    May be caused by structural, metabolic or psychogenic (functional) disorders
  95. Supraatentorial disorders
    • -Above the tentorium cerebelli
    • -Produce changes in arousal by:
    • -Diffuse dysfunction or localized dysfunction
    • -Caused by disease processess affecting the cerebral cortex or subcortical white matter
    • -Disorders outside the brain but within the cranial vault (extracerebral)
    • -Disorders within the brain substance (intracerebral)
  96. Infratentorial disorders
    • -Below the tentorium cerebelli
    • -Produce a decline in arousal
    • -Direct destruction or compression of the reticular activating systems and its pathways
    • -Brainstem may be destroyed by direct invasion or by indirect impairment of its blood supply
  97. Metabolic disorders
    Alterations in arousal
    • Produce a decline in arousal by alterations in delivery of energy substates as occurs with hypoxia, electrolyte disturbances or hypoglycemia
    • -Metabolic disorders caused by liver or renal failure cause alterations in neuronal excitability because of failure to eliminate drugs
    • -All systemic diseases that eventually produce nervous system dysfunction are part of this category
  98. Psychogenic alterations in arousal
    • -Unresponsiveness
    • -May signal general psychiatric disorders
    • -Although appearing unconscious, the person is physiologically awake and the neurologic examination reflects normal responses
  99. 5 patterns of neurologic function are critical to the evaluation process
    • -Help to determine the extent of brain dysfunction
    • 1. Level of consciousness
    • 2. Pattern of breathing
    • 3. Pupillary reaction
    • 4.Oculomotor repsonses
    • 5. Motor responses
  100. Level of consciousness
    • -Most critical clinical index of NS function
    • -A person who is alert and oriented to self, others, place and time is considered to be functioning at the highest level of consciousness. This implies full use of all the person’s cognitive capacities.
  101. Patterns of breathing
    • -helps evaluate the level of brain dysfunction and coma. Rate, rhythm, and pattern should be evaluated. 
    • -When consciousness decreases, the lower brainstem centers regulate the breathing pattern by responding to CO2 levels (posthyperventilation apnea).
  102. Pupillary changes
    indicate the presence and level of brainstem dysfunction because brainstem areas that control arousal are adjacent to areas that control the pupils.
  103. Oculomotor responses
    • -resting, spontaneous, and reflexive eye movements
    • -Persons with a metabolically induced coma generally retain ocular reflexes even when other signs of brainstem damage are present.
  104. Motor responses
    helps to evaluate the level of brain dysfunction and determine the most severely damaged side of the brain. Pattern of response noted may be 1. Purposeful; 2. Inappropriate, generalized motor movement; 3. Not present.
  105. Vomitting, yawning and hiccups
    • complex reflex-like motor responses that are integrated by neural mechanisms in the lower brain-stem.
    • -Vomiting often accompanies CNS injuries that 1) Involve vestibular nuclei or its immediate projections (particularly when double vision) 2. Impinge directly on the floor of the fourth ventricle or 3. Produce brainstem compression secondary to increased intracranial pressure.
  106. Brain death (total brain death)
    • Brain is damaged and can never recover (irreversible) and cannot maintain the body's internal homeostasis.
    • -State law defines brain death as irreversible cessation of function of the entire brain including the brainstem and cerebellum
    • -Abnormality must result from structural or known metabolic disease and must not be caused by a depressant drug, alcohol poisoning or hypothermia
    • -An isoelectric or flat EEG for 6-12 hours
  107. Cerebral death or irreversible coma
    • -Death of the cerebral hemispheres exclusive of the brainstem and cerebellum.
    • -Brainstem may maintain internal homeostasis
    • -May remain in a coma or emerge into a persistent vegetative state or a minimally conscious state
  108. Persistent vegetative state
    • Complete unawareness of the self or surrounding environment and complete loss of cognitive function
    • -Individual does not speak and comprehensible words or follow commands
    • -BP and breathing are maintained without support
  109. Minimally conscious state
    May collow single commands, manipulate objects, gesture or give yes/no responses, have intelligible speech and have movements such as blinking or smiling
  110. Locked-in syndrome
    • -Complete paralysis of voluntary muscles with the exception of the eye movement
    • -Cannot communicate through speech or body movement but is fully conscious
    • -Vertical eye movement and blinking are means of communication
  111. Awareness
    • -Content of thought
    • -Encompasses all cognitive functions including awareness of self, environment, and affective states
  112. Selective attention
    • -Orienting
    • -refers to the ability to select specific information to be processed from available competing environmental and internal stimuli and to focus on that stimulus
  113. Selective attention deficits
    • Can be temporary, permanent or progressive
    • Include seizure activity, parietal lobe contusions, subdurmal hematomas, stroke, gliomas, metastatic tumors, late Alzheimer dementia, frontolobal dementia, psychotic disorders
  114. Memory
    Recording, retention and retrieval of information
  115. Amnesia
    • Loss of memory and can be mild or severe
    • -retrograde and anterograde amnesia
  116. Retrograde amnesia
    Difficulty retrieving past personal history memories or past factual memories
  117. Anterograde amnesia
    The inability to form new personal or factual memories but memories of the distant pass are retained and retrieved.
  118. Executive attention deficits
    • Include the inability to maintain sustained attention and a working memory deficit. Inability to set goals, and recognize when an object meets a goal.
    • ADHD is an example
  119. Pathophysiologic mechanisms that operate disorders in awareness
    • 1. Direct destruction caused by ischemia and hypoxia or indirect destruction resulting from compression
    • 2. The effects of toxins and chemicals or metabolic disorders
  120. Agnosia
    • Defect of pattern recognition-a failure to recognize the form and nature of objects
    • -Can be tactile, visual or auditory
  121. Dysphasia
    • -Impairment of comprehension or production of language with impaired communcation
    • -Aphasia is a more severe form of dysphasia
    • -results from dysfunction in the left cerebral hemisphere (Broca area) and Wernicke area and the subcortical and cortical connecting networks.
  122. Aphasia
    • A more severe form of dysphasia
    • -Inability to communicate using language
  123. Expressive dysphasia
    Loss of ability to produce spoken or written language with slow or difficult speech
  124. Receptive dysphasia
    Inability to understand written or spoken language
  125. Acute confusional states
    • Transient disorders of awareness and may have either a sudden or gradual onset
    • -Delirium can be considered a type of ACS
  126. Patho of Acute confusional states
    Widely distributed neural network involving the reticular activating system of the upper brainstem and its projections into the thalamus, basal ganglion, and specific associated areas of the cortex and limbic areas
  127. Delirium (hyperactive confusional state)
    • -Associated with ANS ovreactivity
    • -Develops over 2 to 3 days
    • -Several NTs are involved like acetylcholine and dopamine
  128. Excited delirium syndrome
    • Aka agitate delirium
    • -Hyperkinetic delirium that can lead to sudden death
    • -Altered mental status. combativeness, aggressiveness, tolerance to significant pain, rapid breathing, sweating, severe agitation, elevated temperature, noncompliance or poor awareness to direction
    • -Inability to become fatigued
    • -Unusual or superhuman strength
  129. Initial goals of Acute confusional state
    • 1. Establish the individual is confused
    • 2. Determine the cause of the confusion (organic or functional)
    • Next step is to differentiate whether the confusion is delirium or an underlying dementia
  130. Dementia
    Acquired deterioration and a progressive failure of many cerebral functions that include impairment of intellectual processes with a decrease in orienting, memory, language, judgment, and decision making
  131. Patho of dementia
    • Mechanisms include neuron degeneration, compression in brain tissue, atherosclerosis of cerebral vessels and brain trauma
    • -Genetic predisposition is associated with neurogenerative diseases like Alzheimer, Huntington and Parkinson diseases
    • -CNS infections including HIV also lead to nerve cell degeneration and brain atrophy
  132. Evaluation and Treatment of Dementia
    • Lab tests and neurophysiologic testing to identify underlying conditions that may be treatable
    • No specific cure exists for most progressive dementias
  133. Alzheimer disease (senile disease complex)
    Leading cause of sever cognitive dysfunction in older persons
  134. Patho of Alzheimer
    • -Include accumulation of neuritic plaques and tangles
    • -These are more concentrated in the cerebral cortex and hippocampus
    • -Degeneration of basal forebrain cholingergic neurons with loss of acetylcholine
    • -Loss of neurons results in brain atrophy with widening of sulci and shrinkage of gyri
    • -Loss of synapses, acetylcholine and other NTs contribute to the decline of memory and attention and loss of other cognitive functions
  135. Neuritic plaques
    Contain a core of amyloid beta protein
  136. Neurofibrillary tangle
    • The tau protein, a microtubule binding protein in neurons detaches and forms an insoluble filament
    • -These tangles contribute to neuron death
  137. Eval and Treatment of Alzheimer
    • -Diagnosis is made by ruling out other causes
    • -Cholinesterase inhibitors have shown a modest effect of cognitive function
  138. Frontotemporal disease
    • Previously known as Pick disease
    • -Second most common degenerative disease of te frontal and anterior frontal lobes
    • -Majority of cases involve mutations of genes encoding tau protein
  139. Seizure disorder
    -Represent a manifestation of disease and not a specific disease entity
  140. Seizure
    A sudden, transient disruption in brain electrical function caused by abnormal excessive discharges of cortical neurons
  141. Epilepsy
    Recurrence of seizures and a type of seizure disorder for which no underlying, correctable cause for seizure can be found
  142. Convulsion
    Sometimes applied to seizures and refers to the tonic-clonic (jerky contract-relax) movement associated with some seizures
  143. Conditions associated with seizure disorders
    • Any disorder that alters the neuronal environment may cause seizure activity
    • -Metabolic disorders, congenital malformations, genetic predisposition, perinatal injury, postnatal trauma, myoclonic syndromes, infection, brain tumor, vascular disease, and drug or alcohol abuse are conditions that may produce seizures
    • Threshold may be lowered by hypoglycemia, fatigue or lack of sleep, emotional or physical stress, fever, large amounts of water ingestion, constipation, use of antipsychotic drugs, withdrawal from antidepressant drugs or hyperventilation
    • -Environmental stimuli like blinking lights can cause seizures
  144. Types of seizures
    Seizures are classified by clinical manifestations, site of origin, EEG correlates, or response to therapy
  145. Tonic phase of seizures
    • -Excitation of the subcortical, thalamic, and brainstem areas
    • -Muscle contraction with increased muscle tone
    • -Associated with loss of consciousness
  146. Clonic phase
    • Alternating contraction and relaxation of muscles
    • -Begins when inhibitory neurons in the cortex, anterior thalamus, and basal ganglia react to cortical excitation
  147. Prodroma
    Early manifestations occurring hours to days before a seizure and may include anxiety, depression, or inability to think clearly
  148. Ictus
    Episode of the epileptic seizure with tonic-clonic activity
  149. Status epilepticus
    In adults is a state of continuous seizures lasting more than 5 minutes or rapidly recurring seizures before the person has fully regained consciousness from the preceeding seizure or a single seizure lasting longer than 30 minutes
  150. Postictal state
    Follows an epileptic seizure and can include signs of headaches, confusion, dysphasia, memory loss and paralysis that may last hours or a day or two
  151. Evaluation and Treatment of seizures
    • Brain imaging and CSF examination help identify neurologic diseases associated with seizures.
    • EEG is used to assess the type of seizure and determine its focus in brain tissue
    • Antiseizure medication, dietary treatments, surgical interventions are some treatments
  152. Primary brain injury
    • Consequence of alterations in cerebral blood flow, intracranial pressure and oxygen delivery
    • Alterations in CSF may be related to three injury states:
    • -Inadequate cerebral perfusion
    • -Normal cerebral perfusion but with an elevated intracranial pressure
    • -Excessive cerebral blood volume (CBV)
  153. Increased intracranial pressure (IICP)
    • May result from an increase in intracranial content (as occurs with tumor growth), edema, excess CSF, or hemmorhage.
    • -Dramatic sustained rises in ICP are not seen until compensatory mechanisms have been exhausted
    • -Dramatic rises in ICP occur over a very short period
  154. Autoregulation
    The compensatory alteration in the diameter of the intracranial blood vessels designed to maintain a constant blood flow during changes in cerebral perfusion pressure is lost with progressively increased ICP
  155. Cerebral edema
    • -Increase in the fluid content of brain tissue
    • -Increased extracellular or intracellular tissue volume
    • -Harmful effects are caused by distortion of blood vessels, displacement of brain tissues, increase in intracranial pressure and eventual herniation of brain tissue to a different brain compartment
  156. Cytoxic (metabolic) edema
    • -Toxic factors directly affect the cellular elements of the brain parenchyma causing failure of the active transport systems
    • -Cells lose their potassium and gain large amounts of sodium
    • -Water follows by osmosis into the cells-cells swell
    • -Occurs in gray matter and may increase vasogenic edema
  157. Interstitial edema
    • -Seen most often with noncommunicating hydrocephalus
    • -CSF from the ventricles into the extracellular spaces of the brain tissue
    • -Brain fluid volume increases predominantly around ventricles, with increased hydrostatic pressure within the white matter
  158. Hydrocephalus
    • Refers to various conditions characterized by excess fluid in cerebral ventricles, subarachnoid space or both
    • -Occurs because of interference of CSF flow caused by an increased fluid production, obstruction within the ventricular system, or defective reabsorption of the fluid
  159. Communicating hydrocephalus
    Defective reabosorption of CSF from the cerebral subarachnoid space and is found more often in adults
  160. Noncommunicating hydrocephalus
    Obstruction within the ventricular systems and is seen more often in children
  161. Patho of Hydrocephalus
    Produces increased pressure and dilation of the ventricles proximal to obstruction. Increased pressure and dilation cause atrophy of cerebral cortex and degeneration of white matter tracts
  162. Acute hydrocephalus
    Presents with signs of rapidly developing IICP. Coma occurs quickly if not treated
  163. Normal pressure hydrocephalus
    • Dilation of the ventricles without increased pressure
    • -develops slowly
  164. Evaluation and Treatment of hydrocephalus
    • Based on physical examination, CT scan and MRI.
    • Can be treated by surgery to resect cysts, neoplasms, or hematomas or by ventricular bypass into the normal intracranial channel or into an extracranial compartment using a shunting procedure
    • -Reduction in CSF is achieved through diuresis or placement of a shunt
  165. Movement
    Complex patterns of activity controlled by the cerebral cortex, the pyramidal system, the extrapyramidal system and the motor units
  166. Hypotonia
    • Decreased muscle tone
    • -Passive movement of a muscle occurs with little or no resistance. Causes include cerebellar damage and pure pyramidal tract damage
    • -Tire easily or are weak
    • -Joints become hyperflexible, extreme joint mobility, muscle mass atrophies
    • -Muscle cells are gradually replaced by connective tissue and fat
  167. Hypertonia
    • Increased muscle tone
    • -Passive movement occurs with resistance to stretch and is caused by upper motor neuron damage.
    • -4 types of hypertonia are spasticity, paratonia, dystonia and rigidity
  168. Hyperkinesia
    • -Excessive, purposeless movement and represents the second broad category of abnormal movements.
    • -Includes tremors,dyskinesias and abnormally involuntary movement
    • -Huntington Disease symptoms
  169. Huntington Disease
    • -Progressive
    • -Neurologic abnormalities
    • -No known treatment for halting degeneration or progression of symptoms
    • -Diseae is fatal
  170. Hypokinesia
    • -Decreased movement
    • -Loss of voluntary movement but still consciouss
    • -Normal peripheral nerve and muscle function
  171. Akinesia
    • -Decrease voluntary and associated movements
    • --Dysfunction of the extrapyramidal system
    • -Deficiency of dopamine  or defect in postsynaptic dopamine receptors
    • -Occurs in parkinsonism
  172. Bradykinesia
    • -Slowness of voluntary movements
    • Difficulty with:
    • -Initiating movements
    • -Continuing movements smoothly
    • -Performing synchronous and consecutive tasks
  173. Parkinson Disease
    • -Complex motor disorder accompanied by systemic nonmotor and neurologic symptoms
    • -Pathogenesis unknown
    • -Gene mutations have been found that influence nerve function
    • Tremor and rigidity
    • -Akinesia/bradykinesia
    • -Postural disturbance
    • -dysplagia
    • -No true paralysis
    • -Nonmotor symptoms include urinary urgency, difficulty concentrating, depression, hallucinations
  174. Secondary Parkinsonism
    • Parkinsonism caused by disorders other than Parkinson disease
    • -Head trauma, infection, neoplasm, atherosclerosis, toxins, drug intoxication
  175. Treatment for Parkinson disease
    • Symptomatic with drug therapy to decrease akinesia
    • -Deep brain stimulation is replacing therapy for those unresponsive to drug therapy
    • -Stem cell implants and gene therapy for future treatments
  176. Paresis
    Partial paralysis with incomplete loss of muscle power
  177. Paralysis
    Loss of motor function so that a muscle group is unable to overcome gravity
  178. Spinal shock
    • Temporary loss of all spinal cord functions below the lesion
    • -Complete flacid paralysis, absence of reflexes, disturbances of bowel and bladder function
  179. Amytrophic lateral sclerosis (ALS)
    • -Sporadic motor neuron disese
    • -Formerly known as Lou Gehrig disease
    • -Neurodegenerative
    • -Involves lower and upper motor neurons
    • -Amytrophic (without muscle nutrition or progressive muscle wasting)
    • -
    • -Scarring of the corticospinal tract in the lateral spinal cord
    • -Higher in males
    • -Unknown cause
    • -Oxidative stress, mitochondrial dysfunction, defects in axonal transport are under investigation
    • -About 60% have a spinal form of the disease with focal muscle weakness beginning in the arms and legs and progressing to muscle atrophy, spasticity, loss of manual dexterity and gait
    • -No associated mental, sensory or ANS symptoms are present
  180. Evaluation and Treatment of study
    • Electromyography
    • -muscle biopsy
    • -Imaging studies
    • -CSF markers
    • -Little treatment is available to alter the course
    • -Rilutek has extended length of time patients do not require ventilatory assistance
    • -Fatal from respiratory failure usually within 3 years of diagnosis-small percentage live 5-10 years longer
  181. Dystonia
    Maintenance of an abnormal posture through muscular contractions. When muscular contractions are sustained for several seconds, they are called dystonic movements. When lasting for longer periods, they are called dystonic postures. These may last for weeks causing permanent, fixed contractures
  182. Decorticate posture
    • Aka antigravity posture or hemiplegic posture
    • Upper extremities flexed at the elbows and held close to the body
    • -Lower extremities are externally rotated and extended
  183. Decerebrate posture/response
    • Increased tone in extensor muscles and trunk muscles
    • -Active tonic neck reflexes.
    • -When head is neutral, all 4 limbs rigidly extended
  184. Basal ganglion posture
    Stooped, hyperflexed posture with a narrow-based, short stepped gait
  185. Hypermimesis
    Manifests as pathologic laughter or crying. Laughter is associated with right hemisphere injury adn crying is with left hemisphere injury
  186. Hypomimesis
    Manifests as aprosody-loss of emotional language. Inability to understand emotion in speech and facial expression. Involves the inability to express emotion in speech and facial expression
  187. Apraxia/dyspraxia
    • Disorder of learned skilled movements
    • -Difficulty planning and executing coordinated motor movements
    • -Difficulty with speaking, writing, using tools or utensils, playing sports, following instructions and focusing
  188. Cerebellar motor movements
    • Associated with ataxia and other symptoms affecting coordinated movement
    • -Primarily influence the same side of the body
  189. Disorders of the CNS and PNS
    • Alterations in CNS function are caused by traumatic injury, vascular disorders, tumor growth, infectious and inflammatory processes and metabolic derangements.
    • Alterations in PNS involved the nerve roots, a nerve plexus, or the nerves themselves, or the neuromuscular junction
  190. Traumatic brain injury
    • Alteration in brain function or other evidence of brain pathology caused by an external force
    • -Most common are motor vehicle accidents for children and falls for adults
    • -Males have the highest incidence rate
  191. Primary brain injury
    • Caused by direct impact and can be focal, affecting one area or diffuse (involving more than one area of the brain)
    • -Can be mild, moderate or severe
    • -Glasgow scale is used to grade severity
  192. Focal brain injury
    • Can be caused by closed (blunt) trauma or open (penetrating) trauma
    • -Closed is more common and involves striking a hard surface or rapidly moving object striking the head or by blast waves
  193. Closed (blunt)  trauma
    • -Closed is more common and involves striking a hard surface or rapidly moving object striking the head or by blast waves
    • -Dura remians in tact
  194. Open (penetrating) injury
    • Penetrating trauma or skull fracture
    • -A break in dura occurs
  195. Closed brain injuries
    • -Specific
    • -Grossly observable brain lesions that occur in a precise location
    • -May be coup or countercoup
  196. Coup
    Injury at the site of impact
  197. Countercoup
    Injury from rebounding and hitting opposite side of the skull
  198. Contusions
    • Compression of the skull at the point of impact produces contusions.
    • Brain bruising from blood leaking from an injured vessel
  199. Epidural (extradural) hematoma
    Bleeding between the dura mater and skull
  200. Subdural hematomas
    bleeding between the dura mater and the brain
  201. Intracerebral hematomas
    bleeding within the brain
  202. Open brain injury
    • Trauma that penetrates the dura mater
    • -Produces focal and diffuse injury
    • -Includes compound skull fracture and missile injuries
    • Crush injury is laceration and crushing of whatever the missile touches
    • Stretch injury is when blood vessels and nerves are damaged without direct contact as a result of stretching
    • -May also include meningeal or cerebral lacerations from projectiles driven into the brain substance
  203. Diffuse brain injury
    • Aka diffusional axon injury (DAI)
    • Involves widespread area of the brain
    • -Whip lash or rotational forces cause shearing of delicate axonal fibers and white matter tracts that project to cerebral cortex
    • -Include mild concussion, classic concussion, mild, moderate and severe DAI
  204. Secondary brain injury
    • -Indirect result of primary brain injury
    • -Trauma and stroke syndromes
    • -Hypotensionm hypoxia, anemia, hypercapnia, hypocapnia.
  205. Primary spinal cord injury
    • -Occurs with initial mechanical trauma and immediate tissue destruction
    • -Occurs if spine is not immobilized properly after injury
    • -May occur in absence of vertebral fracture or dislocation from longitudinal stretching
  206. Secondary spinal cord injury
    • Pathophysiologic cascade of vascular, cellular, biochemical events that begins within a few minutes after injury and continues for weeks.
    • -Traumatized cord is replaced with acellular collagenous tissue, usually in 3 to 4 weeks
  207. Vertebral injuries
    • result from acceleration, deceleration or deformation forces occurring at impact.
    • -These forces cause vertebral fractures, dislocations, and bone fragments that can cause compression to the tissues
    • -Can also cause shearing of tissues
  208. Neurogenic shock
    • Also called vasogenic shock
    • -Occurs with cervical or upper thoracic cord injury
    • -May be seen in addition to spinal shock
    • -Caused by absence of sympathetic activity through loss of supraspinal control and unopposed parasympathetic tone mediated by the intact vagus nerve
  209. Low back pain (LBP)
    • Affects the area between the lower rib cage and gluteal muscles and often radiates into the thighs
    • -Primary cause of disability worldwide
    • -Idiopathic or nonspecific and precise diagnosis
    • -Common causes include degenerative disk disease, spondylolisthesis, spinal osteochondrosis, spinal stenois and lumbar disk herniation
  210. Degenerative disk disease DDD
    • -Process of normal aging as a response to continuous vertical compression of the spine
    • -Genetic component involving the genes that code the cartilage intermediate layer protein
  211. Herniated vertebral disk
    Displacement of nucleus pulposus or annulus fibrosus beyond the intervertebral disk space
  212. Radiculopathy
    Compression or inflammation or both of a spinal nerve resulting from disk herniation
  213. Cerebrovascular disorders
    • Most frequently occurring neurologic disorder
    • -Any abnormality of the brain caused by a pathologic process in the blood vessels is referred to as a cerebrovascular disease
  214. Cerebrovascular accidents (CVAs)
    • -3rd cause of death in women and 5th leading cause of death in men
    • -Persons with hypertension and type 2 diabetes have a fourfold increase in stroke incidence and eightfold increase in stroke mortality
    • -Classified as ischemic, hemorrhagic, or associated with hypofusion
    • -Poorly or uncontrolled arterial hypertension
    • -Smoking
    • -Insulin resistance and diabetes mellitus
    • Congestive heart disease and peripheral vascular disease
    • -Atrial fibrilation
    • -Chlamydia
  215. Ischemic stroke
    Obstruction to arterial blood flow to the brain from thrombus formation, an embolus, or hypoperfusion related to decreased blood volume or heart failure
  216. Transient ischemic attacks (TIAs)
    • Episodes or neurologic dysfunction lasting no more than 1 hour and resulting from focal cerebral ischemia
    • -Include weakness, numbness, sudden confusion, loss of balance or a sudden severe headache
    • -Imaging usually reveals a brain infarction
    • -Will most likely have a stroke within 90 days after TIA
  217. Thrombotic strokes
    • -Arterial occlusions caused by thrombi formation in arteries supplying the brain or intracranial vessels
    • -Develops from atherosclerosis and inflammatory disease processes that damage arterial walls
  218. Embolic stroke
    • Fragments that break from a thrombus formed outside the brain, usually in the heart, aorta or common carotid artery.
    • -Other sources of embolism include fat, air, tumor, bacterial clumps and foreign bodies
  219. Treatment of Stroke
    • Focused on:
    • 1. Restoring brain perfusion in a timeframe that does not contribute to reperfusion injury
    • 2. Counteracting the ischemic cascade pathways
    • 3. Lowering cerebral metabolic demand so that the susceptible brain tissue is protected
    • 4. Promoting tissue restoration
    • Thrombolysis, using a tissue-type plasminogen activator (tPA) is given within 3-4.5 hours of onset of symptoms
    • Anticoagulants are used as well
  220. Hemorrhagic stroke (intracranial hemorrhage)
    • Can occur is brain tissue or subarachnoid or subdural spaces
    • Primary cause is hypertension
    • -Other causes include tumors, coagulation disorders, trauma, illicit drug use (cocaine)
    • -A mass of blood is formed as bleeding continues in brain tissue. Adjacent brain tissue is deformed, compressed and displaced producing ischemia, edema and IICP and necrosis
    • -Can occur because of cerebral hemorrhage, hypertension, intracranial aneurysm
    • -No signs or symptoms unless ruptured
    • -vascular malformations (AVM)
  221. Intracranial aneurysms
    May result from arteriosclerosis, congenital abnormality, cocaine use, trauma, inflammation, and vascular sheer wall stress
  222. Aneurysm
    • -Often asymptomatic
    • -Dizziness, headacahe and cranial nerve compression
    • -Symptoms varies depending on location
    • -Diagnosis before a bleeding episode is made through arteriography
    • -Treatments are both medical (control of hypertension) and surgical (microvascular clipping or placement of endovascular coils)
  223. Arterious malformation (AVM)
    • -rare, congenital vascular lesions
    • -Mass of dilated vessels between the arterial and venous systems without an intervening capillary bed
    • -May occur in any part of the brain and vary in size
    • -Can extend from the cortex to the ventricle
    • -Abnormal blood vessel structure
    • -Abnormally thin and have complex growth and remodeling
  224. Subarachnoid hemorrhage
    • Escape of blood from a defective or injured vessel into the subarachnoid space
    • -Symptoms similar to meningitis
    • -Blood increases ICP and produces an inflammatory reaction
    • -Blood coats nerve roots, clogs arachnoid granulations and obstructs foramina within the ventricular system
  225. Kernig sign
    Straightening the knee with hip and knee in a flexed position produces pain in the back and neck regions
  226. Brudzinski sign
    passive flexion of the neck produces neck pain and increased rigidity.
  227. Headache
    • Common neurologic disorders and is usually a benign symptom
    • -Can be associated with brain tumor, meningitis, or cerebrovascular disease
  228. Migraine
    • Episodic neurologic disorder characterized by a headache lasting 4 to 72 hours
    • Diagnosed when two of the following symptoms occur: unilateral head pain, throbbing pain, pain worsens with activity, moderate or severe pain intensity
    • And at least one of the following: nausea and/or vomiting or photophobia and phonophobia
    • -Have an increased risk of epilepsy,depression, anxiety disorders, cardiovascular disease and stroke
    • -Chronic migraines occur at least 15 days in a month for more than 3 months
    • -Associated with overuse of analgesic migraine medications, obesity, and caffeine overuse
  229. Cluster headaches
    • One of a group of disorders referred to as a trigeminal autonomic cephalagias
    • -Up to 8 attacks per day
  230. Tension type headache (TTH)
    • Most common type of headache
    • -Treated with ice, and more severe forms with aspirin or nonsteroidal antiinflammatory drugs
    • -Chronic TTH are best managed with tricyclic antidepressant and behavioral and relaxation therapy
  231. Meningitis
    • Inflammation of the brain or spinal cord
    • -Infectious meningitis may be caused by bacteria, viruses, fungi, parasites, or toxins
    • -May be acute subacute or chronic
  232. Fungal meningitis
    • Chronic
    • -Much less common than bacterial or viral
    • -Those with impaired immune responses or alteration in normal body flora
  233. Viral meningitis
    • -AKA aseptic or nonpurulent meningitis
    • -Thought to be limited to the meninges
    • -Identifiable bacterium cannot be found in CSF
    • -Managed pharmacologically with antiviral drugs and steroids
  234. Bacterial meningitis
    • -Primarily an infection of the pia mater and arachnoid, the subarachnoid space, the ventricular system, and the CSF
    • -Meningococci and pneumoccoci are most common pathogens. These are inhaled. Epithelial cells to the mucosal barrier to the bloodstream, then cerebral blood vessels, across the blood brain barrier and infect the meninges
    • -Predisposing conditions are otitis or sinusitis, immunocompromised status, and pneumonia
  235. Clinical manifestations of meningitis
    • -Fever, tachycardia and chills
    • -Meningeal irritation manifestations include throbbing headache, severe photophobia, nuchal rigidity, positive Kernig and Brudzinski signs
    • -Decrease in consciousness, cranial nerve palsies and seizures
  236. Treatment for meningitis
    • Rapid diagnosis
    • -Antibiotic administration
    • -Supportive treatment
  237. Brain abcesses
    • -Abcesses, localized collections of pus, may form within the parenchyma of the brain or spinal cord but are rare
    • Classified as epidural (associated with osteomyelitis in a cranial bone) subdural (arise from a sinus infection or a vascular stroke) or intracerebral (arise from a vascular source)
  238. Spinal cord abcesses
    • Classified as epidural or intramedullary
    • -Epidural usually originate as osteomyelitis in a vertebra. The infection then spreads into the epidural space
  239. Clinical manifestations of brain abcesses
    • 1. spinal aching
    • 2. severe root pain, accompanied by spasms of the back muscle and limited vertebral movement
    • 3. Weakness caused by progressive cord compression
    • 4. Paralysis
    • Usually with spinal injury
  240. Encephalitis
    • Acute febrile illness, usually of viral origin with nervous system involvement
    • -Most common forms are caused by bites of mosquitos, ticks or flies
    • -Herpes simplex type 1 is the most common sporadic cause
    • -may occur as complication of systemic viral dsieases such as polio, rabies or mono or after recovery of viral infections such as rubella, varicella, ruboela, or yellow feet.
  241. Treatment of encephalitis
    • May include antiviral agents, antibiotics, and steroids
    • Usually symptomatic treatment
  242. Multiple sclerosis
    • Chronic inflammatory disease involving degeneration of CNS myelin, scarring (sclerosis of plaque formation) and loss of axons
    • -Caused by an autoimmune response
    • -Risk factors include smoking, vitamin D deficiency, and Epstein-Barr virus
    • -Autoreactive T and B cells cross the blood-brain barrier and recognize myelin and oligodendrocyte autoantigens triggering inflammation and loss of oligodendrocyes (myelin producing cells)
    • -Most common initial symptoms are paresthesias of the face, trunk or limbs, weakness, impaired gait, visual disturbances, or urinary incontinence. Intention tremor and slurred speech may occur
    • -Mechanisms of exacerbations or blocked conduction caused by inflammation and demyelination
    • -No single test available to diagnose or rule or MS
    • -Elevated levels of CSF IgG  are found in about 2/3 of patients
    • -Treatment goal is prevention of exacerbations, prevention of permanent neurologic damage and control of symptoms. -Disease modifying drugs are initiated with diagnosis and include corticosteroids, immunosuppressants, and immune system modulators as well as plasmaphoresis
  243. Gullian-Barre Syndrome
    • Rare demyelinating disorder caused by a humoral and cell-mediated immunologic reaction directed at the peripheral nerves
    • -Usually occurs after a respiratory or GI infection
    • -Can vary from paresis of the legs (rubbery legs), to complete quadriplegia, respiratory insufficiency and ANS instability. IV immunoglobulin or plasmapheresis is used during acute phase
    • -Ascending paralysis
    • -Sinus tachycardia, hypovolemia, hypocholemia
    • -EMG to diagnose
  244. Myasthenia Gravis
    • Acquired chronic autoimmune disease mediated by antibodies against the acetylcholine receptor at the postsynaptic membrane of the neuromuscular junction
    • -More common in women
    • -Thymic tumors, pathologic changes in thymus are associated with disorder
    • -Results from a defect in nerve impulse transmission at the neuromuscular junction. Blocks ACh receptors causing diminished transmission of the nerve impulses
  245. Clinical manifestations of Myasthenia Gravis
    • Muscles of the eyes, face, mouth, throat and neck usually are affected first. Respiratory muscles of the diaphragm and chest wall can become weak and impair ventilation
    • -Myasthenia crisis can develop as the disease progresses and occurs when severe muscle weakness causes extreme quadriplegia, respiratory insufficiency with SOB and extreme difficulty swallowing
    • Cholinergic crisis may arise from anticholinesterase drug toxicity with increased intestinal motility...
  246. Diagnosis of of Myasthenia Gravis
    • Made on the basis of a response to endrophonium chloride (Tensilon), results of EMG studies and detection of anti AChR or MuSK antibodies
    • With IV admin, immediate improvement in muscle strength usually persists for several minutes
    • -Anticholinesterase drugs, steroids, and immunosuppresant drugs are used to treat
  247. Spinal cord tumors
    They may be extramedullary, extradural, intradural extramedullary or intradural intramedullary
Card Set
Patho Exam 2
Patho Exam 2