Bio Flashcards

Question

Limbic System (Subcortical brain area): Amygdala function? -Kluver-Bucy syndrome

Answer 1

-attaches emotional significance to sensory input -strongly implicated in fear, aggression and emotional memory -controls the fear response and is involved in memory of fear - linked to PTSD -related to aggression - Kluver-Bucy Syndrome - removal of amygdala - apathy, hypersexuality, hyperphagia (excessive eating), agnosias (problems with recognition)

Answer 2

-moderates or decreases aggression -damage to septum = septal rage syndrome

Answer 3

-regulation and coordination of movement -establishing posture -send info to premotor cortex and motor cortex -basal ganglia are INHIBITORY - they put the breaks on movement and release the breaks in order to move voluntarily

Answer 4

1) caudate nucleus 2) putamen 3) substantia nigra 4) globus pallidus 5) subthalamic nucleus Huntingtons: -presence of unwanted movements -degeneration of caudate nucleus and putamen -continuous thrusting movements of the face and limbs Parkinsons: -slow and steady loss of dopaminergic neurons in the substantia nigra -results in tremor, rigidity, bradykinesia (slowed movements) Two other disorders: Tourette's and OCD

Answer 5

-provides EXCITATORY inputs responsible for maintaining smooth movement and coordinating motor activity -supports our ability to maintain balance -involved in motor learning Ataxia - lack of coordination of voluntary movements in the absence of weakness or sensory loss

Answer 6

-extension of spinal cord, 10 of 12 cranial nerves begin here 1) pons 2) medulla 3) reticular formation Pons and Medulla -sleep, respiration, movement, cardiovascular activity Reticular Formation -set of nuclei -awareness, attention, and sleep -reticular activating system (RAS) - projects to the thalamus- involved in sleep-wake cycle, filter for incoming sensory info, mediates alertness

Answer 7

1) Dendrites -receive info from other neurons by picking up NTS in the synaptic cleft 2) Cell Body (soma) -integrates info from dendrites -contains nucleus - regulates cell activity and controls hereditary characteristics eg DNA 3) Axon -tube-like structure that transmits information

Answer 8

-at start, outside cell excess sodium (Na+), inside excess potassium (k+) -when stimulus of sufficient charge reaches the resting neuron, sodium rushes in, creating an AP -Potassium then moves out -AP travels along the axon to the terminal buttons, releases NTs into synaptic cleft -some NTs then bind to dendrites of next neuron -also, reuptake occurs- pre-synaptic terminal neurons re-uptake some NTs in synaptic cleft All or None -if stimulation is sufficient, neuron files to the full extent. if not, it doesn't fire at all. Absolute Refractory -period after firing where neuron can't fire regardless of stimulation while Na+ and K+ levels are restored outside and inside neurons Relative Refractory -after absolute refractory, where very intense stimulation is required to cause firing

Answer 9

1) classical NTs (the basic ones) 2) peptide NTs Agonist = any substance that enhances the effect of the NT Antagonist = any substance that inhibits effect of NT Excitatory NTs = increase likelihood of action potential (e.g., acetylcholine, norepinephrine, glutamate) Inhibitory NTs = decrease likelihood of AP (e.g., GABA, endorphins)

Answer 10

-one of the most common NTs -involved in 2 significant functions: 1) voluntary movement 2) memory and cognition -poison of black widow spider affects ACh and causes paralysis -prevalent in hippocampus -deficiencies of ACh observed in Alzheimers

Answer 11

1) Dopamine (DA) -thought, movement, and emotion -linked to reward system of the brain -dopamine hypothesis of schizophrenia- psychotic symptoms result from excess dopamine or hyperactivity of dopaminergic system -parkinsons = degeneration of neurons in substantia nigra (basal ganglia). L-Dopa treats Parkinsons 2) Norepinephrine (NE) -aka noradrenalin -significantly involved in mood -NE deficiency --> depression -NE excess --> mania -pain perception -sleep -causes blood vessels to contract and HR to increase

Answer 12

-mood, sleep, appetite, aggression, sexual activity, pain perception -dysregulation of serotonin --> suicidality and impulsivity -deficiencies implicated in mood disorders -low 5HT + low NE = depression -low 5HT + high NE = mania

Answer 13

1) Gaba and 2) Glycine -major inhibitory NTs in the CNS -calming effect -anxiety and epileptic seizures associated with insufficient levels of Gaba -Benzodiazepines are Gaba agonsits - increase Gaba and reduce overarousal 3) Glutamate -most common NT -major mediator of fast excitatory synaptic transmission -abnormal glutamate transmission suspected in schizophrenia, ASD, OCD and depression

Answer 14

-long chains of amino acids -endogenous opioids: 1) enkephalins and endorphins - help regulate stress and pain -substance P - involved in pain regulation

Answer 15

1. Thyroid Disorders -hyperthyroidism -hypothyroidism 2. Diabetes -type 1 diabetes -type 2 diabetes -gestational diabetes 3. Other Endocrine Disorders -hypopituitarism + hyperpituitarism -Addison's disease and Cushing's disease

Answer 16

1) Hyperthyroidism -excessive secretion of thyroxin -weight loss despite increased appetite, heat sensitivity, sweating, diarrhea, tremor and palpitations, fatigue, agitated depression, insomnia, impaired memory and judgment, can involve hallucinations and delusions -most common form = Grave's disease 2) Hypothyroidism -undersecretion of thyroxin -unexplained weight gain, sluggishness, fatigue, impaired memory and intellectual functioning, sensitivity to cold OF NOTE: thyroid disorders are one of the first medical disorders to suspect when psyhiatric symptoms. Hyper mimics anxiety or manic episode. Hypo mimics depression

Answer 17

-Type 1 = pancreas does not produce insulin -Type 2 = body develops resistance to insulin -Gestational = develops during pregnancy -insulin regulates blood sugar Hallmark = Hyperglycemia -excessive glucose or blood sugar levels -classic symptoms = 3 P's 1) polyuria = increased urination 2) polydispia = increased thirst 3) polyphagia = increased appetite -meds treating diabetes can lower blood sugars too much --> hypoglycemia -symptoms: nervousness, irritability, trembling, cold sweat, fatigue, rapid HR, hunger, headache, confusion

Answer 18

Type 1 -Insulin Dependent Diabetes Mellitus (IDMM) -develops before age 30 -life-long insulin -children manage regimen well, become less compliant as adolescents Type 2 -Non-Independent Diabetes Mellitus (NIDMM) -can sometimes be controlled by diet and exercise alone -often requires meds or insulin injections -major risk factors = obesity and sedentary lifestyle -rise in type 2 diabetes in kids attributed to increased inactivity and obesity -African Americans and Hispanics have higher risk Gestational -pregnant women develop high glucose level -may precede Type 2 -1-3% of pregnancies

Answer 19

Hypopituitarism -undersecretion of pituitary growth hormones -dwarfism and pubertal delay in children - in adults: gonadal failure (e.g., impotence, infertility) as well as others (e.g., hypothyroidism, diabetes, adrenocortical insufficiency) Hyperpituitarism -oversecretion of pituitary growth hormones -startling skeletal overgrowth - gigantism or acromegaly

Answer 20

Corticosteroids - secreted by adrenal cortex - involved in use of energy resources, inhibition of anitbody formation, and inflammation Addison's Disease -undersecretion of corticosteroids (adrenal insufficiency) -symptoms: apathy, weakness, irritability, depression, GI disturbance Cushing's Disease -oversecretion of corticosteroids -symptoms: agitated depression, irritability, emotional lability, difficulties with memory and concentration, suicide -physically- adiposity = swelling of face, neck, trunk

Answer 21

1) Aphasia 2) Apraxia 3) Agnosia 4) Agraphia 5) Alexia 6) Amnesia 7) One-Sided Neglect

Answer 22

Aphasia = loss of language abilities due to damage in the brain (lesion) -specific location of lesion determines the type of aphasia 1) Broca's Aphasia; 2) Wernicke's Aphasia; 3) conduction aphasia; 4) global aphasia; 5) anomic aphasia; 6) transcortical aphasia

Answer 23

-an expressive or motor aphasia -lesions to the dominant (left) frontal lobe -severe problem with speech production and articulation (dysarthria) -speech is slow and effortful- short phrases and lengthy pauses -articles (the, an, a), conjunctions and other small words are omitted -comprehension mostly intact -difficulty with word finding, naming objects, repeating phrases -people with this have awareness of it -broken (broca) or choppy speech

Answer 24

-receptive or sensory aphasia -lesions in the dominant (left) temporal lobe -no language comprehension - can't follow verbal commands or repeat phrases -speak fluently, but speak nonsense -unaware of the problem (anosognosia)

Answer 25

-relatively rare -lesion in connecting pathway between receptive and expressive areas -intact language comprehension and speak fluently -cannot repeat verbal phrases -speak fluently but make no sense -can execute verbal commands because still comprehend language

Answer 26

-widespread damage to language regions of the cortex -most language functions impaired including fluency, comprehension, repetition and naming

Answer 27

-problems recalling words or names -speak in a round-about way (circumlocution) -use descriptions to express a word they can't remember -damage to parietal or temporal lobe

Answer 28

-caused by damage outside the main language regions -3 types: transcortical motor aphasia, transcortical sensory aphasia, transcortical mixed aphasia - similar to Broca's, Wernicke's, and Global respectively EXCEPT ability to repeat words and phrases remains intact

Answer 29

-inability to carry out voluntary or purposeful motor movements -understands and is willing to perform movements but cannot execute -many different types: -difficulty carrying out motor command voluntarily but performing it involuntarily (e.g., scratch nose) -inability to carry out complex tax in sequence (e.g., socks before shoes) -no longer being able to perform task with necessary object (e.g., tries to write when given screwdriver) -difficulty plan + coord movements needed for speech (apraxia of speech) -difficulty drawing, copying or constructing simple figures (constructional apraxia)

Answer 30

-loss of ability to recognize sensory stimulus e.g., objects, people, sounds, shapes, smells -caused by damage in the parietal, temporal, or occipital regions 1) Prosopagnosia -inability to recognize a familiar face -retrograde and anterograde -occurs despite processes being intact e.g., visual perception, alertness, attention -injuries to areas of the visual association cortex 2) Anosognosia -lack of awareness of a disability or the nature of one's illness -e.g., Wernicke's not recognizing they're speaking gibberish -deficits in frontal or perietal lobes

Answer 31

-partial or complete loss of ability to write -problems with letter formation, spelling, word selection, grammar, or spatial arrangement -left hemisphere damage eg frontal, temporal or parietal lobes

Answer 32

-aka word-blindness -loss of ability to read and/or comprehend meaning of written words and sentences -most common cause is stroke to dominant (left) hemisphere

Answer 33

-partial or total memory loss 1) Retrograde -loss of pre-existing memories -usually temporally graded - harder to remember recent memories relative to old -episodic memory more affected than semantic -can be short (2 years) or extensive (decades) -even if extensive, memories for facts and events of childhood/adol intact 2) Anterograde -loss of ability to form new memories -forget new information, new people, new events within a few seconds -memory does not transfer from short- to long-term memory

Answer 34

-most often result of stroke in right hemisphere -in this case, no awareness of objects to their left -may eat from only right side of plate, write on right side of page, shave or put makeup on the right -may forget to dress the left side of body, walk into furniture on the left

Answer 35

-Delirium, Major NCDs, Mild MCDs, and subtypes -Major NCD: definition is broad- individuals with decline in a single domain cam receive diagnosis -Mild NCD: less severe levels of cognitive impairment --> interference with independence in daily activities -cause of NCD should be stated as part of diagnosis

Answer 36

Decline in one or more of 6 domains 1) complex attention (sustained, divided attention, processing speed) 2) executive function 3) learning and memory 4) expressive and receptive language 5) perceptual-motor 6) social cognition

Answer 37

1) Alzheimer's disease 2) vascular disease 3) Lewy body disease 4) multiple etiologies 5) Parkinson's disease 6) Huntington's disease 7) frontotemporal lobar degeneration 8) HIV infection 9) prion disease (e.g., Creutzfeldt-Jakob disease) 10) another medical condition 11) traumatic brain injury 12) substance/medication use 13) unspecified

Answer 38

-hallmark: disturbance in attention and awareness -rapid onset (hours to days) -course is fluctuating -includes a cognitive disturbance -need evidence that symptoms have a physiological cause in order to diagnose (e.g., medical condition, infection, substance intoxication or withdrawal) -sometimes called an acute confusional state -different from NCD because acute onset, fluctuating course, and often reversible -can be superimposed on a major NCD (e.g., major NCD due to Alzheimer's disease, with delirium) -can occur at any age, most common with older adults -most common cause: drugs/meds and infections -once suspected or diagnosed, look for underlying cause -reorientation techniques or memory cues e.g., calendar, clock, family photos -most common meds are antipsychotics (e.g., Haldol) -benxos used to manage withdrawal delirium

Answer 39

-most common major NCD up to 80% of NCDs -prevalence increases with age -more prevalent in women because they live longer

Answer 40

Early symptoms 1) memory problems 2) apathy and depression Later Symptoms 1) disorientation 2) confusion 3) problems with judgment 4) behaviour changes 5) gait and motor problems -as it progresses, people need help with basic activities of daily living -in the final stages, lose ability to communicate, fail to recognize loved ones, become bedridden

Answer 41

-amyloid plaques (deposits of protein fragment beta-amyloid) -neurofibrillary tangles (twisted strands of the protein tau) -neuronal damage and death throughout cortex and within brain structures - especially hippocampus and amygdala -decrease of NT ACh

Answer 42

1) pre-clinical - biomarkers indicate early disease but no symptoms 2) mild cognitive impairment (MCI) - mild but noticeable changes in thinking that don't affect ability to carry out daily activities 3) dementia due to Alzheimer's disease -now thought to begin up to 20 years before the presence of symptoms

Answer 43

-agent called Amyvid can help diagnose - picked up in a PET scan -proton MR spectroscopy also being used -etiology unclear but evidence for genetic component - particularly first-degree relatives -progressive disease -cortical in nature- memory, language and movement most affected -two principals of management 1) support caregivers 2) treat what is treatable -drugs: Aricept (donepezil) and Cognex (tacrine) give modest albeit temporary improvements in cog functioning -no treatment that slows or stops AD

Answer 44

-second most common NCD -10-15% of NCD in older adults -twice as common in males than females -results from small cerebrovascular accidents (CVAs) or strokes -location of brain injury determines how functioning is affected Initial symptoms -impaired judgment or ability to make plans -onset is abrupt, course is stepwise - plateaus followed by further degeneration -half of those diagnosed die within 2-3 years -age of onset usually younger than Alzheimer's -no meds can reverse effects of strokes -aspirin, anticoagulants and antihyperintensives can reduce risk of future stroke

Answer 45

-involves abnormal clumps of the protein alpha-synuclein (also found in Parkinson's Disease) -symptoms: similar to Alzheimer's, PLUS visual hallucinations, sleep disturbances, muscle rigidity, other parkinsonian movement features (e.g., shuffling gait)

Answer 46

-most commonly involves Alzheimer's disease + another disease such as vascular disease or Lewy bodies -research shows this is more common than previously thought

Answer 47

-movement disorder marked by tremors, rigidity, and bradykinesia (slowed initiation of movement), and shuffling gait -commonly co-occuring with neuropsych symptoms like depression or NCD -depression may precede motor symptoms by several years -as PD progresses, neurocognitive symptoms are quite common - prevalence rate of major NCD due to Parkinson's up to 40% -subcortical- affects processing speed and EF -incidence is 1/10th that of Alzheimer's -abnormalities include alpha-synuclein aggregates (also found in NCD with Lewy bodies) beginning in substantia nigra of basal ganglia -aggregates cause degeneration of nerve cells that produce dopamine -L-Dopa (a precursor to dopamine) is used to treat movement components of Parkinson's -does not alter the progression of the disease or decrease symptoms of major NCD

Answer 48

-fatal condition -results from autosomal-dominant gene -symptoms become apparent between 30- and 50-years old earliest symptoms -non-specific changes in personality and mood e.g., irritability, apathy, disinhibition -all patients experience a progressively deteriorating major NCD (memory loss and lack of reasoning) - slowly develops alongside psychological symptoms -choreiform movements: frequent, discrete, brisk jerking movements of the pelvis, trunk, and limbs -athetosis: slow writhing movements -facial grimaces -all may begin after 10 years of onset -involves basal ganglia: caudate nucleus and putamen -motor symptoms result from significant reduction in ACh and GABA which triggers excess of dopamine -genetic counselling is an important intervention for those with a family history -child whose parent has gene for Huntington's has 50% chance of getting it

Answer 49

-umbrella term - describes a diverse group of rare disorders affecting the frontal and temporal lobes Typical Symptoms: -changes in personality and behaviour e.g., problems with judgment, explosive temper, disinhibition, poor impulse control -difficulty with language -Pick's disease and progressive supranuclear palsy are examples

Answer 50

-prior to highly active antiretroviral therapy (HAART) major NCD was a common source of morbidity and mortality in HIV patients -AKA Aids Dementia Complex (ADC) -cognitive symptoms: memory problems (LTM remains intact), attention and concentration, language difficulties -motor: weakness, lack of coordination, unsteady gait, jerky eye movements -behaviour/mood: apathy, withdrawal, lack of motivation, personality changes, inappropriate affect, mood swings, hallucinations

Answer 51

-rare, degenerative, fatal brain disorder -results from an infectious misfolded protein (prion) that triggers other proteins throughout the brain to misfold and malfunction -results in rapidly progressive major NCD -symptoms: problems with muscular coordination, personality changes, impaired orientation, memory, judgment, thinking, problems with vision -average duration from onset of symptoms to death is 4-6 months -one variant is believed to be caused my consumption of products from cattle affected by mad cow

Answer 52

-accumulation of CSF in the brain's ventricles causing increased intracranial pressure -caused by over-production or malabsorption of CFS - mal-absorption more common -symptoms: urinary incontinence, unsteady gait, NCD -can sometimes be cured and symptoms reversed with a shunt in the brain to drain excess fluid

Answer 53

-involves NCD that results directly from a head trauma -nature and extent of impairment depends on location and extent of brain injury -in many cases, posttraumatic amnesia is present + some persisting memory impairment and EF issues -others: attention, regulating mood, aggression, apathy, changes in personality -head trauma = leading cause of brain injury in children and young adults -two types of head trauma: closed- or open-head injuries

Answer 54

-skull is not pierced or cracked -loss of consciousness is common Types: 1) concussions; 2) contusions

Answer 55

-most common head injury -may cause short a short- or long-term loss of consciousness + retrograde and anterograde amnesia -retrograde amnesia typically includes amnesia for events just before the injury and the incident itself (not for remote events) -brain injuries are microscopic, widespread, and tend to cause functional (rather than structural) damage Postconcussion Syndrome -constellation of somatic and psych symptoms: headaches, dizziness, fatigue, diminished concentration, memory deficit, irritability, anxiety, insomnia, hypochondriacal concern, hypersensitivity to noise and light -most common symptoms: irritability, fatigue, headache, dizziness -psych symptoms typically heal in same period of time as physical injuries

Answer 56

-bruises -more serious than concussions -result from severe blow to the head that leads to bleeding and bruising of the brain Coup-Countrecoup: bruising beneath the point of impact as well as on the opposite side of the brain -cerebal swelling is common and is potentially life-threatening -localized, macroscopic, structural damage -often at the frontal or temporal lobes -frontal lobe syndrome: lack of foresight and concern, EF problems, irresponsibility, loss of insight -temporal lobe syndrome: irritability and hostility

Answer 57

-e.g., gunshot wounds -many with open-head injuries do not lose consciousness -neurological signs are highly specific: effects of injuries resemble surgical removal of a small area of cortex

Answer 58

-may continue for 2-3 years but the bulk of recover is within first 6-9 months -recovery of memory functions is typically slower than general intelligence -final level of memory performance is lower than for other cog functions -as memory recovers, first remember more remote events and then events coming closer and closer to the trauma -may never remember the event itself or moments leading up - head injury disrupts consolidation

Answer 59

-impairment persists beyond intoxication and withdrawal Korsakoff's Syndrome -common cause of alcohol-induced major NCD -results from chronic thiamin (Vitamin B1) deficiency related to longstanding alcohol abuse -most significant problem: anterograde amnesia -also retrograde amnesia most often of recent memories Confabulation -replacement of a gap in memory with false information that is believed to be true -also, lack of insight, limited spontaneous conversation, EF problems, disorientation, apathy, labile irritability

Answer 60

-occurs in people who are depressed and have cog impairments resembling NCD -in older people, depression symptoms look like NCD Distinguishing Features: -those with pseudodementia complain about memory loss, those with NCD often don't have insight -those with pseudodementia regain mental functions after depression lifts

Answer 61

Gate Control Theory -Melzak and Wall (1965) -sensations of pain not directly related to activation of pain receptors -mediated by neural gates in spinal cord that allow signals to move onto the brain -pressure stimulation closes gates - rubbing hurt area can relieve pain -psych factors e.g., thoughts and mood sig affect gates - depression and bereavement may open gates Acute Pain -begins suddenly -triggered by clearly defined cause -resolves when underlying cause is healed Chronic Pain -persists after injury is healed -affects people physically and emotionally -physical: tense muscles, limited mobility, lack of energy -emotional: depression, anger, anxiety -common complaints: headaches, low back pain, cancer pain, arthritic pain, neuropathic pain Centralization of Pain Theory -sensitization to pain occurs when brain is exposed to repeated pain signals or nerve stimulation -bc of neuroplasticity, neurons develop a memory for responding to pain signals -brain responds more quickly when exposed to same signals in the future -lowered pain threshold and stronger pain response -once centralization occurs, takes larger doses of analgesics to overcome it -some argue for pre-emptive analgesia to prevent or decrease neural plasticity -recommendation is meds on a time-contingent schedule NOT a pain-contingent schedule re: addiction

Answer 62

Types of sleep: 1) non-rem; 2) REM Beta waves = alertness and attention - you beta be awake Alpha waves = relaxation - "aaaaah" Sleep Cycle = 4 NREM followed by REM Stage 5 Stage 1) brief transitional stage between wakefulness and sleep - THETA WAVES Stage 2) sleep spindles - bursts of rapid rhythmic brain activity. body temp and HR start to slow Stages 3) and 4) - DELTA waves - stage 3 transition between light and very deep sleep, stage 4 is deep sleep - HR slowed but keep muscle tone Stage 5) REM Sleep - REM, increase respiration rate, increased brain activity- paradoxical sleep - while brain becomes more active, muscles become more relaxed. Most dreaming happens here -deeper stages less frequent in second half of night and REM more prominent -time in REM decreases with age: newborns 50%; 4-5 y/o 20-25%; older adults 18% -waken during NREM - 30% dream, normal and logical dreams -waken during REM - most have dream that is bizarre and illogical -NREM = physically restorative -REM = psychologically restorative -sleep deprivation: impairs memory, concentration, decision making; disrupts metabolism; increases stress hormones -long-term deprivation = increased risk car accidents -dream deprivation (waking during REM episodes) causes REM rebound

Answer 63

-electric currents passed through brain deliberately triggering a seizure -severe depression, treatment-resistant bipolar, acute psychosis, catatonia -memory loss - confused and disoriented up to 45 mins after -anterograde amnesia - typically resolves a few weeks after treatment -retrograde amnesia - takes longer to resolve - most experience some permanent loss of memory for events during ECT period as well as a few days to a few weeks beforehand -bilateral ECT = greater memory impairment -unilateral ECT = less memory impairment and can be as effective if electrical dose is suffucient

Answer 64

EEG -electrodes on scalp - electrical activity in cortex -changes in brain activity -diagnosis of brain conditions especially seizures -localizing source of seizure during the event PET and SPECT Scans -nuclear imaging -demonstrate activity or functioning of brain -small amount of radioactive material injected -measure metabolism and blood flow -eg cancer shows up brighter bc have higher metabolism rate MRI, FMRI and MR Spectroscopy -uses magnetic fields and radiowaves to create images -MRI imaging - picks up scars or lesions -fMRI - brain activity and functioning - how blood flows within brain during specific task - more activity = more blood flow = brighter on scans -MR spectroscopy - dete4cs metabolic changes that may be consistent with certain disease processes CT Scan -test of structure -combines series of X-ray views and creates cross-sectional images of brain, bones, soft tissues

Answer 65

Tension -most common -band-like tightness, ache or pressure around head -bilateral pain, dull and steady -most can function normally -more common in women Migraines -second most common -often involve unilateral throbbing pain -moderate to severe intensity -pain interferes with or is worsened by normal physical activity -associated features: nausea/vomiting, sensitivity to light and sound -15-20% of people experience an aura (e.g., visual distortion, hand numbness) prior to headache -ocular/retinal migraines = visual disturbances like flashing or bright lights, floating geometric shapes, scotomata (blind spots), loss of peripheral vision Cluster Headaches -recurring headaches that occur in groups or cycles over a period of days or weeks -appear suddenly -severe, debilitating pain in one side of the head -often accompanied by watery eye/nasal congestion/runny nose on same side of head -affect 0.1% of population -more frequent in men

Answer 66

-perceptual condition of mixed sensations -stimulus in one modality (e.g., vision) elicits a sensation/experience in another modality (e.g., olfaction); or a perception of a form (e.g., letter/number) induces a different perception in the same modality (e.g., colour) -runs in families -Vladimir Nabokov and David Hockney have it

Answer 67

-Hans Selye -model of response to long-term stress -three stages 1) Alarm -bodily mobilizes resources to cope with stress (fight or flight) -sympathetic nervous system activated, release of adrenaline and cortisol -immune functioning is lowered while body on high alert -physical symptoms: headache, fatigue, diarrhea 2) Resistance -alarm reaction subsides and body adapts to stressor -level of resistance to illness above normal 3) Exhaustion -occurs in response to chronic, unrelenting stress -body's resources are exhausted -immunity is greatly lowered -can be significant loss of health and death

Answer 68

-Rosenstock -multicausal - in addition to psychosocial factors, there are 6 constructs that predict health behaviours 1) perceived susceptibility to disease 2) perceived seriousness of the disease 3) perceived benefits of preventative action 4) perceived barriers to preventative action 5) cues to action e.g., media information 6) self-efficacy

Answer 69

-antipsychotics -antidepressants -antianxiety agents -mood stabilizers -stimulants

Answer 70

Thorazine (chlorpromazine)*** Prolixin (fluphenazine) *** Haldol (haloperidol)*** Trilafon (perphanazine) *** Serentil (mesoridazine) Navane (thiothixene) Orap (pimozide) Loxitane (loxapine) Moban (molindone) Stelazine (trifluoperazine) Mellaril (thioridazine)

Answer 71

Clozaril (clozapine)*** Risperdal (risperidone)*** Zyprexa (olanzapine)*** Invega (paliperidone)*** Seroquel (quetiapine)*** Geodon (ziprasidone)*** Abilify (ariprazole)***

Answer 72

-first-gen 1950s have a long history of effectively reducing positive symptoms of schizophrenia, but are only minimally effective at treating negative symptoms or cognitive symptoms -second gen 1990s thought would help with negative symptoms but don't. They have less severe side effects Mechanism: -are to some extend dopamine D2 antagonists - lower levels of dopamine by blocking postsynaptic dopamine receptors

Answer 73

Schizophrenia -effective in reducing positive symptoms -no sig effect on negative or cognitive symptoms Other Psychotic Disorders -e.g., delusional disorder, brief psychotic disorder, schizoaffective disorder Bipolar -atypical antipsychotics in conjunction with mood stabilizers or antidepressant meds to treat mania Others -Delirium, Tourette's, ASD (decrease oppositional behaviour, emotional lability, irritability) -PTSD and MDD -NCDs but the FDA says death rates higher for elderly patients

Answer 74

-common side effects: sedation and drowsiness, orthostatic hypotension (dizziness when standing up) -weight gain and sexual dysfunction -for typical antipsychotics (especially Haldol, Prolixin, and Trilafon, which are higher potency), most sig side effects are extrapyramidal symptoms -risk of tartive dyskinesia reduced with atypical anyipsychotics Anticholinergic Effects -can be cause by both typical and atypical -dry mouth (most common), constipation, urinary hesitancy or retention, blurred vision, dry eyes, photophobia (light sensitivity), nasal congestion, confusion, decreased memory -typically diminish in first month but do not fully disappear -drying out or holding in Extrapyramidal Symptoms (EPS) -movement-related symptoms- some of which are the most damaging side effects of antipsychotics -managed through use of anticholinergic agents (ACAs) like Cogentin (benzotropine) and Artane (trihexyphenidyl) -far more likely in typical than atypical, especially Haldol, Prolixin and Trilafon which are higher potency -symptoms include: dystonia (acute and painful muscle spasms), parkinsonism (mask-like face, shuffling gate, drooling, resting tumor, rigidity, bradykinesia), and akathisia (unpleasant restless feeling particularly in legs) Tardive Dyskinesia -most commonly involves abnormal movement of the lips, tongue, jaw (e.g., lip smacking, grimacing, chewing, rolling and protruding tongue) -many involve trunk and arms as well -generally occurs after longer period of treatment (e.g., 1 year+) -higher risk of TD with typical antipsychotics - 20-40% of those taking typical antipsychotics get it -not dangerous, but stigmatizing -best treated through prevention- monitoring and re-assessing every 6 months to see if med can be discontinued or dosage lowered -occasionally, symptoms start only once a med has been discontinued or lowered -no established treatment -oddly, antipsychotics CAN serve as a short-term treatment for TD -anticholinergic agents typically exacerbate TB -may be reversible - 50% experience full remission after stopping antipsychotics Metabolic Effects -atypical antipsychotics frequently cause major weight gain and changes in metabolism - increased risk of diabetes/high cholesterol -regular monitoring of weight, glucose levels and lipid levels Neuroleptic Malignant Syndrome (NMS) -rare - less than 1% -potentially lethal -severe muscle rigidity, altered consciousness, autonomic instability (e.g., heart rate and blood pressure changes), high fever -requires emergency medical attention Agranulocytosis -potentially lethal side effect of Clozaril (clozapine) -Clozapine only given to patients who have failed on all other antipsychotics -sudden drop in the white blood cell (granulocyte) count that results in very high risk of serious infection due to immune suppresion

Answer 75

-do not cause addiction, dependence, or tolerance -withdrawal only happens when high dose is suddenly stopped -symptoms might include GI distress, headaches, insomnia, nightmares -overdoses not highly lethal unless a full 30-60 day supply taken at one time -more lethal when combined with another drug e.g., tricyclic antidepressant

Answer 76

SSRI/SNRI, Tricyclic, MAOIs, Other

Answer 77

Prozac, Serafem (fluoxetine)*** Zoloft (sertraline)*** Paxil (paroxetine)*** Effexor (venlafaxine)*** [SNRI] Lexapro (escitalopam)*** Luvox (fluvoxamine) Celexa (citalopram) Cymbalta (duloxetine) [SNRI]

Answer 78

Elavil (amitryptyline)*** Anafranil (clomipramine)*** Tofranil (imipramine)*** Sinequan (doxepin)*** Asendin (amoxapine) Vivactil (protriptyline) Surmontil (trimipramine) Norpramin (desipramine) Pamelor, Aventyl (nortriptyline) --> can sometimes be recognized by the ending "amine" or "tyline"

Answer 79

Nardil (phenelzine) Marplan (isocarboxazid) Parnate (tranylcypromine) Ensam (selegiline) patch

Answer 80

Wellbutrin (bupropion)*** Desyrel (trazadone)*** Ludiomil (maprotiline) Remeron (mirtazipine)

Answer 81

-SSRIs newest most widely prescribed, well-tolerated, few side effects, minimal lethality -TCAs - highly effective but potential side effects are more serious and can be fatal in overdose -MAOIs - oldest class of antidepressants, especially effective in treating atypical depression (increased appetite and need for sleep), interact dangerously with certain foods and medications

Answer 82

-block reuptake of serotonin/norepinephrine, increasing their levels in the brain -Wellbutrin (bupropion) is an anomaly - increases dopamine -typically takes a couple weeks for meds to take effect

Answer 83

Major Depressive Disorder -all antidepressants equally effective in treating typical depressions -SSRIs = fewer and less distracting side effects than others, and are safer, first line of treatment Bipolar Disorder, Depressed -used in combination with mood stabilizer when treating depression in bipolar - to minimize risk of inducing manic episode -prozac, paxil, zoloft, and wellbutrin are common Anxiety/Trauma/OCD -panic disorder: SSRIs, TCA Tofranil (imipramine), and MAOIs used in addition to antianxiety agents like Xanax and Ativan -OCD: SSRIs and TCA Anafranil (clomipramine) -PTSD: SSRIs -Social Anxiety Disorder: SSRIs -GAD: SNRI Effexor (venlafaxine) and TCA Tofranil (imipramine) Chronic Pain -responds well to many TCAs Bulimia Nervosa -antidepressants are common -only FDA approved is Prozac (fluoxetine) -studies have also shown efficacy for other SSRIs, TCAs, and MAOIs Premature Ejaculation -SSRIs and TCA Anafranil (clomipramine) Other Uses: -severe bereavement -anorexia nervosa -premenstrual dysphoric disorder -enuresis -childhood sleepwalking or night terrors -persistent depressive disorder (dysthymia) -borderline personality disorder

Answer 84

SSRIs -far fewer side effects than TCAs and MAOIs -headaches, nervousness, restlessness, insomnia, GI distress - fade over time -if there is sexual dysfunction, may be helped by adjusting the dose or switching to another -black box warning of potential risk of suicidal thinking or attempts for children and adolescents TCAs -may cause severe anticholinergic effects (e.g., dry mouth, blurred vision, constipation, urinary hesitation, confusion, memory problems) -frequent effects: sedation, orthostatic hypotension, weight gain, nausea, sexual dysfunction -linked to increased risk of heart disease - contraindicated in patients with heart conditions, high blood pressure or seizures MAOIs -frequently cause orthostatic hypotension, weight gain, edema, sexual dysfunction, and insomnia -tyramine-induced hertensive crisis - can't eat foods high in tyramine - can trigger dangerous increase in blood pressure requiring immediate medical attn. Symptoms: severe headache, stiff neck, palpitations, sweating, nausea, vomiting -certain meds should be avoided e.g., MAOIs can react with SSRIs - serotonin syndrome - potentially life threatening

Answer 85

-do not cause dependence, tolerance, or addiction -abruptly stopping can cause non-life-threatening withdrawal symptoms -TCAs and MAOIs highly lethal when used to attempt suicide via overdose -lethality further increases when combined with alcohol -SSRIs and other are not very lethal

Answer 86

1) Anxiolytics (BZs) 2) Sedative/Hypnotics (BZs) 3) Non-Benzodiazepine Anxiolytics 4) Non-Benzodiazepine Sedative/Hypnotics

Answer 87

Xanax (alprazolam)*** Klonopin (clonazepam)*** Valium (diazepam)*** Ativan (lorazepam)*** Librium (chlordiazepoxide) Tranxene (clorazepate) Paxipam (halazepam) Serax (oxazepam)

Answer 88

Restoril (temazepam)*** Halcion (triazolam)***

Answer 89

Buspar (buspirone)***

Answer 90

Ambien (zolpidem)*** Sonata (zaleplon) Lunesta (eszopiclone)

Answer 91

-divided into two categories: 1) anxiolytics - major function anxiety reduction; 2) sedative/hypnotics - main purpose is to induce sedation and improve sleep -non-benzo anxioltyics and sedative/hypnotics - eg buspirone - low potential for abuse and dependence, but typically requires 2-4 weeks for clinical response and can't be taken as needed -beta-blockers usually used to treat high blood pressure and other heart conditions -inderal (propranolol) - a beta blocker that can prevent physical symptoms that occur with social phobia

Answer 92

-GABA agonist -increased GABA = reduced anxiety, increased sedation, muscle relaxation, and reduction in seizures

Answer 93

Anxiety Disorders -because of high potential for abuse/dependence, benzos should only be prescribed for short periods -consider underlying cause of anxiety e.g., medical illness, illicit drugs, withdrawal for CNS depressants -Panic Disorder: Xanax (alprazolam) and Ativan (lorazepam) + SSRIs or TCAs drug of choice in long-term -GAD: Xanax (alprazolam) and Klonopin (clonazepam). Buspar (buspirone) + antidepressants -Other anxiety disorders: minor role in treating SAD, Phobias, PTSD, OCD - antidepressants much more common Sleep Problems -BZs are best used for short-term (less than 7 days) sleep problems precipitated by acute stress or jet lag -issues with tolerance and dependence -rebound insomnia - discontinuing causes insomnia -disrupt sleep cycle and suppress REM - REM rebound - vivid, disturbing dreams that interfere with sleep Other Clinical Issues -Klonopin (clonazepam) sometimes used to treat acute mania -BZs sometimes used to treat akithesia and alcohol withdrawal -play a role as antivconsulsants (particularly Klonopin), muscle relaxants, and in anesthesia

Answer 94

-most common = drowsiness and dizziness -others: mild cognitive impairment, impaired coordination, nightmares, headaches, upset stomach, memory problems -side effects of Buspar: dizziness, headaches, nausea, lightheadedness, excitement and insomnia -beta-blockers side effects (they are generally well-tolerated): sexual dysfunction (up to 10% males developing impotence), fatigue, dizziness, shortness of breath, angina, cold hands and feet, difficulty sleeping, nightmares

Answer 95

-physiological and psychological dependence are possible -BZs vary greatly in how quickly they take effect and how long they last (half-life) - the most addictive are those with rapid onset (= buzz) and short half-life (= mini-withdrawal) - e.g., Xanax -taking BZs as needed (PRN) encourages dependency -can develop tolerance to BZs -BZs and alcohol are cross-tolerant - those who have tolerance to BZs also have increased tolerance to alcohol (hence BZs use to decrease alcohol withdrawal) -withdrawal syndrome for BZ can be fatal - only gradual taper with doc monitoring - never abrupt stop -stage 1 symptoms: tremors, sweating, agitation, increased autonomic reactions -stage 2 symptoms: hallucinations and panic -stage 3: single or multiple grand mal seizures -BZs rarely fatal when taken alone, easily fatal when taken with alcohol or other CNS depressants -BZs should be avoided for older adults - BZ use in older adults = increased risk of falls and fractures, MVAs, cog impairment -BZ use should be limited in patients with history of alcohol or drug dependence

Answer 96

1) Lithium 2) Anticonvulsants

Answer 97

Eskalith (lithium carbonate) Lithobid (lithium citrate)

Answer 98

Tegretol (carbamazepine)*** Neurontin (gabapentin)*** Depakote (divalproex)*** Depakene (valproic acid)*** Lamictal (lamotrigine)*** Trileptal (oxcarbazepine) Topamax (topiramate)

Answer 99

-lithium first mood stabilizer - 1970s -1990s anticonvulsants started to be used as mood stabilizers - were initially meant to treat seizures -specific mechanism of action is largely unknown

Answer 100

Bipolar Disorder -lithium most often used -long time to take effect: 1-3 weeks for insomnia, 6-8 weeks for depression - because of this, may be combined with atypical antipsychotic for manic episodes and with an antidepressant for depressive episodes -after several months, drug has a prophylactic (preventative) effect - cuts in half the number of episodes and reduces severity -used for schizoaffective disorder, bipolar type -anticonvulsants are also used, often when lithium doesn't work or is contraindicated Other Clinical Uses -depression - lithium or anticonvulsant may be added if antidepressants alone are ineffective -impulse control disorders (e.g., intermittent explosive disorders) -occasionally used as part of treatment of cyclothymic disorder and BPD -anticonvulsants used for pain relief for some neurological chronic pain disorders like trigeminal neuralgia

Answer 101

-lithium side effects: fine hand tremors, gastric distress (e.g., nausea, diarrhea, bloating), weight gain, sedation, hair loss, acne, plyuria (excessive peeing) and polydipsia (excessive thirst) -period blood tests required when taking lithium to make sure levels are in a therapeutic range + monitor for thyroid or kidney problems -lithium toxicity - potentially fatal, always a medical emergency. Symptoms may initially mimic the flu - vomiting, abdominal pain, severe diarrhea. Other signs = sever tremor, ataxia, coma, seizures, confusion, irregular heartbeat. Can occur when a patient is on a stable dose and complying with doctor's orders. Can also occur as result of an overdose -anticonvulsants side effects: drowsiness, dizziness, headache, diarrhea, nausea, vomiting -may increase risk of suicidal thoughts and behaviours

Answer 102

-lithium alone does not cause tolerance, addiction, dependence, or withdrawal -non-compliance is a major issue -lithium contraindications include pre-existing heart disease, thyroid disease, renal damage, and pregnancy -always require close monitoring while on lithium because of effects on body symptoms + many drug interactions -anticonvulsants = no dependence, tolerance, withdrawal

Answer 103

Ritalin (methylphenidate)*** Adderall (amphetamine)*** Concerta (methylphenidate)*** Dexedrine (dextroamphetamine)*** Strattera (atomoxetine)*** - an SNRI, non-stimulant med that is FDA-approved to treat ADHD but note warning of increased suicidal thoughts in kids and adolescents

Answer 104

-increase release of dopamine and norepinephrine (the catecholamines) AND by blocking their reuptake

Answer 105

ADHD -response typically occurs within the first two days of administration Other Clinical Uses -sometimes used for treatment-resistant depression, treatment-resistant obesity, narcolepsy, and chronic medically debilitating conditions (e.g., AIDS, cancer)

Answer 106

-loss of appetite -insomnia -headaches -GI distress (stomach aches or nausea) -may temporarily suspend growth in children Other Side Effects -anxiety, irritability, dysphoria, increases in HR and BP -can occasionally bring about movement disorders (tics) Drug Holidays (structured treatment interruptions) -benefits: relief from side effects -drawbacks: possible negative impact on social development and peer relations

Answer 107

-can cause psychological dependence and drug abuse -street value as uppers -can cause physical dependence, tolerance (esp when used for narcolepsy), addiction, and withdrawal -withdrawal: increased appetite, increased weight gain, increased sleep, decreased energy, and uncommonly, paranoid symptoms -overdose is rarely lethal bc of large discrepancy between therapeutic doses and lethal doses