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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 |Pages |

|Neuropsychiatry – 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 tegmentum(nucleus 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 result 2) 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. Glutamate(GABA (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 drugs |

|5-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 A STEp.

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), 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)

 

All atypical antipsychotics act on and cause weight gain and diabetes xcept Ziprasidone.

Clozapine: Atypical antipsychotic. “closes” many receptors (antihist, antichol, antiα adren). Agranulocytosis seizures (high dose) side effect. SDA: low EPS, tardive dyskinesia, and –ve symptoms of schizo. D4 receptor axn!

 

riSPeridOne: Schizo, Psychotic Old people. (age associated psychosis and dementia) SDA that elevates prolactin. Low doses atypical, high doses typical

 

OLAnzapine: GranOLA makes you fat and sleepy. Improves mood in phases of bipolar and schizo.

Quetiapine: Crazy ass PD pts w/ schizo. Queso w/ cholesterol biosynthesis inhibited (animals not humans)

 

Ziprasidone: Zerotonin 1D antagonist, 1A agonist. Inh reuptake of both 5-HT and NE. No significant weight gain.

 

Aripiprazole: DA2 antagonist and partial agonist

 

Mood disorder – disturbance in emotional state. Pt can feel dysthymia, depression, hypomania, mania. *no differences in ethnicity, education, marital status, income.

 

I.                    Primarily Depressive

Major depressive – 2 wks depressed mood or loss of interest

Dystymic –

Depression NOS – depressed mood, anhedonic, appetite, sleep

*In major depression w/ psychotic features, the delusions and hallucinations R congruent.

-5-10% MDD pts develop mania

-up to 15% of MDD will die by suicide during the recovery phase, mood↓ while energy↑.

Double depression is dysthymic disorder and precedes MDD.

 

Dysthymic disorders depressed mood for at least 2 yrs.

II Depressive disorders w/ mania Bipolar I. Dx simple are manic or hypomanic episode. Elevated, expansive, irratible. ↓ sleep, talkative, distractibility, rambling thrush, and period of 7 days.

 

Mania. Hypomanic →manic → psychotic

Mixed presentations- suicidal. 1° manic then followed by depression. Mean age of onset early 20s. 90% individuals w/ manic episode will have successive reps. Early onset – worse progrnosis

*Bipolar is the MOST inheritable psychotic disorder.

Bipolar II and hypomanic – unlike mania – delusions/hallucinations cannot be present. Inflated self esteem does not reach a delusional grandiose level. 4 days of symptoms

Depression common psychiatric disorder. Pure depressive yndromes are the 2D’s: Depression (recurrent symptoms >2 wks). Dysthymia (>2 yrs). Depression associated w/ mania includes Bpolar disorder and cyclothymic disorder (cycle b/w depression and mania). Depression can be

1)      reactive or 2° (most common; response to real stimuli of grief, illness…)

2)      endogenous (genetic; can’t experience ordinary pleasure)

3)      manic depressive disorder (bipolar)

Best trx is psychological trx and meds. ECT is used for MDD pts that don’t resond to antidepressants.

Symptoms of depression SIG Energy Capsules**

TCA’s: mixed inh NE and 5-HT reuptake pumps. “off switches” of amine transmission.

-“I’m Am 3 circles” Imipramine (enuresis/anorexia) and Amitryptyline. Axns of antimusc, antihist, anti adreno only contribute to toxicity. Nortryptiline used for Nordic migraines. Migraines result as a deficiency of 5HT in blood vessels in brain (vasodilation).

 

Heterocyclics: 2nd gen – insomnia side effect. “MTA in Boston” Maprotiline, Trazodone (5 HT autoreceptor block; ↑ 5HT release; priapism) Amoxapine (severe neurotroxicity w/ seizure) and Bupropion.

3rd gen – “Vanessa Nancy Mirtaz” Venlafaxine, Nefazodone, Mirtazapine.

*azodone cousins 2nd letter/term of both mnemonics

Short ½ life Trazodone/Venlafaxine b/c Travis and Vern are short.

SSRI can’t be used to OD. Fluoxetine – anorexia. Minimal autonomic toxicity, demethylated active metabolite Norfluoxetine.

 

MaoI – axn allows more amines to accumulate presynaptically and more to be released.

Hydrazide “make you a Phene (fiend) for Is (ice)”. Phenelzine and Isocarboxazid.

Nonhydrazide “make you a transsexual”. Tranylcypramine

Inhibition persists after drugs are no longer detectable in plasma.

Great for atypical depression. Consider tyramine side effects and mixture with SSRI can cause 5HT syndrome.

 

Clinical indications of Antidepressants. “Are DOPE Stuff Baby Girl” ADHD, Depression, OCD, Pain/Panic disorder, Enuresis, Social phobia, Bulimia, GAD.

Antidepressants are most successful in trx pts that r:

1) slow (psychomotor retardation) 2) sleepless (sleep disturbances)

3) sexless (↓ libido) 4) satiety less (weight loss/poor appetite)

 

TCA’s and 2nd/3rd gen agents differ in degree of sedation and antimusc effects.

Li and antidepressant can trx depression, Li by itself prevents relapses.

Blood plasma drug level determination should be obtained in postabsorptive state. When evaluating the state of pts (abt 1/3) that don’t respond to antidepressants, consider the 5 D’s: Dx, drug, dose, duration of trx, different trx.

 

Inhibition of P450 3A4 can occur at high [] of Nefazoodone and Fluvoxamine. Can lead to fatal arrhythmias.

 

TCA OD can include; coma, resp depression, agitation, neuromuscular irritability, hyperpyrexia, bowel/bladder paralysis.

 

MaoI OD can include agitation, delirium, neuromuscular excitability, obtunded consciousness, seizures, shock, hyperthermia.

Li prevents mood swings in pts with bipolar affective disorder.

 

Pts w/ cyclic attacks of mania have many symptoms of paranoid schizo. Gradiocity, Bellicosity, Paranoid thoughts, overactivity. “manics @ G.O.P.B.”

Li affects electrolytes and their transport (inh Na+/H+ exchange), same for neurotransmitters (inh NE/DA release), and 2nd messengers (PLC, IP3 pathway inh)

 

Li carbonate preferred Trx for bipolar affective disorder and can also trx EtOHism, aggression, some childhood episodic changes of mood aggression, and also can produce nausea/tremor. It is easily measured in body fluids, NOT metabolized, and interacts with diuretics, new NSAIDs, all neuroleptics xcept clozapine. Side effects are on ion dep. Systems like kidney, heart, thyroid. Can lead to diabetes insipidus (polydisia, polyuria) Therapeutic OD common. Li toxicity in newborns is manifested by lethargy, cyanosis, poor suck and moro reflexes, and hepatomegaly.

-can be substituted by carbamazipine or valproic acid (used 4 epileptics).

 

Amoxapine, fluoxetine, and venlafaxine can all act on DA, NE, and 5HT reuptake pumps.

Uric acid is found in brain tumors. Ascorbic acid found in human uterine cervical cancers.

 

Carbamezipine block Na+/K+ channels used 4 trigeminal neuralgia.

 

Thinking (have ideas n make new ones) vs language (encode ideas into symbols)

 

Disorders of Thought process or form: loose associations, word salad, racing thoughts, flight of ideas, circumstantiality, tangentiality, neologisms, clang associations, thought blocking.

Disorders of thought content: delusions, ideas of reference, poverty of content, overvalued ideas, obsessions, phobias, suicidal ideas, homicidal ideas.

 

Psychosis – break w/ reality

 

Table 11-4 from BRS

 

Schizo subtypes: disorganized (disheveled appearance, inappropriate emotions), catatonic (bizarre posture, lack of coherent speech), paranoid (delusion of persecution), undifferentiated (symptoms of more than 1 type), residual (1 previous schizo episode)

***** make sure that you know your axes as there were questions on both exams about them!!!!!

Axis 1

Axis 2

Axis 3

Axis 4

Axis 5

NEUROPSYCHIATRY - EXAM 2 MATERIAL

Trx of Dementia

Cholinesterase Inhibitors: Improvement of cognitive function, global clinical state, ADL and behavior.

Mechanism: ( ACh concentration, Dual action meds (tacrine and rivastigmine) may contribute to rapid rise of ACh (more side effects & greater effectiveness)

Side effects: (gastric acid secretion (dose dependent

), Heart Block. Central activity (nausea, vomiting, weight loss and sleep disturbance). May exacerbate asthma/pulmonary conditions. OD mimics organophosphate poisoning.

Donepezil - Reversible AchE, ( nicotinic receptor density–associated with enhanced synaptic strengthening through long term potentiation

Galantamine - Reversibly and competitively inhibits AchE, Nicotinic cholinergic modulator– affecting NE, 5HT, GABA and Glutamate. Neuroprotective by inducing antiapoptotic proteins and calcium signals. ( Nicotinic receptor density–long-term potentiation. Found naturally in daffodil bulbs

.

Rivastigmine - AChE and Butyrlycholinesterase(BuChE) Inhibitor (equal affinity)

Psuedoirriversibly inhibits AchE Possibly more effective in late stage AZ– more potent with GI AchE. More region specific (greater GI) than other AchEs. Severe vomiting/esophageal tear if not titrated slowly. Only AChEI to demonstrate efficacy in Parkinson’s Disease Dementia

Tacrine: AChE and BuChE inhibitor– reversible.

Also myalgia, rash, and liver toxicity

-clinically indicated for Alzheimer’s Disease– mild to severe (as per cognition and behavioral impairment), Vascular Dementia, Mild Cognitive Impairment, Traumatic Brain Injury, DLB, Down’s Syndrome, ADD, etc.

Memantine: NMDA receptor antagonist (noncompetitive) 5HT3 receptor antagonism (hence absence of GI complaints) For Moderate to Severe Dementia (AZ)

Also for MCI, vascular dementia, HIV/AIDS, etc May be used with AChE

Interferes w/ glut activity in AZ. Dizziness, headache, constipation, seizure, and thought disorganization/psychosis.

Unproven therapies: NSAIDs, estrogen replacement, vitamin E, b-amyloid vaccinations

Delirium (Toxic-metabolic encephalopathy)

: Disturbance in consciousness. Reduced ability to focus, sustain, shift attention, impaired cognition and memory impairment. Hallucinations and absence of insight and judgment. Affects terminally ill pts > post surgical pts > hospitalized pts. Risk factors: age, hx of cns/AIDS/drugs, dementia

Most patients recover and delirium lengthens hospital stay, increases risk for complication. Caused by generalized dysregulation of neurotransmission; GABA-Glutamate dynamic. NMDA receptor up regulation seen in Alcohol Dependence associated with withdrawal syndrome. elevated levels of Acetylcholine

Trx: Address the underlying medical condition ( atypical antipsychotics at low dose. Avoidance of both Benzodiazepines and Anticholinergics recommended

Cognitive Disorders:

Dementia – disorder of thought; slow insidious onset w/o attributable cause. irreversible

- memory impairment, aphasia, apraxia, agnosia, or disturbance of executive fxn

Delirium – disorder of sensorium; sudden onset w/ attributable cause. Transient

Diagnosis of Cognitive disorder involves clinical features, history, and MMSE.

Normal aging: memory impairment, decreased attention span, slowed learning, Retained: vocabulary, language ability, and general information. EEG changes: slowing of background alpha rhythm ( ................
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