“How to Survive” Guide –5th Year 1
TABLE OF CONTENTS
Hello everyone!
This is the first study guide for 5th year classes, and as such, we do not have enough advice to make individual guides for each class. In this guide, you will find advice for each class you have to take, including neuropsychiatry, systemic pathology, epidemiology, and pathophysiology. And, last but certainly not least, the much dreaded, much feared USMLE Step 1. Good luck.
Topic / PagesNeuropsychiatry – Advice / 2
Neuropsychiatry – Exam 1 Information (from Akeem Marsh) / 3-11
Neuropsychiatry – Exam 2 Information (from Akeem Marsh) / 12-20
Systemic Pathology / 21-22
Epidemiology / 23
Pathophysiology / 24
Physical Diagnosis / 25
Comprehensive Basic Science Exam / 26
The Final Step of Sophie: USMLE Step 1 / 27-31
How to Survive: 5th Year
Galina Borodulina (Class of 2007)
Barry Ladizinski (Class of 2007)
Akeem Marsh (Class of 2007)
Shayla Syed (Class of 2007)
NEUROPSYCHIATRY- ADVICE AND INFORMATION
Advice from Akeem Marsh
The name Neuro-Psychiatry, doesn’t that sound very sophisticated and medical professional-ish. Well that it certainly is, but not one course, much like it’s predecessor Behavioral Medicine, that you will not have to lose sleep over. In many ways, this is just an extension of Behavioral Medicine so advice is really not necessary. I can say nothing at all and half of you, maybe more will still get A’s haha. Having said that, I will still provide some information that those of you that like this sort of thing may find helpful.
What you learn in this class mostly is about psychiatric illnesses (dementia, psychosis, schizophrenia, attention deficit disorder, …) and how to treat all these diseases. I think this class, unlike Behavioral Medicine, was completely lecture notes oriented. Your written exams will be in the same format as they were in behavioral medicine, about 30-50 multiple choice questions and you will find them to be very easy. I have some notes compiled together and they are derived from all of the lecture notes. You may find these helpful because it condenses everything together sort of succinctly and I added in some mnemonics as well.
The best books to use for this course are in my opinion Behavioral Science BRS and PreTest in Psychiatry (yes, Step 2 psychiatry). I think that is the MOST relevant for both your coursework and your miniboard. The Behavioral Science PreTest is a shameful book in the pretest series and those of you that decide to invest in it, and I know some will unfortunately, will probably regret that purchase as it is completely irrelevant. PreTest in Psychiatry is good for both coursework and for the miniboard.
I have heard of two different versions of the miniboard, either one heavily centered on ethics questions and one with a lot of drug questions. In any case, if you even study for your Neuro-Psychiatry course at all, you should be well prepared for your miniboard. The ethics questions will be like Patient Doctor all over again asking questions about how one should interact with patients (common sense) or the drug filled exam, which you should be ready for anyway because that is mostly what Neuro-Psychiatry is about.
Enjoy this “vacation” while it lasts because when you get hit with the real stuff, i.e. pathology, you will have to work a bit harder than you did for this course. If you care to use them, the notes that I made are attached to this file in the following pages. Happy Studies!
Advice from Shahla Syed
The hardest part of neuropsych is learning the drugs - if you can do that, you will be just fine, and I would recommend going back to Katzung again for this. Of course you have to learn the psychopathology as well, but I found that less difficult than learning drugs (I've always had trouble with pharm).
NEUROPSYCHIATRY- EXAM 1 MATERIAL
Marijuana increases weight (associated munchies).
Leptin signaling blocked by suppressors of cytokines. Leptin signaling stops in severely obese pts. Signaling center is located in the arcuate nucleus of the hypothalamus. leptin = weight by stimulation of appetite. Leptin is produced by the ob gene.
Orixegenic - appetite. Anorixegenic - appetite.
Anorexia xtreme weight loss, refusal to eat despite normal appetite. Bulimia however involves binge eating, tooth enamel erosion.
Trx anorexia: TCA’s (imipramine), 5HT – fluoxetine, phenfluoramine, heterocyclics: isocarboxazid, phenelzine, and trazodone.
Long term Trx for obesity: ObeSity – Orlistet and Sibutramine
Short term Trx for obesity: a short obese girl named Zoe Torp.
Zonisimine and Torpiramate
SSRI - weight for 6 mos. Antidepressants - glucose levels
Phase 3 of clinical trial antidepressant. Endocannibinoid receptor block (Radafaxine is Rad b/c it stops ur high.)
Selective 5-HT2c Agonist – Rimonabant and phenfluoramine
CeFiLIstat blocks absorption of Fat by inh. LIpase.
Mutation in mahogany mg gene is what es weight. Having a fxning mg gene doesn’t work well at weight control. Mg gene related to agouti pigment gene, and nearly identical to attractin produced by activated T cells that stimulates attraction between cells.
ADHD – Impulsivity, fidgeting, distracted ez, difficulty following directions. at least 6 mos. Occurs b4 age 7. impaired behavior in at least 2 settings. 3 types: combined, inattentive, hyperactive-impulsive. All more common in boys. Girls get inattentive type. Pts r at risk for drug abuse, accident, and dropout. Caused by possible reticular activating system (frontal lobe) or in NE. Strong genetic component; multigene disorder (D4 receptor, DA transporter, synaptosomal-associated protein 25). Stimulants calm children with ADHD. There are different affects between children and adults with ADHD b/c there is more DA released in adults for their lack of autoreceptor activity. Trx Dextroamphetamine and Methylphenidate (both indirect acting sympathomimetics), Pemoline (liver fxn tests shud be done b/c jaundice) and Modafinil (1B agonist). [Dexter Must Make Peace.] Drugs can also trx narcolepsy, weight loss, and rarely supplement PD. Side effects include GI symptoms, headache, muscle twitch, and hallucinations.
Cocaine affects DA release and reuptake.
Conduct Disorder – Aggressive behavior and infringement upon the rights of others > 12 mos. Usually comorbid with ADHD, ODD, learning disability. More common in boys. Same risks as ADHD. Multifactorial etiology. Trx multimodality, psychotherapy, and drugs: antipsychotics, SSRIs, and ithium
Affects on DA release: amphetamine > Ritalin > caffeine
ODD – Disobedient, hostile, defiant behavior to authority > 6 mos. More common boys, may lead to development conduct disorder. Multifactorial or unknown etiology. Trx no drugs, just psychotherapy and behavioral management skills.
Psychoanalysis
Psychoanalytic Psychotherapy
Supportive Psychotherapy
Cognitive Behavioral Therapy
Depression: Monoamine depletion by unknown disease process, stress, drugs. MAO inh. (isocarboxazid, phenelzine, tranylcypramine) Relieve depression by monoamine. TCA’s inh monoamine transport. Same affects as MaoI. 3 main neurotransmitters are DA, 5-HT, NE. Prozac 5-HT. MAO destroys NE, NE reuptake pump terminates axn of NE, NE receptors react 2 NE release.
4 groups of treatment: 1) TCA’s 2) Heterocyclics 3) SSRI (prozac)
4) MAO: side effects tyramine (cheese, wine, pickled pigs feet, aged meats, beer) and hypertensive crisis, serotonin syndrome (muscle rigidity, CV collapse, hyperthermia)
Biological basis of Schizophrenia is unknown.
Mesolimbic DA pathway: ventral tegmentumnucleus accumbens. Associated with this pathway pleasure, reward, reinforcing behavior, drugs of abuse, and chocolates. Hyperactivity ( DA) here gives +ve psychotic symptoms (emotional behaviors, auditory hallucinations, delusion, thought disorder) and plays a role in aggressive/hostile behavior in schizo.
*all known antipsychotic drugs are capable of treating +ve psychotic symptoms are blockers of DA receptors (D2).*
Mesocortical DA pathway: ventral tegmentum limbic cortex . –ve schizo symptoms (5 A’s: attention deficit hyperactivity, affective flattening, alogia, avolition, anhedonia) could be localized to dorsolateral prefrontal cortex. –ve symptoms due to burnout of neuronal symptoms excitotoxic overactivity of glutamate systems. DA deficit (-ve symptoms schizo) can be 1 or 2 (inh by excess 5-HT OR antipsychotic blockage of D2 receptors).
Nigrostriatal DA pathway: sub nigra basal ganglia (striatum). EPS and motor control.
Deficiencies Parkinson’s (Rigidity, Akinesia/bradykinesia, Tremor) and Akathisia (restlessness), dystonia (twisting movements). Blocking D2 receptors mock deficiencies. Chronic blockade causes Neuroleptic-induced tardive dyskinesia. Hyperactivity of DA – chorea, dyskinesias, and tics.
Tuberinfundibular DA pathway: Hypoth Ant Pit. Active inh prolactin release. Postpartum, activity is ed. ed prolactin causes galactorrhea, amenorrhea, sexual dysfxn. ed prolactin occurs after chronic blockage of D2.
Schizo onset late teens/early 20s. Symptoms; odd behavior, es facial expression, moderate depression, elevated HVA in body fluids. Incidence s in pts w/ fetal obstetrical complications. Anatomic features include wide sulci, ventricle size, frontal and medial temporal lobes (gliosis) and hippocampus (disordered orientation of pyramids). Causes:
1) toxic or genetic result2) poor neuronal migration (occurs in epilepsy as well)
3) inadequate synaptic selection (mutations in synapsin 1:2, possibly D2)
4) poorly innervated
*synapsin sux in schizo. D2 antagonists worsen symptoms
(Give GABA to epileptics, but NOT glutamate. GlutamateGABA (Glut. Decarboxylase) GABA Glutamate (GABA Transaminase) Glutamate is excitotoxic by inducing apoptosis/cell death.
HaloPEridol – Has Potency and EPS.
SDA (serotonin DA antagonist) – block both 5-HT2A and D2.
Clozapine blocks histamine and cholinergic as well. Less EPS than typical used as Trx for Tardive Dyskinesia and has agranulocytosis as a side effect.
Anxious pts trx w/ antidepressant. Venlafaxine drug of choice. Mood in depression and anxiety of GAD. Venturous for trxing 2 disoders.
Clomipramine (TCA) and Fluvoxamine (SSRI)– trx OCD
High comorbidity of depression and anxiety.
SSRIs (fluoxetine, paroxetine, sertraline, fluvoxamine) are used for pts with depression, anxiety disorder subtypes, panic disorders and social phobia.
Buspirone – 5-HT1A partial agonist is a generalized anxiolytic. Other 5-HT1A agonists are flesinoxan, sunepitron, adatanserin, ipspapirone. Advantages vs BZDs include no interaction with EtOH, BZDs, sedative hypnotic agents, absence of drug dependance with long term use, ease of use in therapeutic onset for antidepressants. Used preferentially in chronic/persistant anxiety comorbid with substance abuse, and elderly pts.
-Buspirone best for 4A’s: Anxiety (chronic/persistent), Abuse (comorbid substance), Aged (elderly), and Autoreceptor Agonist.
Mechanisms of action of drugs5-HT1A agonist / Antidepressants / BZD anxiolytics
Adaptive neuronal and receptor events / Adaptations in neurotransmitter receptors / Occupy BZD receptors
ALL 5-HT1A agonists have presynaptic axns for anxiety and postsynaptic axns for nausea/dizziness.
GAD + MDD = MAD. Subsyndromal anxiety + subsyndromal depression = subsyndromal mixed anxiety depression (anxious dysthymia). MDD + subsyndromal anxious depression. GAD + dysthymia = GAD w/ depressive symptoms
Enkephalins – are mood altering
Orthoquinone (free radical) produced from DA. Neurodegenerative from L-Dopa.
Brain derived neurotrophic factor:
-sensory neurons: nodose, dorsal root ganglion
-spinal motor neurons, basal forebrain cholinergic neurons, substantia nigra DA neurons, facial motor neurons, retinal ganglion cells
Nomifensine and Bupropion help depressed by blocking reuptake pump.
Pargyline is a Mao inh.
Pramipexole is a D2 agonist.
Idocoxane, Clonidine, Reserpine, Yohimbine ALL have 2A autoreceptor axn.
ICaRYs is an automatic flight machine.
Serotonin can be found in intestine and pineal gland. Gastric carcinoid syndrome contains excess 5-HT, and the test for this checks levels of 5-HIAA.
Fenfluramine enhances 5-HT release.
CisApride s Appetite in Children.
Drugs involved in cholinergic transmission:
-hydroxybutyrate – Gaba B receptor inh NE release
Vesamichol – inh Ach storage
Physostigmine, donepezil, galantamine AchE inh
Troxypyrrolium/hemicholinium inh uptake of choline by presynaptic membrane
Bungarotoxins + botulinum inh Ach release at presynaptic terminal
Curare/Rabies nAChR
Vigabatrin inhibits GABA Transaminase and is used to treat childhood epilepsy.
Spastic paralysis is a GABA B disease, and Baclofen trxs.
*Flumazonil is the only antagonist for BZD. *Flumazonil says F#ck BZD!
Lennox Gestaut Syndrome – mixed seizure and MR. Tonic seizure activity in sleep. Trx Toperamide, Filbarmate, Lamotipine.
West syndrome muscle contraction and MR. 1-2 sec duration, peaks faster. Trx Topiramide, vigabactrin, corticosteroids.
Diazepam (Valium). Good Anxiolytic. IV for Status Epilepticus. Tetanus.
-makes you take ASTEp.
Chlorazepate and Oxazepam are BZDs that live forever in your body and produce metabolites that live forever.
Alprazolam (xanax)– anxiety and depression. Like venlafaxine
Triazolam – pts will experience “rebound” insomnia after discontinued use after long trx.
Zolpidem/Zolepion – work on BZ1 receptor. Trx sleepwalk
- sedatives (anxiolytics) anxiety and exert a calming effect while hypnotics produce drowsiness and encourage “natural sleep”. Sedatives at high doses can have hypnotic effects.
BZDs are MOST imp sedative hypnotics. Barbiturates are sedative hypnotics that cause undesirable psychologic and physiologic dependance. Other sedative hypnotics include: piperidinediones, propanediol carbamates, alcohols (EtOH, chloral hydrate, paraldehyde), buspirone, zolpidem. Sedative effects can be obtained w/ blockers, clonidine, antipsychotic tranquilizers, TCAs, and anti-histamines.
*Redistribution of drug from CNS 2 other tissues is an imp feature of the biodisposition of sedative-hypnotics. Thiobarbiturates are RAPID. Sedative hypnotics are detectable in breast milk. (can depress CNS in nursing infants)
Anxiety is an expected, normal, and transient response to stress. Pathological anxiety requires 4 criteria: 1) autonomy (no recognizable triggers) 2) intensity (> pts capacity to bear discomfort) 3) duration (persistent symptoms) 4) behavior (impairs coping)
Anxiety differs from fear which is a sense of dread and foreboding that occurs in response to an external threatening event. Symptoms include autonomic arousal, “going to die” or “lose control”, avoidance or compulsions, and worry/apprehension/obsessions.
Etiology is central NE systems (locus coerulus) and GABA (limbic), modulated by serotonergic and neuropeptides. Is most prevalent psychiatric disorder. risk among pts with 1st degree relatives w/ anxiety. Physical, psychosocial, and quality of life affected.
Organic causes of anxiety: thyroid, NE, drugs (cocaine, caffeine, EtOH, narcs, sed-hypnotics).
Panic disorder – recurrent unexpected panic attacks (episodes of intense anxiety peak w/in 10 mins) More common in women. Late teens – 30 y/o. Runs in family. Hard to diagnose b/c symptoms include cardiac, pulmonary, GI, neurological, autonomic arousal, psychological. Trx antidepressants (paroxetine, sertraline) and high potency BZDs (alprazolam/clonazepam). Agorophobia seen in some pts w/ panic disorders. Anxiety abt or avoidance of places or situations from which escape might be embarrassing.
GAD – excessive anxiety/worry. Occurs more days than not > 6mos. More common in women. Child or adolescent. 3/6 (restlessness, ez fatigability, difficulty concentrating, irritability, muscle tension, insomnia). Trx cognitive behavioral therapy and antidepressants, BZDs, buspirone.
Phobia – persistent, excessive unreasonable fear of situations or objects. 10% gen pop. Exposure to stimulus provokes anxiety. Trx BZDs to anxiety and cognitive behavior therapy.
-social phobia (fear of public scrutiny). Trx SSRI, BZDs, blockers.
OCD – recurrent, intrusive, unwanted thoughts or compulsive behaviors/rituals. Four criteria: 1) intrusive/inappropriate 2) not simple worries 3) attempts made to ignore/neutralize 4) obsession recognized as a product of his/her mind
OCD is Trx w/ ClOmipramine b/c it has an O and C. Cognitive Therapy is good as well.
PTSD ntense fear, helplessness, or horror b/c of an experience that was a threat of death, injury or severe harm. 1% prevalent in gen pop , and higher among those who experience trauma. Symptoms > 1 mon. subtypes include acute (<3mos), chronic (>3mos), delayed onset (onset >6 mos). Trx only sertraline, paroxetine and Exposure based log therapy.
Antipsychotic drugs
Parkinson’s patients need L-Dopa + a cholinergic antagonist. Typicals are all D2 antagonists.
Phenothiazine derivatives: suppress hiccups
1)aliphatic – chlorpromazine [sleepy, less EPS than haloperidol b/c has antichol activity]
2)piperadine – thioridazine
3)piperazine – trifluoperazine and thiethylpiperazine (motion sickness)
Haloperidol is a butyrophenone and causes MOST EPS b/c it lacks antichol activity.
Thiothixene is a thixanthene.
Neuroleptics cause psychomotor and affective indifference. Sedation caused by phenothiazines. Sedation caused by phenothiazine derivatives involves minimal motor coordinations. Known as “tranquilizers” b/c calm, ↓ agitation/hyperactivity w/o ↓ wakefulness. Chemoreceptor trigger zone of reticular formation has D2 receptors blocked by neuroleptics. Neuroleptics ↓ nausea from other drugs, pregnancy, radiation, cancers but NOT nausea 2° to bowel obstruction or motion sickness. **Side effects occur in ALL neuroleptic pts
Apomorphine and bromocriptine (AntiPD) have structure similar to DA.
Chlorpromazine and Haloperidol (neuroleptics) have structural overlap.
Chlorpromazine, thioridazine, Molindazine, Loxapine, Trifluoperazine, Thiothixene, Haloperidol, Fluspirilene. Of the previous drugs listed: From left to right, ↑ risk of orthostatic hypotension, and at the top have high dose/low potency. From right to left, you have ↑ risk of developing PD symptoms and low dose/high potency.
Neuroleptic induced Parkinsonism (EPS): Rigidity, Akinesia, Tremor.
Neuroleptic Dyskinesias and Dystonias (involuntary motions of hip, jaw, tongue). Acute dystonia needs diphenhydramine for trx. Neuroleptic induced Akathisia (tremendous restlessness despite rigid stiffness).
Mechanism of above symptoms: Neuroleptic drug offsets the normal balance b/w cholinergic and DA inputs into the neurons of the striatum. Anticholinergic such as Procyclidine, Trihexylphenidyl, and Benztropine restore lost balance. Balance could also be restored with L-Dopa, but this would antagonize the neuroleptic and induce psychosis.
*when the Rat Does Act, Pet The Belly.*
After 1 to 2 mos of neuroleptic therapy, most pts will develop tolerance to side effects and won’t need the anticholinergic but 25% of pts will.
Tardive Dyskinesia (“chewing gum motion”). Long term DA receptor blockade. Striatal nerve cells synthesize more DA receptors, thus making the cells supersensitive to small amts of DA. Trx w/ clozapine (D2/5-HT2A receptor agonist)
Phenothiazine induced obstructive jaundice is due to a hypersensitivity. Dermatitis/Photosensitivity: pts sensitive to sunlight, exaggerated sunburn. UV light readily oxidizes chlorpromazine. Drug accumulates in melanin containing tissues (eye, skin, sub nig). Prolactinemia (breast swelling, galactorrhea)