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272 Cards in this Set
- Front
- Back
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Where are the three herniations of the brain
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cingulate Gyrus
Tentorium Foramen Magnum |
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What symptoms will you get with tumor in the PFC? Motor Cortex? Temporal Lobe? Ocipital Lobe?
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Personality change
Seizures on one side of body seizures Hemianopia |
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Ring enhancing lesions are caused by?
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Abscess
Metastases primary tumors hematomas |
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What do Glial Tumors look like?
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no boundaries
grows through infiltrations |
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What are the Hystological criteria for Gliomas?
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Cellularity
Pleiomorphism Mitosis Necrosis Angiogenesis |
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What are secondary Glioblastomas?
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P53 Mutation
Starts out as low grade astrocytoma turns to Anaplastic astrocytoma then turns into secondary |
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What is primary glioblastoma de novo?
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EGFR amplification
straight into Primary |
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what are the five common sites for meningiomas?
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Parasagital
Falcine Olfactory Groove Sphenoid Ridge Foramen Magnum |
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What is a contra coup lesion?
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Caused by single falls when the head strikes a fixed object. Damage is 180 deg. from site of impact
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What is coup lesions?
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stationary head is struck with a hard moving object.
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What is a gliding contusion?
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when the whte matter seperates.
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What is Kernohan's notch phenomenon?
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unilateral downward compression of the brain through the tentorial causes the third nerve and cerebral peduncle on the opposite side of lesion to be squeezed. May cause paresis ipsilateral to lesion and pupilary dysfunction contralateral.
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What are the primary brainstem traumas?
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closed head injury by angular acceleration
basal skull fracture hyperextension of neck |
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What are Duret Hemorrhages?
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torn blood vessels caused by displaced brain caudally.
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What is Black brain?
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Dead brain with no blood in it.
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How recurrent is depression?
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2/3 of the cases are recurrent.
Risk of recurrence rises with each episode. |
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Does antidepressents prevent suicide?
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YEs, not enough data, but they reduce suicidal ideation. Pts. also receive clinical intervention.
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Does Genetics play a factor in depression?
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Yes.
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What does personal, permanent and pervasive mean in terms of depression?
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Personal - taking blame for outcome
Permanent - outcome remains the same in each situation Pervasive - relating the failed outcome to failure in everything in life. |
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What do the antidepressent drugs focus on?
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Limbic system and monoamines.
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What are some diagnostic criteria for depression?
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Depressed mood
loss of interest cahnge in weight, sleep Fatigue. NOT DUE TO SUBSTANCE ABUSE |
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What is the difference between Bipolar I and II?
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I = > 1 manic or mixed episode
no need for depressed episode. II = Hypomanic and Depressed episode |
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What is the goal of antidepressents?
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To reduce suicide.
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How long does treatment last?
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At least one year to prevent relapse.
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What are the different types of antidepressents?
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SSRI
SNRI NDRI SARI NASSA - alpha 2 antagonist and serotonin antagonist MAOI TCA |
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What is remission?
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remission is when the disease no longer exists and the pt no longer meets the criteria
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What is the criteria for manic episode?
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one week period with elevated/irritable mood.
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What are some symptoms of mania?
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Always associated with marked social, occupational impairment.
Poor insight suicidal ideations memory impairment |
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What is mixed episode?
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duration of at least one week.
symptoms impair functioning anxiety agitation pressured speech no need for sleep |
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What is the peak age for bipolar?
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15-19 years old
youth is mor severe |
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What systems are affected by depression?
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Brain - dec. neurogenesis
Cardio - dec. HRV and incr. platlet stickiness Autonomic system - incr. sympathetic Endocrine - Incr. HPA Immune - decr. CMI, incr. cytokines |
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What is the leading cause of disability worldwide?
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depression
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What is Huntington's?
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abnormal expansion of polyglutamine tractscausing intranuclear fimlamentous inclusions
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What is Picks?
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Tau filament inclusions. causes frontotemporal dementia. No amyloid plaques.
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What is Crautzfeld Jacob Dis?
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spongiform encephalitis. causing severe dementia, visual disterbances, myoclonus.
Has amyloid fibrils. |
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What deficits occur with alzheimers?
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memory and cognitive
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describe hytological braing with AD?
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atrophied wth enlarged ventricle.
contains neurofibrillary tangles of tau and senile plaques which accumulate in limbic region. |
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What does Tau do?
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it stabalizes microtubles for axonal support.
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What is PD?
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contains intraneuronal filamentous inclusions known as Lewy Bodies. Lewy bodies contain alpha synuclein. depletes the Substantia Nigra of DA.
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What is the common factor for neurdegenerative diseases?
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They all involve mifolding of protein.
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What does an alzheimers gross brain look like?
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has narrowed gyri and widened sulci. Hipicampus is effected.
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What are senile plaques?
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AB peptides known as APP. formed extracllularly.
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Where are tauopathies mostly seen?
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In Glial cells more so than neurons. in frontotemporal lobes.
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What are the thre laws of pharmacology?
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Drugs Work
Drugs have side effects The number of side effects increase the longer the drug is on the market. |
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What is pharmacodynamics? Pharmacokinetics?
Pharmacoeconomics? psycopharmacotherapy? |
pharmacodynamics - How does the med work.
Pharmacokinetics - what are the dosing strategies pharmeconomics - is it cost effective psychopharm - what does the patient think about med. |
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What are the properties of receptor regulation?
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Desensitization
down regulation up regulation |
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What are the four DA pathways?
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Nigostriatal - motor move'ts
Mesolimbic - attention, pleasure Mesocortical - processing Tuberoinfundibular - prolactin inhibition |
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Where is NE made?
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Locus Ceruleus.
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What symptoms arise when alpha 1 receptors are blocked?
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dizziness
Hypotension Drowsiness Sexual dysfunction |
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What is Serotonin syndrome?
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agitation, hypervigilance,
confusion, tremor. |
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What do TCA's effect?
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serotonin reuptake,
Muscarinic ACh receptors antiadrenergic effects (alpha 1). |
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Are MAOIs long lasting?
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YEs they irreversibly bind to MAO therefore, the body needs to make more.
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What is MAC?
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Minimum Alveolar Concentration -
is analogous to EC50, the midpoint of the concentration effect curve in a population. |
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Whatorgans acheive equilibrium from anesthesia the quickest?
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Organs with good blood flow acheive equilibrium first. Brain, heart. Last = fat
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Who will reach anesthetic equilibrum first? high cardiac output or low?
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Low cardiac output pts.
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How does inhalation anesthetics affect blood pressure? Ventilation?
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it decreases it. respiratory rate increases.
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How does solubility of anesthesia in the blood affect the onset?
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Low solubilty will acheive anesthesia quicker.
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what type of base is a local anesthetic?
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Weak base.
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What are the two types of local anesthetics?
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Amides and esters
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What are the different properties between amines and esters?
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Esters have short half lives (unstable), Amides undergo hepatic biodegredation, Esters produce allergic PABA.
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How do local anesthetics work?
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They block the Na channels from generating an AP. It binds to the internal membrane of the Na channel. It binds to the channel when it is open or inactivated. It unbinds in the resting state. The weak base is uncharged when it enters the cell then binds to H+ and attaches to Na channel.
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Why is epinephrine used with anesthesia?
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it vasoconstricts the vessels decreasing absorption so the anesthesia works longer.
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How are Esters metabolized? Amides?
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Esters are hydrolyzed by pseudocholinesterase which creates PABA. Amides are metabolized in the liver.
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What determines potency of anesthesia?
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Higher lipophilic (high partition coefficient) = more potent. Therefore, not as much is needed.
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What determines duration of anesthesia?
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More lipophilic = longer duration because it isn't reabsorbed by the blood from the nerve.
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What determines speed of onset of an anesthetic?
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Pka. The pKa that is closer to the body pH will have a faster onset.
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What are the symptoms of anesthetic toxicity?
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Muscle twitching
numbness of tongue Coma Respiritory arrest CVS depression |
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How can you tell which anesthetics are amides?
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they have two "i" in their name.
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Which anesthetic is more toxic?
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Amides because they are metabolized in the liver.
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What do you do for CNS toxicity of an anesthetic?
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halt injection, yperventilate with 0xygen if seizures occur.
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How is bupivicain different in terms of toxicity?
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Cardiovascular toxity occurs before CNS.
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How do you treat cardiac toxicity from anesthesia?
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inject lipid emulsions into the blood to absorb anesthesia from the heart.
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What is EMLA?
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anesthetic that contains lidocaine, prilocaine and a mixture of others.
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What are sedatives and Hypnotics used for?
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anxiety disorder
convulsive disorder insomnia |
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What are barbituates used for? Why?
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poor anxiolytic, but good for anesthesia. Binds to GABA and makes cell more neg.
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How do Barbituates effect cardio and respiratory?
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decreases blood pressure and suppresses ventilatin drive.
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What are benzodiazepienes used for?
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sedation
hypnosis anxiolysis |
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How does Benzos effect cardiovascular?
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decreases blood pressure which causes increase in heart rate.
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What are the treatments for sleep disorder?
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Search for medical disorder - hyperthyroidism
Search for psych disorder - depression Good sleep hygeiene |
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What is Cognitive-behavioral therapy? What is the goal?
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The patients problematic thoughts, emotions, and behaviors are addressed and HW is assigned to enhance learning and memory. The goal is for the patient to become self sufficient.
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What is "case formulation" in CBT?
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the explanation about the pts. condition- how it started, and developed. It involves family history and personal development focusing on schemas.
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What is a schema?
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patient's belief and views of the world and self.
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What are some techniques pts. can benefit from learning skills?
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monitoring own behavior
monitoring own thinking Ask socratic questions practice new behavior |
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What are some advanced schema techniques?
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Role Playing
Guided imagery |
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What are 3 key elements of a CBT session?
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Setting an agenda
mood check bridge from previous session |
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When is psychodynamic therapy advised?
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Major depression
panic disorder PTSD Cluster B, C |
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What are some assumptions for psychodynamic therapy?
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Problems are not the symptoms
past experiences are replayed in the present. |
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What are the main techniques of psychodynamic therapy?
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look for repetitive patterns
uncover meaning unconcious Therapist needs a relationship with pt. to enable learning |
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What are the drug types we need to know for substance abuse?
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nicotine
sedatives - alcohol, benzos and hypnotics stimulants opioids cannabinoids hallucinogens - LSD, PCP, ecstasy |
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Is adiction a disease?
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Yes, relapse and remission,
involuntary behavior, no cures. |
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What is addiction/Dependence?
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Drug use out of control.
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What is the neurological effect of drugs?
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to activate reward systme and increase DA in nucleus accumbens.
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What factors determine addiction?
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agent (drug)
Host environment |
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What is tolerance?
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reduction in drug effect with repeated administration.
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How is cross tolerance helpful?
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useful in choosing detox.
heroin - medthadone alchol - oxazepam |
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Is tolerance neccessary for addiction? withdrawl?
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neither is necessary nor sufficient.
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What is sensitization?
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reverse of tolerance. increase effect with repeated dosing.
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What factors lead to relapse?
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psychiatric problems
social problems |
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What is cue induced craving?
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a compulsion, difficult to resist a drug craving caused by cues previously associated with drug use.
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What is the mechanism of action of LSD?
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involves serotonergic system (post-synaptic) H/E exact mechanism is unknown.
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What is the 1/2 life of LSD?
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3hrs.
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What CNS effects does LSD have?
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Euphoria
Labile mood halluconations overflow of one sensory system to another. |
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What are the side effects of chronic use of LSD?
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no permanent damage
bad trips flashbacks |
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What is the mechanism of PCP?
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not understood
acts as antagonist of NMDA- glutamatereceptors |
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What are CNS effects of PCP?
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euphoria
speedy uncommunitive oblivious numbness in hands and feet distortion of body image auditory and visual hallucinations |
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What are the effects of chronic PCP use?
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dulled thinking
loss of impulse no clear evidence of brain damage. |
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What is the mechanism for ecstacy?
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belived to be DA and serotonergic.
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What are the effects of ecstacy?
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dry mouth
increased heart rate increased BP euphoria loss of boundaries hallucination |
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Does psychosocial intervention prevent suicide?
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No evidence.
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Is suicide behavior viewed as primary problem or symptom in CBT?
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primary problem.
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What is involved in the initial seesions when dealing with suicide?
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safety plan
recognition of suicide thoughts coping strategies information for reaching out to friends contacting professionals |
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What do the middle sessions of suicidal therapy involve?
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behavioral strategies
affective coping strategies cognitive strategies |
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What are the aims of cognitive therapy for suicide attempters?
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preventing repeat attempts
reducing the severity of risk factors increase use of health services |
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What are the effects of opioids?
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CNS - analgesia, euphoria, sedation
C-V - vasodialation Eye - pupil constriction Lungs - resp. depression GI - decrease in contractions |
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What are opioids used for?
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severe pain.
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What are the withdrawl symptoms of opioids?
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craving, dysphoria, over activity of CNS.
sweating yawning anxiety |
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What is the mechanism of opioids?
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stimulate DA neurorecptors
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what are the benefits of methadone?
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oral
long lasting blocking dose - no effects of opiate will be felt if used. |
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What is a unit of alcohol?
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14g.
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Where is alcohol absorbed? How?
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in the small intestine. passive diffusion - therefore, not saturable.
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Who has a higher BAL for a given dose, Male or Female? why?
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Femaale - alcohol enters fat slowly therefore it stays in the blood longer.
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How is alcohol metabolised?
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3 key enzymes -
Alcohol Dehydrogenase (liver) Oxidative pathway in liver by microsomal ethanol oxidizing system ( MEOS) Acetaldehyde dehydrogenase (ALDH). |
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How does ADH work?
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in liver and stomach.
More in men than women, T/f women have higher BAL. First order kinetics. |
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How does MEOS work?
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kicks in when ADH is saturated. More you drink more you make.
Zero order kinetics. |
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What effects does chronic alcohol have?
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Loss of White and grey matter,
reduced brain metabolism, wernickes/kersakoff syndrome - cerebellar signs and memory loss in the frontal lobe Vasodialation increased blood pressure |
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What is fetal alcohol syndrome?
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microencephaly,
floppy baby ETOH crosses placenta. |
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How is Panic disorder defined?
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having panic attacks which are periods of intense fear or discomfort. Reach a peak in ten mins.
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What are the symptoms of a panic attack?
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heart palpitations
sweating shortness of breath chest pain feeling of choking |
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What is agraphobia?
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anxiety of being in situations where escape is difficult.
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What is social phobia?
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characterized by persistent extremem fear of situations. exposed to unfamiliar people.
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Do pts. experience withdrawl with benzos?
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Yes after 4 weeks of use the meds need to be carefully discontinued before stopping.
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What is the treatment for GAD?
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antidepressants, SSRI, TCA, Benzos, buspirone, CBT
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What is the prevelance of GAD?
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lifetime prevelance is about 5%.
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What are the symptoms of GAD?
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twitching, cold, clammy hands, sweating.
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What are the diagnostic criteria for GAD?
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excessive anxiety for more days than not for 6 mos.
anxiety is difficult to control causes distress. |
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What is the main NT that is linked to anxiety and what type of receptor is it?
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GABA-A is the main inhibitory receptor.
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What pathway when excessive causes dysfunctional arousal?
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Sympathetic - norepinephrine.
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what two types of meds should the pts. start with if pt. has anxiety disorder?
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Benzo and SSRI - b/c SSRI takes a few weeks to become effective.
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What are SSRIs used for?
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GAD
PD PTSD social anxiety disorder depression OCD Pain |
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What are the benefits of benzos for anxiety?Drawbacks?
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benefits -
effective rapid onset well tollerated Drawbacks- sedation cognitive impairment dependence interaction with alcohol |
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Can B-blockers be used for anxiety?
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Yes. for performance anxiety not for GAD.
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What are the benefits of CBT for anxiety disorders?
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very effective
more long term benefit than meds provides comorbid benefit lower relapse rate apon discontinuation. |
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pathways that are effected by anxiety disorders have what primary task?
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axiety arises from a multilayered system that has the task of assessing potentil threats and preparing responses to them.
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What two areas in the brain are responsible for threat appraisal and memories?
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PFC and hippocampus.
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What are benzos good for? what are they not good for?
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anxiety disorders.
not good for- OCD stress disorder, PTSD. |
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Does a stress response = anxiety?
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NO!
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What is the purpose of anxiety and its factors?
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Threat assessment and response.
Detection descrimination rapid response Return to baseline memory function |
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Do the number of threatened events change your response?
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Yes,
Behavioral response changes depending on the threat level. Higher threat needs less trial for response. |
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What are the mechanisms of stress?
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Stress response - locus ceruleus, hypersensitive to incoming stimuli
Limbic system - hippocampus, source of emotional response Integrated system - PFC and amygdala, multiple layers of feedback |
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What is the treatment for anxiety disorders?
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monoamines, GABA - Benzos
psycotherapy |
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What type of stressors precipitate PTSD?
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Only serious threat to life or limb.
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What are the four symptoms of PTSD?
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Dissociation -time stands still
intrusion - rexperience avoidance hyperarousal |
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What is the difference between ASD and PTSD?
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ASD has the same symptoms but last no longer than 1 month.
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When is the onset for PTSD?
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PTSD may not manifest for months to years later. This is called delayed onset PTSD.
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What is the impact of experience on acquiring PTSD?
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Double edge sword depending on how the individual responded to the previous experience. If they had PTSD then they are likely to get it again, if they did not had PTSD then they are not as likely to get it.
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What is the biological mechanism of PTSD?
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there is a higher rate of turnover of the catecholamines in PTSD. PTSD pts. have decreased basal cortisol levels and hightened sensitivity to negative feedback in the HPA axis. Pts. are sensitized to neutral stimulants as well as egative feedback.
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What is the treatment for PTSD?
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Controversial, some get therapy immediately other wait a few weeks. Antidepressents can also be used.
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What part of the brain is damaged by PTSD? Why? and what is the consequence?
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Hippocampus, because of high levels of cotisol destroy it. Therefore habituation and descrimination fail and feedback is heightened.
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What is the treatment for PTSD?
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restore social support and anitdepressents, sedatives, hypnotics.
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What is the purpose of the HPA axis?
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Fight or flight response.
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What is the patheway of the HPA axis? and what NT and hormones are released?
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The hypothalmus secretes CRF which upregulates the ACHT in the pituitary. ACHT activates the adrenal gland to produce glucocorticoids (cortisol). Cortisol inhibits CRF and ACTH production. Cortisol and the catecholamines are used for the fight or flight response.
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What are the two receptors for glucocorticoids?
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GR - intracellular (broadly expressed in every cell) has a low affinity for cortisol and is responsible for neg. feedback.
MR - has hig affinity for cortisol adn maintains HPA tone. |
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What do corticosteroids do?
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promote gluconeogenesis
inhibits immune and inflamitory rxn inhibits reproduction system decreases bone mass alters memory maintains fluid balance feedback regulation of HPA. |
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What is he cortisol concentration in the body lok like?
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it is at the highest after waking up. Then wanes and increases a little in afternoon. at lowest point at night.
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How is the hippocampus affected by stress?
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MR receptors in the hippocampus get activated and there is a decrease in the number of dendrites.
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What is CRF? what does it do? and where is it located?
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Corticotropin releasing factor. initiates HPA response. It is located mainly in the hypothalmus but also in other places in the brain.
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What are the effects of CRF?
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Loks like stress response.
increased sympathetic activity increased arousal alteratins in behavior suppression of growth hormone. |
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How are HPA and depression related?
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Hyperactive HPA system gives you a chronic level of cortisol and causes loss of circaidian rhythm.
Less feedback inhibition. |
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How is parenting related to the HPA axis?
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a seperated child or abused child has higher HPA activity than normal child. This can cause mental illness.
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What are the clinicl features of OCD?
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obsessive
compulsive awareness of excessiveness Marked distress |
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What are the thre clinical courses of OCD?
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unremitting and chronic
Phasic with periods of complete remission Episdic with incomplete remission |
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Is OCD genetic?
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Genese play a big role.
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What part of the brain is effected by OCD? and what is the consequence?
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abnormal high function of the orbital cortex cn caudate nucleus. There is a disregulation balance in the basal ganglian pathway.
The defensive Macros predominate due to increase activity of the striatum. |
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What is the treatment for OCD?
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SSRI
CBT |
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What is the difference between OCD and OCPD?
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In OCD the person is bothered by the obsession in OCPD the person sees the obsession as normal.
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How is anorexia characterized?
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disturbed sense of body image abid fear of obesity.
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What is the epidemiology of Anorexia?
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Females
Genetics play a role. |
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what are the two subtypes of anorexia?
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restrictive - don't eat
binge/purge |
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Why is anorexia dangerous?
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It causes elecrolyte imbalance and loss of fluid. Cardiomyopathy.
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What is the treatment for Anorexia?
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Intervention. no meds can help the disorder.
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How is Bullimia different than anorexia?
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Bullimics know they have a problem and have normal weight.
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How is billimia diagnosed?
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two binge episodes a week for 3 mos.
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What are the treatments for bullimia?
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psycotherapy and antidepressents.
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What are the two types of Bullimia?
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Purging
non purging - fasting or excersice. |
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What is the criteria for night eating syndrome?
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morning anorexia
evening hyperphagia awakenings consumption of snacks |
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What is effected during night eating syndrome?
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There is a delay in circadian rhythm while the circadian sleep rhythm is intact
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What is the mechanism of benzos?
|
GABA-A receptor activation
similar to barbituates, alcohol there is a tolerance and withdrawl. |
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What are the symptoms of benzo withdrawl?
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anxiety
agitation sensitivity to light insomnia |
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What are some treatments for insomnia?
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look for underlying cause
sleep hygiene antihistamines non benzo hypnotics antidepressants |
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What is a physical dependence? is it normal? How is it different than addiciton?
|
tolerance with withdrawl
and is a normal response. and addiction is when you use more than intended with unsucceful efforts to cut down. |
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What are the effects of marijuana?
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euphoria
aniolysis umotivated memory problems bad balance. |
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What is the active ingredient in marijuana?
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THC.
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How long until marijuana has a peak effect?
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10 mins. inahaled
2hrs eaten. |
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How is marijuana detected?
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Urine samples can be positive 96 hrs. after joint. Plasma not urine correlated with time and amount used.
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What is legal THC used for?
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chemotherapy and AIDS related wasting.
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What are the two types of cannabinoid receptors and where are they located?
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CB1- Brain: Hypothalmus controls apetite, basal ganglia involves motor hippocampus involves memory
fat, kuver CB2- lymphocytes. |
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Which receptor do endocannabinoids bind to?
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CB1
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What are cannabinoids useful for?
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treatment of the disorder of motivation and reward systmem that induce drug addiction and abuse.
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What is the criteria for alcohol dependence?
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maladaptive alcohol use and
3 of: tolerance withdrawl more than desired desire to cut down effects personal life |
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How does alcohol affect the brain?
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it acutely stimulates and chronically disrupts brain reward pathway.
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What is the pathway model for addicts in the brain?
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a memory (cue) triggers the hippocampus, than the drive and salience are from the nucleus accumbens and VTA and the control is mediated by the prefrontal cortex.
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What drives stimulant epidemics?
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low perceived risk and increase supply.
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What brain pathway is involved with cocaine?
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mesocorticolimbic system. VTA is activated causing DA to be released from the nucleus accumbens and rewarding effects in the PFC. Glutamate is also released by VTA to create euphoria.
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What are the toxic effects from cocaine?
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vasospasm
seizures cardiac arrythmias hypertension |
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How is cocaine euphoria and plasma levels related?
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it is not the amount of cocaine in the plasma but the increase of level that creates the euphoria.
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What are the four types of cocaine cravings?
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cocaine induced craving
cue induced craving stress induced craving baseline craving. |
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What are treatments for stimulant abuse?
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intervention
AA individual and group therapy |
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Do opioids provide analgesia?
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Yes
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What type of receptor does morphine bind to?
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Mu opioid receptor in the CNS.
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What is supraspinal analgesia?
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peri-aquaductal grey and thalamus neurons decend in the dorsal horn. In the dorsal horn these terminals inhibit pain impulses. Mediated by Mu receptors.
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What is spinal analgesia?
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mediated by kappa and delta receptors in the dorsal horn.
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What causes the euphoric properties of morphine?
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binding of Mu receptors in the VTA, nucl. accumbens and cotex increasing DA release to cause reward.
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What are some side effects to opioids?
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respiration depression
antitussive constipation constriction of pupils dialation of peripheral circulation. |
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What is the treatment for opioid abuse?
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naloxone or methadone.
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what is the onset of morphine?
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1 min if IV
10 min if IM lasts for 3-4 hrs. |
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What are the withdrawl symptoms from opioids?
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anxiety
agitation diarrhea pupil dialation |
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What factors contribute to schizophrenia?
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Genes and environment play a factor in schizo.
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What part of the brain is effected by schizo?
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dysbindin hippocampus is much smaller in pts. with schizo. There is progressive grey matter loss. Interneuron development is also decreased.
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What is the pathway involved in schizo?
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Primary lesion in PFC preventing inhibitory response. This leads to increase in DA.
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What are the types of treatments for schizo?
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typical and atypical antipsychotic. atypical increases the volume of the hippocampus.
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What is schizophrenia?
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syndrome of abnormal thought, feeling and behavior with delusions and hallucinations.
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What are the symptoms of schizophrenia?
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delusions
hallucinations disorganized speech disorganized behavior negative symptoms all greater than 2 mos. |
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Is there a higher incidence of schizophrenia in urban pop?
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yes.
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what is affected by schizophrenia?
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limbic system without gross alterations.
cingulate gyrus hippocampus orbitofrontal |
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What are the positive symptoms of schizophrenia?
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delusions
hallucinations abnormal behavior and thoughts. |
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what are the negative symptoms of schizophrenia?
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disturbed affect
alogia (lack of speech) |
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What prognosticators represent a good outcome for schizophrenia?
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later and abrupt onset.
level of premorbid functioning. more developed brain has less neg. symptoms = better outcome. |
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What are the subtypes of schizophenia?
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paranoid - delusions and hallucinations
disorganized - disorganized behavior and speech catatonic - abnl motoric/posturing or speech undifferentiated |
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What are the treatments for schizophrenia?
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antipsychotic affect DA in the basal ganglia, temporal lobes and frontal lobes
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What are the differences between typical and atypical antipsychotic meds?
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atypical also improve depression and some neg. symptoms.
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What is the difference between hepatic steatosis and cirrhosis?
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steeosis = fty deposition within the liver
cirrhosis = fibrosis |
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What are the effects of inhalants?
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vasodialation
increase HR smooth muscle relaxation (used for sexual activity) |
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What are the toxicity effects of amphtamines? what is it similar to?
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hyperthermia
tachycardia hypertension Cocaine |
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What are the two reasons for chest pain related to cocaine? how are they treated?
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Myocardial ischemia - oxygen, aspirin NO beta blockers
Aortic disection - beta blocker AVOID apirin |
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What is the most common infection for drug abuse?
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Staph Aureus.
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What is the most severe complication of drug abuse IDU?
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endocarditis caused by staph a or other bacteria. Pt. will have new murmur.
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What meds can be used for anxiety?
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SSRI, TCAs, MAOI,
Benzos best for GAD. |
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What type of receptor do benzos bind to?
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GABA specific BZ-1.
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What are the two types of GABA receptors?
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BZ-1 for sleep
BZ-2 for anxiety, cognition, memory |
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What type of GABA receptor does hypnotic agents act on?
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BZ-1.
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What are the four pathways involved with DA?
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nigrostriatal - motor (Parkinsons)
Mesolimbic - attention, pleasure Mesocortical - processing tuberoinfundibular - prolactin inhibition. |
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What are the three classes of antipsychotic and what are their side effects?
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High potentcy - effect alpha 1 (orthostatic hypotension)
Mid - more anticholenergic (more sedative, dry mouth) Low- most anticholinergic. |
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What are the four pathways for ACh?
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Nucleus Basalis - learning, memory
Striatal interneurons - motor function Lateral Tegmental - arousal Peripheral - cardiac, GI |
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What is Neuroleptic Malignant Syndrome?
|
Rxn to antipsychotics that causes thermal dysregulation and muscle rigidity.
stop neuroleptic and start supportive care. |
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What is the different effects of typical from atypical antipsychotics?
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typical stop the positive symp. may worsen neg.
atypical improves both. |
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What medications are used for bipolar disorder?
|
Lithium
antiepileptic atypical antipsychotic. |
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What is the side effect for lithium?
|
slurred speech, muscle twitching, memory problems.
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How does nicotine have the effect it has? what does is change?
|
Nicotine has direct and indirect on several NTs - dopamine, NE
it effects the function of cardiovascular, endocrine and skeletal |
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What receptors interact with nicotine?
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nicotine acetycholine receptors.
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What part of the brain is effected by nicotine?
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Nucleus accumbens releases DA
amygdala releases serotonin. |
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Why do people smoke?
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positive reinforcement and negative reinforcement.
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What are the treatments for smoking?
|
non pharm.
meds. physician counseling is the strongest motivation to quite. |
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What are the 5 A's for a physician when coming across a pt. who smokes?
|
ask about smoking
advise on quitting asses willingness assist with treatment arrange follow-up |
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what are pharm. treatments for nicotine addiction?
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gum, patch, spray, inhaler, Zyban.
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How does smoking alter antipsychotic meds?
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changes enzyme activity so pt. needs more meds.
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Why is smoking more addictive?
|
quicker to the brain = more addictive.
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What are the signs of nicotine dependence?
|
smokes when waking up
difficult from refraining smokes one pack/day |
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What populations are affected by smoking?
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Women
pregnant psychiatric adolescents |
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What is the most used illicit drug?
|
marijuana
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Do women stop drug use during pregnancy?
|
23% stop during first trimester
93% stop by third trimester most relapse after delivery. |
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|
what are the highest rates of use of drugs?
|
younger age
unmarried less education |
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|
what disrtuptions of pregnancy are caused by drugs?
|
nicotine - spontaneous abortion and premature delivery
Cocaine - pontatneous abortion, abruptio placentae, premature delivery, fetal demise. |
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What are the neonatal effects from drug use?
|
growth retardation, jittery and withdrawl.
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What are the signs and symptoms of neonatal withdrawl from opiates, alcohol and benzos?
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irritability, trmulousness, increased muscle tone.
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What are the signs of neonatal withdrawl from marijuana and nicotine?
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irritability, tremors, startle.
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What are the signs for neonatal withdrawl from cocaine?
|
increased muscle tone and drowsiness.
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What effect do drugs that block NMDA and activate GABA receptors have on neonates?
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apoptosis of neurons.
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What disruptions are caused by nicotine in neonates?
|
neuronal proliferation and differentiation an disruption of cholinergic and catecholaminergic systems. affects memory and sleep.
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What are Fetal alchohol syndrome symptoms?
|
growth retardation
cns disfunction craniofacial abnormalities |
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|
What are the treatments for pregnent women who abuse drugs?
|
abstinence based AA
methadone Provide access to mother and father. |
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|
How are alcohol effects different for adolescents than adults?
|
mor vulnerable.
the effects on learning and memory at a lower dose adolescents are less sensitive to alcohol and morot impairment. |
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|
What vulnerabilites are there to drug abuse?
|
family
genetic environment. |
