Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
514 Cards in this Set
- Front
- Back
|
Psychoanalytic etiologies of anxiety?
|
Psychoanalytic:signal, incomplete repression
|
|
|
Behavioral etiologies of anxiety?
|
Behavioral: classical conditioning, operant conditioning, negative reinforcement, positive reinforcement
|
|
|
Learning theory of anxiety?
|
faulty distorted or counterproductive thinking pattern
|
|
|
Biologic theory of anxiety?
|
physiological signs associated w/release of epinephrine, which causes anxiety
|
|
|
Where are the majority of noradrenergic neurons in the CNS? What is the significance?
|
Locus Ceruleus
role in regulating fear and anxiety |
|
|
Where are the cell bodies that release serotonin?
|
Raphe Nuclei
|
|
|
Average age of onset for panic disorder and genetic?
|
25 y/o
15-18% of first degree relatives affected |
|
|
Common comorbidities with panic disorder?
|
depression (70%)
alcoholism |
|
|
What neurobiological substances are associated with increased panic disorder?
|
Yohimbine (alpha2 adrenergic receptor antagonist), Sodium lactate infusion (increases NE), dopamine, Caffeine, Locus Ceruleus (firing NE), blood flow increase to right parahippocampus, mitral valve prolapse
|
|
|
What neurobiological substances are associated with decreased panic disorder?
|
serotonin, GABA,
|
|
|
What kinds of drugs are used to treat panic disorder?
|
SSRI, Benzodiazepines, TCA, MAOI
|
|
|
What drug is specifically not used in panic disorder?
|
Buspirone
|
|
|
What are some medical conditions that can present like panic or anxiety disorder?
|
hyperthyroidism, pehochromocytoma, caffeine intoxication, amphetamine or cocaine intoxication, cardiac or respiratory conditions, neurologic conditions
|
|
|
What is negative reinforcement?
|
frequency of behavior is increased by removing an unpleasant stimulus
|
|
|
What is positive reinforcement?
|
increases frequency of behavior by pairing it with rewarding stimulus
|
|
|
Def of Obsessive Compulsive Disorder
|
Presence of either obsessions or compulsions which cause distress or are time consuming
|
|
|
Epidemiology of OCD
|
2-3% lifetime prevalence
onset between 10 and 23 years |
|
|
What neurobiological substance and area of the brain are implicated in OCD?
|
serotonin
increased activity in caudate nuclei, orbital gyri, and cingulated gyri |
|
|
How is OCD managed with drugs?
|
SSRIs, clomipramine
|
|
|
How is OCD managed w/surgery?
|
cingulotomy, subcaudate tractotomy, anterior capsulotomy
|
|
|
What are the stages of hypnotics/sedatives?
|
Sedative-->Hypnotic-->General Anesthetic
|
|
|
Mechanism of Benzodiazepines?
|
potentiate the action of GABA receptor Cl channel complex, bind to gamme-2 subunit,
|
|
|
Uses of benzodiazepines?
|
preanesthetic medication, ideal hypnotic, relieves anxieties with minimal interference with cognitive function and wakefulness
|
|
|
CV Effects of Benzodiazepines?
|
lower BP, increase HR at anesthetic doses
|
|
|
Names of benzodiazepines?
|
-epam
-olam |
|
|
Side Effects of Benzodiazepines?
|
impair driving and motor skills, lassitude, incoordination, reaction time, BAD interaction with alcohol, can have paradoxical effects
|
|
|
Withdrawl from Benzodiazepines?
|
insomnia, seizures
|
|
|
Mechanism of Barbiturates?
|
lack specificity of benzos, tolerance problems, high liability for abuse, potentiate GABA receptor-channel, supress glutamate channel activity, supress voltage gates Ca channels
|
|
|
Uses for barbiturates?
|
antagonize CNS effects of other drugs, emergency treatment for convulsions, intravenous general anesthetic
|
|
|
Barbiturate naming?
|
-barbital
|
|
|
Part of brain that is especially sensitive to barbiturates?
|
mesencephalic reticular activating system
|
|
|
Effects of Barbiturates?
|
decrease BP, RR,
increase: enzyme,protein, and lipid content of hepatic smooth ER, |
|
|
Pharmacokinetics of Barbs?
|
some highly lipid soluble=rapid uptake by brain
binds to plasma albumin, metabolized by liver enzymes (longer effects in cirrhosis) |
|
|
Bad effects of barbs?
|
CNS hangover, ethanol interaction, antihistamine interaction
|
|
|
Eponymonic Rhythm in Barb poisoning
|
Cheyne-Stokes
|
|
|
Other effects of Barb poisoning?
|
drop in BP, hypothermia, dilatation
|
|
|
Treatment for Barb poisoning?
|
dialysis, hemoperfusion
|
|
|
Non-Benzodiazepine Hypnotics?
|
zolpidem, zaleplon, eszopiclone
Ramelteon |
|
|
Action of Zolpidem, Zaleplon, and Eszopiclone?
|
potentiate GABA(a) receptor activity but are selective for isoforms with alpha1 subunits
|
|
|
Action of Ramelteon?
|
agonist at MT1 and MT2 melatonin receptors, no GABA effects,
|
|
|
Benzodiazepine Antagonists
|
Flumazenil
|
|
|
Use of Flumazenil?
|
reversing CNS depressant effects of benzo OD, hasten post-surgical recovery
|
|
|
Is there a link between genetics and suicide?
|
Yes, independent of psychiatric illness. Higher concordance in monozygotic twins
|
|
|
CNS Implicated in Suicide?
|
central serotonin system, low CSF 5-HIAA, serotonin deficiency
|
|
|
RFs for Suicide
|
95% have diagnosable mental disorder
alcohol dependence, schizophrenia |
|
|
Suicide Risk Indicators/Assessment?
|
*past attempt*
warnings, history of violent behavior, withdrawal from friends, giving away possessions, loss of interests, |
|
|
Management of suicidal patient?
|
don't leave alone, assess lethality
|
|
|
What are the "brake" regions?
|
orbital frontal cortez, anterior cingulate cortex, increased by SSRI's
|
|
|
What are the "drive" regions?
|
limbic regions, dropped by anticonvulsants
|
|
|
What is the role of serotonin in violence?
|
acts on 5-HT2 receptors in prefrontal cortical regions, deficiency results in disinhibition of aggression
|
|
|
What is the role of catecholamines in violence?
|
increased noradrenergic receptor sensitivity
|
|
|
What genotype is associated with childhood aggression?
|
5-HT2a TYR
|
|
|
What is psychosis?
|
loss of touch with reality testing and impairments in the thought processing, can include hallucinations and delusions
|
|
|
DSM Definition of Schizophrenia
|
6 months with an active phase of at least 1 month including 2 or more Sx
delusions, hallucinations, disorganized speech, disorganized or catatonic behavior, negative symptoms |
|
|
Negative Sx of Schizophrenia
|
apathy, poor hygiene, poor motivation, social withdrawal, affect flattening, alogia (speech poverty), anhedonia, avolition
|
|
|
Is there a difference in the epidemiology of schizophrenia in men and women?
|
Men: early onset (10-25 y/o)
Women: 25-35 y/o, |
|
|
What are the 5 subtypes of Schizophrenia?
|
paranoid, disorganized, residual, undifferentiated, catatonic
|
|
|
Paranoid Schizophrenia
|
primarily delusions and/or auditory hallucinations
|
|
|
Disorganized Schizophrenia
|
disorganized thoughts and/or behavior
|
|
|
Residual Schizophrenia
|
negative symptoms or attenuated positive symptoms
|
|
|
Undifferentiated Schizophrenia
|
variable
|
|
|
Catatonic Schizophrenia
|
mutism and/or negativism
|
|
|
What are the three stages of the schizophrenia disease course?
|
Prodrome: apathy, social withdrawl, or attenuated positive Sx
Acute: bizarre behavior, impairment of functioning, unsafe behaviors Residual: similar to prodrome but occurring after and acute episode |
|
|
Poor prognostic factors for Schizophrenia?
|
early/insidious onset, poor premorbid functioning, family history of Schizophrenia and primarily negative sxs
|
|
|
Good prognostic factors for Schizophrenia?
|
later and more acute onset of illness, good premorbid functioning, no fmaily hx and primarily positive sxs
|
|
|
Stress-Diathesis Model of Mental Illness?
|
Genetic disposition plus environmental stressor (e.g. psychological trauma) and/or biological stressor (e.g. infection, drugs)
|
|
|
What are the prenatal stressors associated with Schizophrenia?
|
Malnutrition
Viral Exposure: influenza in 2nd trimester Seasonal Delivery:late winter-Spring Obstetric: in utero hypoxia |
|
|
What is the dopamine hypothesis of the pathophysiology of Schizophrenia?
|
excess dopamine in the mesolimbic dopamine tract of the brain might be responsible for positive Sx, decreased dopamine in mesocortical tract may be responsible for negative and cognitive Sx
|
|
|
Is Schizophrenia a neurodevelopmental or neurodegenerative disease?
|
considered neurodevelopmental with abnormal migration of cells during brain development, fronto-temporal gray matter loss after disease onset
|
|
|
What is the effect of excess dopamine in the mesolimbic tract?
|
positive Sx of Schizophrenia
|
|
|
What is the effect of decreased dopamine in the mesocortical tract?
|
negative Sx of Schizophrenia
|
|
|
What are other medical causes of psychosis?
|
Medications (steroids)
Seizure disorder (temporal lobe epilepsy) TBI Hormone Dysregulation (hypo/hyperthyroidism) |
|
|
What is the action and what disease does Chlorpromazine (Thorazine)?
|
Schizophrenia
an antihistamine used to reduce psychotic Sx because i blocks the dopamine D2 receptors |
|
|
What other neurotransmitters are hypothesized to be involved in Schizophrenia?
|
Serotonin: excess can cause psychosis (LSD)
GABA: people with Schizophrenia have a loss of GABA in hippocampus Glutamate: PCP is a glutamate antagonist, underactivity of glutamate can cause psychosis |
|
|
What is schizoaffective disorder?
|
A chronic psychotic disorder meeting criteria for schizophrenia, except intermittent mood episodes (mania, hypomania or depression) are superimposed on the psychosis.
There must be a period of at least two weeks during which the psychosis exists without evidence of a concurrent mood episode |
|
|
How are antipsychotics primarily secreted?
|
50%: P450
50%: kidney |
|
|
Is there a difference in the effectiveness for reducing positive Sx of psychosis for typical and atypical antipsychotics?
|
No
|
|
|
Which type of antipsychotics are more effective in the treatment of negative Sx?
|
Atypical agents
|
|
|
What drug is sometimes used with people who do not respond to traditional antiopsychotics?
|
Clozapine
|
|
|
How long should pharm treatment for schizophrenia be done before thinking about trying something else?
|
4-6 weeks
|
|
|
What are the 4 major dopamine pathways in the brain?
|
Nigrostriatal, Mesolimbic, Mesocortical, Tuberoinfundibular
|
|
|
Nigrostriatal Dopamine pathway
|
cellbodies in the ventral tegmental area
projection to the basal ganglia controlling movement, blocking dopamine in this pathway causes extrapyramidal side effects site of action of typical antipsychotics |
|
|
Mesolimbic Dopamine Pathway
|
cell bodies in ventral tegmental area
projections to nuclei in limbic system blocking dopamine decreases hallucinations and delusionsM |
|
|
Mesocortical Dopamine Pathway
|
cell bodies: ventral tegmental
projections: cerebral cortex (limbic and frontal) modulates negative and cognitive Sx greater site of action for atypical antipsychotics |
|
|
Tuberoinfundibular Dopamine Pathway
|
cell bodies: hypothalamus
projections: anterior pituitary controls prolactin secretion blocking dopamine removes inhibition of prolactin secretion-->galactorrhea, gynecomastia, and amenorrhea |
|
|
What dopamine tract is most effected by typical antipsychotics?
|
Nigrostriatal
|
|
|
What dopamine tract is most effected by atypical antipsychotics?
|
Mesocortical (modulates negative and cognitive sx)
|
|
|
What kind of typical antipsychotics have the highest affinity for D2 receptors?
|
High potency
thus lowest blockade of cholinergic, andrenergic, and histaminergic receptors have most EPS |
|
|
What are some high potency typical antipsychotics?
|
fluphenazine, haloperidol, pimozide, thiothixene, trifluoperazine
|
|
|
What are some moderate potency typical antipsychotics?
|
loxapine, molindone, perphenazine
|
|
|
What is the difference between high and low potency typical antipsychotics?
|
Low requires larger dose due to lower D2 affinity, thus more cholinergic, andrenergic, and hisaminergic side effects, and less EPS
|
|
|
What are some low potency typical antipsychotics?
|
chlorpromazine, mesoridazine, thioridazine
|
|
|
What drug can cause permanent pigmentation of the retina? What kind of drug is it?
|
Thioridazine
low potency typical antipsychotic |
|
|
What type of antipsychotics have the highest risk of tardive dyskinesia?
|
Typical
|
|
|
What are the effects of muscarinic (cholinergic blockade by antipsychotics?
|
dry mouth, constipation, urinary retention, blurred vision, precipitation or narrow angle glaucoma
|
|
|
What are the effects of alpha-1 andrenergic blockade by antipsychotics?
|
orthostatic hypotension, lightheadedness, tachycardia, sedation, and sexual dysfunction
|
|
|
What are the effects of histamine-1 blockade caused by antipsyhotics?
|
sedation, weight gain, fatigue
|
|
|
What is Neuroleptic Malignant Syndrome? (NMS)
|
uncommon, potentially fatal adverse reaction to antipsychotics marked by elevated temperature, autonomic instability, delirium, rigid muscle tone & elevated CK, developing over 24-72 hours. Risk factors include dehydration, heat exhaustion, and poor nutrition.
|
|
|
What makes atypical antipsychotics different from typicals?
|
antagonize serotonin 2A and D2, more selective for mesolimbic pathway (less EPS),
|
|
|
What are some atypical antipsychotics?
|
Clozapine, Risperidone, Olanzapine, Quetiapine, Ziprasidone, Aripiprazole
|
|
|
What is receptors to clozapine antagonize? What are significant SEs of clozapine?
|
5-HT2A, D1,2,4
SE: antihistamine and anticholinergic SEs, Agranulocytosis |
|
|
What receptors do risperidone antagonize? What are it's SEs?
|
5-HT2A, D2, and ά-1
SEs: orthostatic hypotension, reflex tachycardia, insomnia, agitation, greater EPS |
|
|
What receptors are antagonized by Olanzapine? Side Effect Profile?
|
5-HT2A, D1-4, histamine-1, muscarinic-1, alpha-1
SEs: drowsiness, drymouth, akathesia, insomnia, weight gain, DM2 and ketoacidosis |
|
|
What receptors are antagonized by Quetiapine? Side Effect Profile?
|
5-HT2A, D2, histamine-1, Alpha-1,2
SEs: orthostatic hypotension, somnolence, weight gaine, DM2, ketoacidosis |
|
|
What receptors are antagonized by Ziprasidone? SE profile?
|
5-HT2A, 5-HT1A, D2, D3, blocks reuptake of monoamines
SEs: dizziness, nausea, postural hypotension BLACK BOX WARNING: can increase QT interval, check baseline EKG first |
|
|
What are the receptors effected by Aripiprazole? SE profile?
|
D2 and 5-HT1A agonist
5-HT2A antagonist SEs: nausea, sedation, anxiety, akathesia |
|
|
What are the receptor targets of Paliperidone? SE profile?
|
antagonist of 5-HT and D2
SEs: hyperprolactinemia, dystonia, akathesia |
|
|
What 2 atypical antipsychotics cause the least disturbances in metabolism?
|
Ziprasidone and Aripiprazole
|
|
|
What are the 3 clusters of Personality Disorders? How can they be remembered?
|
A: Odd eccentric "Weird"
B: Dramatic, erratic, labile "Wild" C: fearful, inhibited "Worried" |
|
|
What are the cluster A personality disorders?
|
paranoid, schizoid, szhizotypal
|
|
|
What are the cluster B personality disorders?
|
narcissistic, antisocial, borderline, histrionic
|
|
|
What are the cluster C personality disorders?
|
avoidant, dependent, obsessive-compulsive
|
|
|
What is the difference between schizoid and schizotypal personality disorder?
|
emotional coldness and aloofness with seclusion vs. interpersonal awkwardness, magical thinking
|
|
|
What is ego-syntonicity?
|
the idea that the abberancies in a personality disorder are in sync with the person's understanding of self so they are not distressing to the patient but to people around the patient
|
|
|
What are the general neurobiological effects of alcohol?
|
GABA binding: depressant
Release of Dopamine and Endorphins (creates positive reinforcement) Inhibits the NMDA (Glutamate System) |
|
|
Quick defining features of alcoholism?
|
tolerance, withdrawal, loss of control, compulsive use, consequences
|
|
|
What is the definition of Type I alcoholism?
|
adult onset with gradually increasing consumption, features of guilt, worry, dependency, and introversion, little family Hx, Men=Women, good treatment response
|
|
|
What is the definition of Type II alcoholism?
|
early onset, strong family Hx, male predominance, antisocial personality disorder, impulsivity, poor treatment response
|
|
|
What are lab values that point to chronic heavy drinking?
|
GGT>35(men), 30 (women)
CDT>20/26 MCV>91 AST>40/33, ALT>46/35, Uric Acid>8.0/6.2 Typical: AST and ALT elevated with AST~2xALT |
|
|
What are the signs and Sx of alcohol withdrawal?
|
autonomic hyperactivity, physiological tremor continuous>8Hz, familial tremor bursts of activity<8Hz, insomnia, nausea, vomiting, visual/auditory hallucinations, psychomotor agitation, anxiety, tonic-clonic seizue
|
|
|
What are delirium tremens?
|
autonomic hyperactivity (tachycardia, diaphoresis, fever, anxiety, insomnia, hypertension), perceptual distortions, tactile or visual hallucinations, fluctuating psychomotor activity, delirium 2-3 days after drinking stops
|
|
|
What is Wernicke's Encephalopathy?
|
Alcohol Induced Persisting Amnestic Disorder
acute, life threatening, Sx: ataxia, ocular motility abnormalities, lateral orbital palsy, confusion, vestibular dysfunction |
|
|
How is Wernicke's encephalopathy treated?
|
Thiamine for 1-2 weeks
|
|
|
What is Wernicke-Korsakoff syndrome?
|
chronic, anterograde amnesia (can't form new memories), sometimes confabulation, treated with Thiamine
|
|
|
What is Mallory-Weiss Syndrome?
|
a syndrome in alcoholics where they develop longitudinal tears at the gastroesophageal junction due to excessive vomiting
|
|
|
How are DTs treated?
|
benzodiazepines
|
|
|
What species are most likely to cause pneumonia in alcoholics?
|
Klebsiella, and Legionella
|
|
|
What neurotransmitter is implicated the most in alcohol's effects?
|
GABA, its release is potentiated by EtOH,
|
|
|
What enzyme is inhibited by Disulfiram (antabuse)?
|
aldehyde dehydrogenase, this causes a build up of acetaldehyde,
|
|
|
What is the physiological response to drinking EtOH while taking Disulfiram?
|
hot feeling face, flushing, vasodilation over whole body, throbiing, and pushing headache, nausea, vomiting, respiratory problems, thirst, CP, hypotension, orthostatic syncope, etc. etc.
|
|
|
What two substances start the metabolism of EtOH?
|
MEOS, and alcohol dehydrogenase
|
|
|
What neurotransmitter's system is ramped up by chronic alcohol abuse leading to the symptoms of withdrawal?
|
Glutamate
|
|
|
What is the purpose and effect of Naltrexone?
|
It is an opioid antagonist use in to treat alcoholism? Takes away the reward feeling
|
|
|
What is the purpose and effect of Acamprosate?
|
to maintain alcohol abstinence in a recovered alcoholic,
|
|
|
What causes blindness in methanol poisoning?
|
buildup of formic acid
|
|
|
What metabolic disorder is caused by methanol ingestion?
|
acidosis
|
|
|
What is the treatment for methanol poisoning?
|
ethanol and hemodialysis
|
|
|
What is the active alkaloid in opium?
|
morphine
|
|
|
What are some of the effects of morphine?
|
analgesia, miosis, constipation, decreased BP, decreased Respiration, euphoria, sleep
|
|
|
What is naloxone and what is it used for?
|
an opiate antoagonist used for treatment of addiction to opium
|
|
|
What are the different classes of opiate receptors?
|
mu, kappa, delta, and mu/delta
|
|
|
What are the mu receptors selective for?
|
endomorphins
|
|
|
What are the delta receptors selective for?
|
enkepahlins
|
|
|
What are the kappa receptors selective for?
|
dynorphins
|
|
|
What are the mu/delta receptors selective for?
|
beta-endorphin
|
|
|
What receptors do most opiate drugs work at?
|
mu
|
|
|
What kind of receptors are opioid receptors?
|
GPCR
|
|
|
What is the effect of cocaine and amphetamines?
|
block biogenic amine uptake systems, enhances biogenic amine release,
|
|
|
What reward site in the brain is implicated in addiction?
|
Medial Forebrain Bundle, especially dopamine containing neurons running from the VTA (ventral tegmental area) to the nucleus accumbens
|
|
|
What are the proposed cellular mechanisms of tolerance?
|
uncoupling of receptors from G-proteins, endocytosis of receptors and their degradation in lysosomes
|
|
|
What is the mechanism of addiction?
|
specific nerves in the brain that mediate cravings, they run from the VTA to the nucleus accumbens
|
|
|
Why do some opiates produce dysphoria rather than euphoria?
|
they act on kappa receptors reducing dopamine release on VTA-->nucleus accumbens pathway
kappa=crappa |
|
|
What is hypochondriasis?
|
Preoccupation with fears of having, or the idea that one has, a serious disease based on the person’s misinterpretation of bodily symptoms.
|
|
|
What is conversion disorder?
|
the conversion of a psychological insult to a somatic symptom without medical explanation
|
|
|
What is somatization disorder?
|
A history of many physical complaints beginning before age 30 years that occur over a period of several years and result in treatment being sought or significant impairment in social, occupational, or other important areas of functioning. 4 pain, 2 GI, 1 pseudoneurological, 1 sexual
|
|
|
What is the definition of factitious disorders?
|
conscious creation of Sx in order to take "sick role", disease forgery, motivation is unknown to patient (distinction from malingering),
|
|
|
What is allostatic load?
|
The ability of an organism to adapt over time
|
|
|
Where in the brain is stress modulated?
|
amygdala, anterior cingulated cortex, HPA axis
|
|
|
What are the Sx of Acute Stress Disorder?
|
sense of numbing or detachment, reduction in awareness of surroundings, derealization, depersonalization, dissociative amnesia
|
|
|
What are the Sx of PTSD?
|
persistent reexperiencing of the event, avoidance of stimuli that cause remembering, arousal, insomnia,
|
|
|
What are RFs for PTSD/ASD?
|
female gender, previous psych illness, homozygosity for short alleles of 5HTTP transporter, low intelligence,
|
|
|
What meds are used in PTSD?
|
SSRIs, beta blockers, atypical antipsychotics
|
|
|
What are the stages of the sexual response cycle?
|
desire, arousal, plateau, orgasm, resolution
|
|
|
What is the hypothesized biological origin of paraphilias?
|
elevated testosterone, Klinefelter's, cortical atrophy, temporal lobe epilepsy,
|
|
|
What are the main features of ADHD?
|
Deficit in rule-governed behavior
Unable to modulate arousal Seek immediate reinforcement Poor motivation when bored or sustained effort required |
|
|
What are the categories of ADHD Sx?
|
Inattention, Hyperactivity, Impulsivity
|
|
|
What are ADHD biological RFs?
|
Fragile X, G6PD deficiency, PKU, resistance to thyroid hormone, lead poisoning
|
|
|
What are pre/perinatal RFs of ADHD?
|
poor maternal health, young age of mother, cigarette smoking, prenatal alcohol, toxemia, eclampsia, postmaturity, extended labor
|
|
|
What are the neuroanatomic/neurochemical findings of ADHD?
|
Deficits in fronto-striatal areas
Dopaminergic dysfunction dopamine transporters Brain volume globally less on average, especially cerebellum Greater rate of abnormal frontal cortical morphology |
|
|
How do stimulants (Ritalin, Focalin, dl-methylphenidate, d-methylphenidate) treat ADHD?
|
not paradoxically, they stimulate protions of the brain that are underactive, prefrontal cortex, and inhibitory functions, increased effect of dopamine and NE
|
|
|
What are the non-stimulant meds for ADHD and what do they do?
|
Atomoxetine: increase dopamine and NE effect in prefrontal cortex
Bupropion, TCAs, Alpha 2 adrenergic agonists, Modafinil |
|
|
What are the diagnostic criteria for autism?
|
onset before age 3, qualitative impairment in social interaction, qualitative impairment in communication, restricted repetitive stereotyped patterns
|
|
|
Is there genetic linkage to autism?
|
yes, strong
|
|
|
Lab work up for autism?
|
serum amino acids, urine organic amino acids, pyruvate lactate, karyotype looking for fragile X, EEG, lead level
|
|
|
What are brain abnormalities that appear on imagine for autism?
|
larger brains in young
smaller brains in old white matter is disproportianately large hypoperfusion and glucose metabolism abnormalities, lower interconnectivity of cortical area chronic tissue changes involving activated microglia, abnormal activation of fusiform face processing area, |
|
|
What are the 3 layers of the cornea from outer to inner?
|
epithelium, stroma, endothelium
|
|
|
What amount of total diopters is covered by the cornea?
|
2/3
|
|
|
What is miosis? What branch of the nervous system does this?
|
pupil closing, parasympathetic
|
|
|
What is mydriasis? What branch of the nervous system does this?
|
pupil opening, sympathetic
|
|
|
Is the ciliary muscle contracted for near or far vision?
|
Near vision: when it contracts the lens rounds up allowing farsighted people to correct their own vision
|
|
|
What is the etiology of presbyopia?
|
It is a farsightedness caused by hardening of the lens over time
|
|
|
What is normal intraocular pressure?
|
~15 mm of Hg
|
|
|
What is the normal pathway of aqueous humor?
|
Production in ciliary epithelium-->posterior chamber-->anterior chamber-->trabecular mechwork--> canal of schlemm-> episcleral veins
|
|
|
What is the equation for Intraocular pressure?
|
IOP=(F-U)/c+Pe
F=total outflow, U=uveoscleral outflow, Pe=uveoscleral venous pressure R=resistance of outflow |
|
|
What is the etiology of open angle glaucoma?
|
a decrease in "c", c=1/Resistance, an increase in resistance
|
|
|
Where is most damage from glaucoma done?
|
optic nerve head because lamina cribrosa is the weakest point of eye
|
|
|
What causes permanent loss of vision in glaucoma?
|
death of ganglion cells
1: from compression of axons reducing transport 2: reduced blood flow causing damage |
|
|
What are the layers at the back of the eye from closest to the vitreous to furthest?
|
Inner Retina (ganlion cells, INL), Outer Retina (photoreceptors), Retinal Pigment Epithelium, Choroid
|
|
|
Where does oxygen come from for photoreceptors?
|
choroidal circulation
|
|
|
Which receptors are susceptible to all colors of light?
|
Cones
|
|
|
Where are cones concentrated the highest?
|
fovea
|
|
|
Is there any retinal circulation in the fovea?
|
No
|
|
|
What kind of defect is present if there is no constriction of the pupil when light is shone in the left eye?
|
disease in left afferent optic nerve
|
|
|
Deficit in what cranial nerve will cause decrease in corneal sensation?
|
V
|
|
|
Deficit in what cranial nerve will cause problems with eye closure?
|
VII
|
|
|
What is the normal tract taken by tears in the eye?
|
Lacrimal Gland--> Lacrimal Puncta--> Lacrimal Ducts--> Lacrimal Sac--> nose
|
|
|
What makes up the uvea?
|
Iris, ciliary body, choroid
|
|
|
What are the three types of cataracts?
|
Cortical, Nuclear (myopia), Subcapsular(worst)
|
|
|
What is the name of the deposits in non-neovascualr (dry) Age Related Macular Degeneration?
|
Drusen
|
|
|
What kinds of meds are used to treat wet ARMD?
|
anti-VEGF
|
|
|
What condition must be considered in an elderly person with amaurosis fugax?
|
Giant Cell Arteritis
|
|
|
What condition is suggested by optic neuritis?
|
Multiple Sclerosis
|
|
|
What is papilledema and what does it suggest?
|
swelling of both optic discs (not just one), it implies increased intracranial pressure
|
|
|
Giant Cell Arteritis?
|
AKA: Temporal arteritis
Idiopathic vasculitis, women 65-80, medium to large arteries in head and neck Histo: granulomatous cell infiltrate giant cells disruption of internal elastic lamina proliferation of intima occlusion of lumen |
|
|
What does the derm mnemonic "SCAT-D" stand for?
|
Size, Color, Arrangement, Type of Lesion, Distribution
|
|
|
What is the name for a non-palpable change of color of the skin?
|
Macule<1cm
Patch>1cm |
|
|
What is the name of a solid raised lesion?
|
Papule<1cm
Plaque>1cm |
|
|
What is the definition of a nodule?
|
a solid, raised lesion>1cm, usually confined to the dermis or subcutaneous tissue
|
|
|
What is the name of a raised lesion filled with clear fluid?
|
Vesicle<1cm
Bullae>1cm |
|
|
What is a pustule?
|
a pus filled papule
|
|
|
What is the definition of scales?
|
flakes or plates of compacted, desquamated layers of stratum corneum
|
|
|
What is crust?
|
drying of exudate or plasm on the skin
|
|
|
What is the name of a permanent fibrotic change that occurs on the skin following damage to the dermis?
|
Scar, Keloid if it grown beyond edges of the original wound
|
|
|
What is lichenification?
|
A thickening of the A thickening of the epidermis with epidermis with
exaggeration of normal exaggeration of normal skin lines. Usually due skin lines. Usually due to chronic rubbing or to chronic rubbing or scratching of an area.scratching of an area. |
|
|
What is an erosion?
|
a slightly depressed area of skin in which part or all of the epidermis has been lost
|
|
|
What is an ulceration?
|
necrosis into the level of the dermis and sometimes of the underlying tissue
|
|
|
What are petichiae, pupura, and ecchymoses?
|
NONBLANCHABLE bleeding that occurs in the skin from pinpoint-->cm-->large patches
|
|
|
What are the four layers of the epidermis from top to bottom?
|
Stratum Corneum
Granular Layer Spinous Layer Basal Layer |
|
|
How often does the skin normally turnover?
|
every 30 days
|
|
|
What is the main kind of cell in the epidermis?
|
keratinocytes
|
|
|
What connects keratinocytes to the epidermal basement membrane?
|
hemidesmosomes (autoimmune destruction of these causes bullous pemphigoid)
|
|
|
What connects keratinocytes to one another?
|
desmosomes(autoimmune attack on these causes pemphigus vulgaris)
|
|
|
What is the mortar that holds the corneocyte bricks together in the stratum corneum?
|
insoluble lipids (ceramides, cholesterol, free fatty acids)
|
|
|
What is filaggrin?
|
a filament aggregating protein that is important for cornified envelope formation and barrier function (mutation causes ichthyosis vulgaris)
|
|
|
Describe melanocytes
|
neural crest derived pigment producing cells located in the stratum basalis
|
|
|
Describe Langerhans cells
|
bone-marrow derived antigen presenting cells that reside primarily in the suprabasal layers
|
|
|
Describe Merkel cells
|
mechanoreceptors that make synaptic contacts and give our sense of touch
|
|
|
What are the major components of the lamina lucida?
|
laminin-5,6
|
|
|
What are the major components of the lamina densa?
|
collagen IV and laminin 1, anchoring fibrils of collagen VII
|
|
|
What are the two layers of the dermis?
|
1. papillary-more fibroblasts, collagen I and III
2. reticular-elastic fibers (elastin and microfibrils from fibrillin 1 [marfans]) |
|
|
Which kind of sweat glands communicate directly with hair follicles?
|
apocrine
|
|
|
What kind of control are eccrine sweat glands under?
|
Cholinergic (response to temp. change, emotions)
|
|
|
What control are apocrine sweat glands under?
|
andrenergic, it is odorous
|
|
|
What are the 5 varieties of psoriasis?
|
Plaque, Guttate, Palmar-plantar, Pustular, Erythrodermic
|
|
|
What is the most common variety of psoriasis?
|
chronic plaque
|
|
|
What form of psoriasis is associated with younger patients and strep infections?
|
Guttate, generally resolves but is replaced with plaque psoriasis
|
|
|
What form of psoriasis is associated with corticosteroid treatment?
|
pustular, patient may also have fevers, high WBC, and hypotension
|
|
|
What is the most severe form of psoriasis that presents with more than 80% of the skin covered?
|
Erythrodermic
|
|
|
What abnormalities can be detected in psoriasis keratinocytes?
|
increased Ki-67, keratin 16 expression, migration in 3-7 days,
|
|
|
What is the genetic correlation with psoriasis?
|
MHC locus of chromosome 6, interleukin 12 and 23 receptor alleles
|
|
|
What is the newly recognized population of T-cell now thought to be a main culprit in psoriasis?
|
Th17 which produce interleukin 17,20, and 22, 23, and STAT 3
|
|
|
What are the treatments for psoriasis?
|
topical corticosteroids, vitamin A or D, phototherapy with UVB, or Psoralen and UVA, acitretin, methotrexate, cyclosporine A, anti-TNF, anti-T
|
|
|
What is the mnemonic for the classic presentation of Lichen (P)lanus?
|
4 p: purple, polygonal, pruritic, papules most commonly in the oral mucosa, flexor surfaces, and genetalia
|
|
|
What infection has lichen planus been linked to without substantiation?
|
Hepatitis C
|
|
|
What are Wickam's Striae?
|
lines of erosion in the mucous membrane associated with lichen planus
|
|
|
What is the clinical presentation of pityriasis rosea?
|
papulosquamous reaction in younger people that is post-viral and starts with a herald patch and Christmas Tree pattern, CD4+ T cell infiltrate
|
|
|
What viruses are associated with pityriasis rosea?
|
HHV 6 and 7, URIs
|
|
|
What is the predominant infiltrate of the skin in secondary syphilis?
|
Th1, CD4
|
|
|
What are the vasculitises of large vessels?
|
Giant Cell
Takayasu's |
|
|
What are vascultides of medium size vessels?
|
Polyarteritis Nodosa
Wegener's Granulomatosis Churg-Strauss Kawasaki |
|
|
What are the vaculitides of small vessels?
|
microscopic polyangiitis
immune complex urticarial vasculitis cryoglobulinemia waldenstrom's collagen EED, |
|
|
What is microscopic polyangiitis?
|
an ANCA associated vasculitis that is primarily affecting the small vessels and 60% have pANCA
Sx: glomerulonephritis, skin ulcers, dyspnea, palpable purpura, penicillin usage or strep infection |
|
|
What is the antibody associated with Churg Strauss?
|
pANCA
|
|
|
What are the Sx of Churg-Strauss?
|
asthma, eosinophilia, necrotizing vasculitis, allergic rhinitis
|
|
|
What is the antibody associated with Wegener's Granulomatosis?
|
cANCA
|
|
|
What are the Sx of Wegener's Granulomatosis?
|
necrotizing vasculitis in upper respiratory tract, lower respiratory tract, and kidneys
|
|
|
What is the DDx for macular purpura and petichiae?
|
ITP, aspirin, renal insufficiency, Vit C def., trauma, valsalva
|
|
|
What is the DDx for macular hemorrhage>1cm :Ecchymoses
|
hepatic insufficiency, Vit K deficiency, Actinic Purpura, Amyloidosis, Platelet function defects like vWD
|
|
|
What is the DDx for classic round palpable purpura?
|
IgG/IgM immune complex mediated vasculitis, IgA Vasculitis (HSP), Cryoglobulinemia, ANCA vasculitis, septic vaculitis (RMSF/meningococcemia)
|
|
|
What is the DDx of non-inflammatory retiform purpura?
|
heparin necrosis, coumadin necrosis, cryoglobulins, septic embolic disease, antiphospholipid syndrome, cholesterol emboli
|
|
|
What is the DDx of inflammatory retiform purpura?
|
IgA Vasculitis (HSP), cryoglobulinemia, ANCA associated vasculitis, septic vasculitis
|
|
|
What are the 5 categories of blister causation?
|
Trauma, Infection, Congenital disease, Autoimmune, Other
|
|
|
What is spongiosis?
|
edema in between keratinocytes
|
|
|
What is acantholysis?
|
dyscohesiveness
|
|
|
What are the 3 kinds of subcorneal vesicles?
|
Miliaria, Bullous Impetigo, Staphylococcal scalded skin syndome
|
|
|
What are the two bugs associated with Miliaria and what distinguishes them?
|
M. Crystallina: in corneum non-inflammatory
M. Rubra: spinosum with neutrophils and spongiosis |
|
|
What causes miliaria?
|
obstruction of the intraepidermal component of eccrine duct
|
|
|
What causes bullous impetigo?
|
staph aureus infection, specifically the exfoliative toxin (serotype II, phage 71)
|
|
|
What causes scalded skin syndrome?
|
staph type II, type 71, acantholysis, Ab bind to desmoglein 1
|
|
|
What are the diseases associated with intraepidermal vesicles?
|
Epidermolysis bullosa simplex,acute eczema, pemphigus vulgaris, Hailey-Hailey, Glucagonoma
|
|
|
What kind of Abs are produced in pemphigus vulgaris? Immunofluorescence?
|
Anti-desmoglein 3, mucosa focus
IgG and C3 |
|
|
What kind of Ab are prominent in Pemphigus foliaceus?
|
desmoglein 1, skin focus
|
|
|
What is the pathophys of paraneoplastic pemphigus?
|
dysregulation of IL-6, mucositis, polymorphous eruption, bronhiolitis,
|
|
|
What is the inheritance of Hailey-Hailey disease?
|
AD
|
|
|
What skin problem is caused by a Glucagonoma?
|
necrotizing migratory erythema, serpiginous erythematous scaly patches with central erosions
|
|
|
What are the diseases that cause subepidermal blisters?
|
Erythema Multiforme/Stevens-Johnson's
Toxic epidermal necrolysis Bullous Pemphigoid Epidermolysis bullosa acquisita dystrophic epidermolysis bullosa dermatitis herpetiformes |
|
|
What kind of reaction is erythema multiforme/Stevens Johnson's?
|
cytotoxic T cell reaction associated with herpes, mycoplasm, or drugs
|
|
|
What kind of drugs cause Toxic Epidermal Necrosis?
|
sulfonamides, antiepileptics, allopurinol
|
|
|
What antibodies are present in bullous pemphigoid? What shows up on DIF?
|
collagen XVII, and Plakin
IgG and C3 |
|
|
What is the reaction that causes Pemphigoid gestationis?
|
IgG1 anti-paternal HLA cross-reactivity with BP180 with complement activation
|
|
|
Where does Cicatricial pemphigoid generally appear?
|
in the oral cavity, eyes, nose, anogenital region, scalp and head of elderly females
|
|
|
What are the antibodies present in Cicatricial pemphigoid?
|
BPAg2, BPAg1, Laminin 5, Beta4 Integrin
|
|
|
What kind of antibodies are present in epidemolysis bullosa aquisita?
|
type VII collagen (anchoring fibrils)
|
|
|
What kind of diseases is Epidermolysis Bullosa Acquisita associated with, what is found on DIF?
|
Autoimmune: Chrohns, Lupus, RA
DIF: IgG and C3 at the floor of the blister |
|
|
What disease is associated strongly with dematitis herpetiformis?
|
Gluten-sensitive enteropathy (celiac disease) anti-Gliadin and anti-endomysial Abs
HLA B8, HLA Dw3 |
|
|
What are the 5 objectives of general anesthesia?
|
analgesia
amnesia loss of consciousness motionlessness abolition of autonomic response to pain |
|
|
What is the therapeutic index of most inhalation anesthetics? Is this good or bad?
|
2-3
bad, very low means the line between harm and help is very fine (LD50/ED50) |
|
|
What is the MAC for inhalation anesthetics?
|
the measure of potency called Minimum Alveolar Concentration
the lower the MAC the more potent the drug |
|
|
What is one way that inhaled anesthetics become more potent, esp. in older patients?
|
lower temp increases potency
n=PV/RT |
|
|
How do you use the MAC to figure out the blood concentration of an inhaled anesthetic?
|
MAC*blood/gas pc
|
|
|
What is the relationship between oil/gas partition coefficient and MAC?
|
MAC is inversely proportional to oil/gas partition coefficient
|
|
|
What happens at 20%, 40%, and 60%, 80%, 105% N2O?
|
20% analgesia
40% excitement and disinhibition 60% amnesia 80% unconsciousness 105%=1 MAC |
|
|
What is the mechanism of N2O?
|
reduces neuronal excitability (membrane hyperpolarization, disruption of synaptic transmission), blockade of nerve conduction
|
|
|
What vitamin does N2O inactivate and how?
|
It inactivates B12 by oxidizing its cobalt atom
|
|
|
What are other negative SEs of N2O?
|
megaloblastic anemia, spontaneous abortions, congenital abnormalities,
|
|
|
What do halogenation and fluoridation do to inhalable anesthetic cmpds?
|
Halogenation: stabilizes and reduces metabolism
Fluoridation: reduces potency and solubility (faster) |
|
|
How do volatile anesthetics work?
|
They enhance the inhibitory response mediated by GABA(A) receptors.
|
|
|
How is the potency of volatile anesthetics measured?
|
It is equal to the oil/gas partition coefficient. The higher the lipid solubility the higher the potency and the smaller the MAC value.
|
|
|
What factor decides the depth of anesthesia induced by an inhalation anesthetic?
|
the partial pressure or gas tension of the anesthetic in the brain (blood)
|
|
|
What are the factors involved in determination of speed of induction and recovery of inhalation anesthetics?
|
blood/gas pc
alveolar vent rate and CO |
|
|
What tissues take up inhaled anasthetics the fastest?What is the slowest?
|
brain, heart, kidney
fat |
|
|
What can help increase arterial tension of an inhaled anesthetic?
|
Increased pulmonary blood flow
Increased ventilation if the lambda is high |
|
|
What are the characteristics of an inhaled anasthetic that will be eliminated quickly?
|
low lambda
low blood/gas pc low oil/gas pc |
|
|
What are the CV side effects of inhaled anesthetics?
|
sensitizes heart to epinephrine induced arrythmias, myocardium depression due to reduction of Ca level, hypotension
|
|
|
What is the mechanism for hypotension with halothan, enflurane, and sevoflurane?
|
lowering of CO
|
|
|
What is the mechanism of hypotension in isoflurane and desflurane?
|
a decreased in SVR
|
|
|
What inhaled anesthetic has the tendency to cause spike and wave seizures?
|
Enflurane
|
|
|
What inhaled anesthetic has teh possibility of causing hepatotoxicity?
Nephrotoxicity? |
Halothane
Methoxyflurane |
|
|
Clinically, how are most IV anesthetics used?
|
For induction of anesthesia, followed by inhalation maintenance
|
|
|
What are the main types of IV anesthetics?
|
Barbs, Propofol, Etomidate, benzos, ketamine, opioids, alpha-2 adrenergic agonists
|
|
|
What three features determine the pharmacokinetics of IV anesthetics?
|
Lipid solubility: high lipid solubility means high brain penetration
resdistribution of the drug: quick redistribution of drug means short action metabolism: single bolus vs. continuous |
|
|
What kind of drug is thiopental?
|
barbituate with extremely rapid onset (<1 min), ultra-short acting
|
|
|
Where is thiopental metabolized?
|
the liver, slowly, can develop toxicity with too much administration (for induction only)
|
|
|
What are the drawbacks of thiopental?
|
most likely to cause myocardial depression, hyperalgesic response to pain at subanesthetic doses, contraindicated in patients with acute intermittent porphyria, must NOT be coadministered with acidic solutions like opioids and muscle relaxants (precipitate in IV)
|
|
|
What are the advantages that propofol has over thiopental?
|
rapid metabolism by liver (phase II) means it can be used for a long time, recovery is more rapid and pleasant
|
|
|
What are the SEs of Etomidate that differentiate it from Thiopental? What is its advantage?
|
myoclonic movements during induction, high incidence of nausea and vomting
least cardio depressive problems |
|
|
How are benzos used for anesthesia?
|
no unconsciousness but do prodice anxiolysis, amnesia, and sedation
|
|
|
What makes Midazolam unique amongst benzos?
|
water soluble delivery, converted to lipid soluble by p450, lack of pain on injection, best amnesiac, shorter half life
|
|
|
What drug is used to reverse Benzo effects?
|
Flumazenil, competitive antagonist of BDZ binding site on GABA(A)
|
|
|
What kind of anesthesia does ketamine produce?
|
dissociative
|
|
|
What is the mechanism of ketamine?
|
blocks the NMDA receptor channel, good for children, has cardiostimulatory properties
|
|
|
What drug is used to speed recovery from opioids due to its antagonistic effects?
|
Naloxone
|
|
|
Why is dexmedetomidine better than clonidine for sedation?
|
they are both antihypertensive alpha-2 adrenergic agonists, dex is more selective for alpha2, patients are rousable
|
|
|
What is the new definition of a TIA that lasts longer than an hour?
|
a small stroke
|
|
|
What are the risk factors for strokes?
|
high age, atherothrombosis, heart disease, race (african americans) have a higher rate regardless of differences in risk factors, HTN, diabetes, smoking
|
|
|
What are the two types of strokes?
|
Ischemic (80%) and Hemorrhagic (20%)
Hemorrhagic has a much higher mortality |
|
|
What causes ischemic strokes?
|
atherosclerosis-->atherothrombosis, clots in heart that travel to brain (AFib), vessel wall proliferation, hypercoagulable states, dissection of vessel, inflammation of brain vessels
|
|
|
What is the pathophysiology of atherosclerosis?
|
Initial formation of atherosclerotic plaque
Deposition of calcium and cholesterol in wall of vessel Proliferation of cells in vessel wall Expansion of plaque Secondary formation of thrombus Composed of platelets initially If flow is very reduced…..secondary clot formation |
|
|
What kind of plaque has a higher risk of causing thrombosis?
|
unstable (with surface inflammatory cells and activated macrophages)
|
|
|
Where in the heart are emboli most likely to form?
|
LV, LA due to AFib
|
|
|
What is the cascade caused by stroke in brain?
|
decreased blood flow-->decline in O2 and glucose-->reduced oxidative metabolism-->failure of Na/K ATPase-->neurons malfunction and die-->clinical deficit
|
|
|
What is normal blood flow in brain?
|
>50 ml/100cc/min
|
|
|
What are the two types of neuronal cell death in stroke?
|
necrotic (short term, Ca into mitochondria, leaky membranes) and apoptosis (days after the ischemic insult)
|
|
|
What are the clinical deficits associated with Left MCA stroke?
|
aphasia, right hemiparesis
|
|
|
What are the clinical deficits associated with Right MCA?
|
neglect syndrome, left hemiparesis
|
|
|
What are the clinical deficits associated with Vertebral Artery?
|
ataxia, crossed sensory Sx
|
|
|
What are the clinical deficits associated with Basilar artery?
|
bilateral weakness, eye changes, CN findings
|
|
|
What are the typical causes of stroke in specific arteries?
|
Carotid: atherothrombosis
MCA/branch: embolism ACA: athero and emboli Small vessels:microathero or lipohyalinolysis Vertebral: athero or dissection Basilar: athero PCA: embolism |
|
|
What are the main acute stroke treatments?
|
Reperfusion: TPA (must be in 3 hrs), mechanical devices
Neuroprotective Agents: falure Avoid hyperglycemia, keep BP up, treat fever |
|
|
What is the ischemic penumbra?
|
the part of brain that you are trying to salvage after a stroke
|
|
|
Why is hyperglycemia bad for stroke?
|
anaerobic metabolism-->lactic acid which kills neurons really well
|
|
|
What is the best treatment for ischemic stroke edema?
|
remove half the skull
|
|
|
What drugs must be avoided if stroke is a risk?
|
HRT (hormone replacement therapy) and oral contraceptives
|
|
|
What is the most common cause of Intracerebral Hemorrhage?
|
trauma
|
|
|
What is done to evaluate a ICH patient?
|
CT and MRI, clotting studies, TOX screen, angiogram
|
|
|
Which is better (MRI or CT) for acute ICH?
|
They are equal
|
|
|
Which modality (MIR or CT) is more sensitive to subacute and chronic ICH?
|
MRI
|
|
|
What are the most common locations for ICH due to HTN?
|
BG, putamen, thalamus, cerebellar, pons
|
|
|
What is the method for measuring the volume of a ICH?
|
(AxBxC)/2
|
|
|
What kind of hemorrhage has a favorable response to surgical evacuation?
|
cerebellar hemorrhage
|
|
|
What treatment should be avoided and what alleles are ICH due to Cerebral Amyloid Angiopathy?
|
AVOID anticoagulation, should never get Warfarin
associated with apolipoprotein e4 and e2 alleles |
|
|
What drugs of abuse can lead to ICH?
|
cocaine, amphetamines, meth because of extreme rise BP or vasculitis due to toxic effects of the drug destroying the wall of the blood vessel
|
|
|
What are the 3 components of intracranial pressure?
|
brain, bone, and CSF
only brain is readily compressible |
|
|
How is ICH treated?
|
Reduce ICP: mannitol, hyperventilation, drain CSF, surgery
Reverse Coagulopathy: FFP, vitamin K Surgery to remove clot: unproven |
|
|
What is the Cerebral Perfusion Pressure?
|
the MABP-ICP
must be over 70 mm of Hg to prevent cerebral damage, |
|
|
What is the new treatment that is being tried for ICH?
|
recombinant activated factor VII, plugs blood vessels but didn't work in phase III
|
|
|
What causes hydrocephalus after and ICH?
|
blood in ventricles obstructing flow
mass effect of hematoma kinking the outflow of ventricles |
|
|
What are the risk factors for subarachnoid hemorrhage?
|
female, HTN, smoking, APCKD, ehlers-danlos, marfans
|
|
|
What parts of brain are supplied by MCA1 segments?
|
Corpus Striatum and associated internal capsule.
|
|
|
What parts of brain are supplied by PCA p4 segments?
|
supply bulk of medial hippocampal formation
|
|
|
What is the most likely place for embolic material to come from that causes a stroke?
|
Left side of the heart, atrial fibrillation
valvular heart disease including prothetic valves, acute MI, left atrial myxoma |
|
|
What is NBTE?
|
non-bacterial thrombatic endocarditis very common in hospitalized patients
|
|
|
Carnahan notch phenomenon causes damage on which side of the brain?
|
contralateral to the mass
|
|
|
What are the most vulnerable neuronal subpops to TGI (Global Ischemia)?
|
Pyramidal Neurons in CA1
Cerebellar Purkinje Neurons Pyramidal Neurons in III, and V |
|
|
What are the cells in the brains that are principally involved in cleaning up a cerebral infarct?
|
macrophages NOT neutrophils (unless septic)
|
|
|
What happens when coagulative necrosis is resolved in the brain?
|
you get liquefactive necrosis, dead brain tissue is eaten up by lipid laden macrophages
|
|
|
How long does liquefactive necrosis last?
|
weeks to months making it impossible to date resolving infarcts without clinical data
|
|
|
What do we call small flame shaped hemorrhages that appear in the brain stem with uncinate herniation?
|
Duret Hemorrhage
|
|
|
Can mass lesions be an etiology for intracerebral hemorrhage?
|
Yes: oligodendroglioma, pilocytic astrocytoma, metastatic melanoma, and metastatic choriocarcinoma
|
|
|
Can vasculitis or vasculopathy be a etiology for intracerebral hemorrhage?
|
Yes, watch out for CAA (cerebral amyloid angiopathy) caused by A beta
|
|
|
What is the most common cause of non-traumatic subarachnoid hemorrhage?
|
rupture of an aneurysm
|
|
|
What is the most common genetic disorder leading to ruptured aneurysms?
|
ADPKD (autosomal dominant PKD)
|
|
|
Where are most aneurysms?
|
Proximal cerebral anterior circulation (90%): especially AComm, PComm from distal ICA, and MCA bifurcation, supraclinoid
|
|
|
What happens to the risk of rupture for a huge aneurysm?
|
It actually goes down slowly, but they represent as mass effect.
|
|
|
What is the deadly complication that can come along with SAH?
|
Vasospasm within 1-2 weeks of procedure and treatment
|
|
|
What is the blood vessel that runs in the epidural potential space and can be torn leading to epidural hematoma?
|
middle meningeal artery
|
|
|
What are the blood vessels that may rupture causing a subdural hematoma?
|
bridging superior cerebral veins
|
|
|
What kind of cells are the source of meningiomas?
|
arachnoid cap cells
|
|
|
What is the most common source of a subarachnoid hemorrhage?
|
aneurysm
|
|
|
What is the pathway from beginning to end of CSF?
|
Lateral Ventricles-->Interventricular Foramina of Monro-->third ventricle-->cerebral aqueduct of Sylvius-->fourth ventricle-->foramina of magendie and luschka-->subarachnoid space-->arachnoid villi-->superior sagittal sinus
|
|
|
What shows up in a lumbar puncture in MS?
|
oligoclonal bands
|
|
|
What is the common cause of non-obstructive hydrocephalus?
|
elderly folks with scaring of pia arachnoid and arachnoid villi preventing resorption into the sinus
|
|
|
What is the source of the brain's anterior circulation?
|
internal carotid artery
|
|
|
Occlusion of which artery from the circle of willis is most likely to cause contralateral motor and sensory loss to the leg?
|
Anterior Cerebral Artery
|
|
|
Occlusion of which artery from the circle of willis is most likely to cause contralateral motor and sensory loss to the arm and face as well as aphasia (on the dominant side)?
|
Middle Cerebral Artery
|
|
|
Lesions of this structure cause conduction aphasia?
|
arcuate fasciculus
|
|
|
What is the source of the brain's posterior circulation?
|
Vertebral arteries
|
|
|
Occlusion to what artery causes Wallenberg's Syndrome (lateral medullary syndrome)?
|
PICA (posterior inferior cerebellar artery)
|
|
|
Occlusion to what artery causes ventral or Weber's syndrome, thalamic syndrome of Dejerine-Roussy, and contralateral hemianopsia?
|
Posterior Cerebral Artery (PCA)
|
|
|
What artery supplies blood to the anterior 2/3 of the spinal cord including the ventral horns, ventrolateral white columns?
|
anterior spinal artery
|
|
|
What artery supplies blood to the posterior third of the spinal cord including the dorsal horn and dorsal white columns?
|
posterior spinal arteries
|
|
|
Where in the spinal cord does sensation ascend from the upper limbs?
|
fasciculus cuneatus, so clearly the fasciculus gracilis does the lower limbs
|
|
|
Where is the second synapse for both clinically significant ascending spinal tracts?
|
VPL of Thalamus
|
|
|
What information is carried by the dorsal column-medial lemniscus pathway?
|
touch, pressure, vibration, proprioception, and sensations
|
|
|
What information is carried by the spinothalamic pathway?
|
pain and temp
|
|
|
What does the lateral corticospinal tract do?
|
carries motor commands to the contralateral limbs
|
|
|
Compression of which root (Dorsal or ventral) causes decreased DTRs?
|
tricky: both can
|
|
|
What causes sciatica?
|
L5/S1 prolapse compressing the S1 dorsal and ventral roots with weakness of foot eversion, plantar flexion, and loss of ankle jerk reflex
|
|
|
What is the result of hemisection of the spinal cord (Brown Sequard Syndrome)?
|
ipsilateral loss of touch, pressure, vibration and proprioception below lesion
ipsilateral UMN signs below the lesion conralateral loss of pain and temperature beginning one or two segments below the lesion ipsilateral anesthesia and LMN signs at the level of the lesion |
|
|
What is the effect of syrungomyelia (central cord syndrome)?
|
cape like distribution of loss of pain and temp sensation
|
|
|
Which cranial nerves have their location/nuclei in the midbrain?
|
I-IV
|
|
|
Which cranial nerves have their location/nuclei in the pons?
|
V-VIII
|
|
|
Which cranial nerves have their location/nuclei in the medulla and spinal cord?
|
IX-XII
|
|
|
In the brainstem, where are the motor nuclei located?
|
(M)edial
sensory are lateral |
|
|
What will be the effect of a UMN lesion of the facial nerve before the facial nucleus?
|
contralateral paralysis of lower face
|
|
|
What is the effect of a LMN lesion of the facial nerve?
|
ipsilateral paralysis of upper and lower face
|
|
|
To what side will the tongue deviate in a LMN lesion of CN XII?
|
ipsilateral to the lesion
|
|
|
To what side will the uvula deviate in a lesion of CN X?
|
deviation away from lesion
|
|
|
What way will the jaw deviate in a lesion of CN V?
|
towards the lesion
|
|
|
What are the deficits in medial medullary syndrome?
|
alternating hypoglossal hemiplegia
contra: hemiparesis and tactile and kinesthetic deficits in body ipsi: flaccid paraysis of the tongue with deviation towards the lesion |
|
|
If CN XII has a lesion in the UMN what way will the tongue deviate?
|
away from the lesion
|
|
|
What are the results of lateral medullary (Wallenberg's syndrome?
|
alternating hemianesthesia
contra: loss of pain and temp from body ipsi: loss of pain and temp from face Ipsi: horner's syndrome |
|
|
With a UMN lesion of the CN X, what direction will the uvula deviate?
|
away from the lesion
|
|
|
What is the result of ventral (Weber's) syndrome of the midbrain?
|
alternating oculomotor hemiplegia
contra: hemiplegia and lower facial paralysis ipsi: oculomotor nerve palsy |
|
|
What are the Sx of Thalamic syndrome of Dejerine-Roussy?
|
stroke of the PCA causing contralateral hemisensory loss in the head and body-->followed by dysesthesia
|
|
|
What are the principal output cells of the brain?
|
Pyramidal
thus more of them in motor cortex |
|
|
What are the principal interneurons of the brain?
|
granular cells
thus more of them in sensory cortex |
|
|
What brain network is associated with spatial orientation and neglect?
|
parieto-frontal
|
|
|
What cortical network is associated with face and object recognition?
|
Occipito-temporal
|
|
|
What cortical network is associated with attention and behavior (executive functions)?
|
prefrontal
|
|
|
What cortical network is associated with memory and amnesias?
|
Limbic
|
|
|
How would one clinically differentiate between dysarthria and broca's aphasia?
|
have the patient write: if it is BA the patient will not be able to write
|
|
|
What would damage to the vestibulocerebellum cause (flocculonodular node)?
|
feeling of loss of equilibrium and vertigo
|
|
|
What would damage to the spinocerebellum cause (vermis and paravermal area)?
|
truncal ataxia and broad based staggering gait
can be caused by alcoholism |
|
|
What would damage to the cerebrocerebellum cause?
|
loss of coordination of voluntary movements, dysmetria, intention tremor
|
|
|
What is the current theory of the origin of headaches?
|
neurogenic inflammation: depolarization of sensory neurons in the trigeminovascular system causing release of substance P, neurokinin A, and calcitonin gene-related peptide (CGRP) which irritate the nerve endings
|
|
|
What is effective treatment for headaches?
|
serotonin agonist activation
5-HT1B --blood vessel 5-HT1D --nerve endings |
|
|
According to the Monroe-Kellie Doctrine (an out growth of the Council of Vhorms) what 3 things are ICP elevated by?
|
1: addition of CSF
2: increased brain tissue volume (edema) 3: addition of blood (hemorrhage) |
|
|
For the umpteenth time, what regions of the brain are particularly susceptible to ischemia?
|
pyramidal neurons of CA1 in the hippocampus
dentate gyrus pyramidal neurons in neocortical layers II, V, VI, purkinje cells of the cerebellum |
|
|
What were we specifically told not to use to treat increased ICP?
|
steroids
|
|
|
What is the current theory of the origin of headaches?
|
neurogenic inflammation: depolarization of sensory neurons in the trigeminovascular system causing release of substance P, neurokinin A, and calcitonin gene-related peptide (CGRP) which irritate the nerve endings
|
|
|
What is effective treatment for headaches?
|
serotonin agonist activation
5-HT1B --blood vessel 5-HT1D --nerve endings |
|
|
According to the Monroe-Kellie Doctrine (an out growth of the Council of Vhorms) what 3 things are ICP elevated by?
|
1: addition of CSF
2: increased brain tissue volume (edema) 3: addition of blood (hemorrhage) |
|
|
For the umpteenth time, what regions of the brain are particularly susceptible to ischemia?
|
pyramidal neurons of CA1 in the hippocampus
dentate gyrus pyramidal neurons in neocortical layers II, V, VI, purkinje cells of the cerebellum |
|
|
What were we specifically told not to use to treat increased ICP?
|
steroids
|
|
|
What is the only neuroprotectant in clinical use? (think Kevin Everett or if you must Meredith Grey)
|
hypothermia (though I am pretty sure Meredith Grey was brain damaged)
|
|
|
What kind of hematoma has the tendency to spread out?
|
subdural
|
|
|
What kind of hematoma has the tendency to stay in a small area?
|
epidural
|
|
|
What is the job of the semicircular canals in the ear?
|
angular rate sensors
|
|
|
What is the job of the otoliths? (utricle and saccule)
|
linear accelerometers
|
|
|
What does the VOR do (vestibulo-ocular reflex)?
|
Allows us to see while head is moving
|
|
|
What does the VSR do (vestibulo-spinal reflex)?
|
allows us to balance, do high performance body movements
|
|
|
What does loss of VOR cause?
|
Nystagmus
|
|
|
What test is used to diagnose Benign Paroxysmal Positional Vertigo?
|
Hallpike Test
|
|
|
What causes BPPV?
|
utricular debris (limestone)
|
|
|
How is vestibular neuritis treated?
|
steroids, and vestibular suppressants
|
|
|
What drugs cause ototoxicity(just dizziness)?
|
aminoglycosides: gentamicin, vancomycin,
|
|
|
What disease causes episodic vertigo with nausea and a full feeling in the ear, roaring noise, and decreased hearing?
|
Menieres Disease (think German "ach! mein ears!!)
|
|
|
How is Menieres treated?
|
salt restriction, diuretic, vestibular suppressant, antiemetic, gentamicin!
|
|
|
How is migraine associated vertigo treated?
|
topiramate, verapamil, nortriptyline
|
|
|
Which is more common, primary or secondary nervous system tumors?
|
secondary
|
|
|
What are generalized Sx of CNS tumor?
|
headache, seizures, personality change
|
|
|
What are localized Sx of CNS tumor?
|
weakness, sensory Sx, gait ataxia, visual changes, language dysfunction
|
|
|
What are the two main subtypes of gliomas?
|
astrocytoma and oligodendroglioma
|
|
|
Is surgical care an option for gliomas?
|
not really, usually they are too diffuse
|
|
|
What is stained for in order to ID a astrocytic tumor?
|
GFAP (Glial Fibrillary Acidic Protein)
|
|
|
What is the most common malignant primary brain tumor?
|
Glioblastoma Multiforme (arising from astrocytes)
|
|
|
What is the typical gross appearance of a glioblastoma multiforme?
|
cerebral tumor that shows on a MRI with contrast with ring enhancement and a central area of necrosis,
|
|
|
What brain tumor is described as having "pallisading necrosis, and microvascular proliferation?"
|
Glioblastoma Multiforme
|
|
|
What kind of brain tumor shows minimal mass effect or edema on MRI?
|
diffuse fibrillary astrocytoma
|
|
|
What is the genetic sign of good reaction to treatment by an oligodendroglioma?
|
1p and 19q loss of heterozygosity
|
|
|
What is the histopathological description classic for oligodendroglioma?
|
fried egg cells (uniform basophilic cells with cleared cytoplasm and small bland nuclei), delicately branching vessels (chicken wire) and microcalcifications
|
|
|
What predisposes one to a meningioma?
|
neurofibromatosis type 2
exposure to ionizing radiation |
|
|
What are the two populations that are generally categorized for with Primary Central Nervous System Lymphoma (PCNSL)?
|
immunocompromised and immunocompetent
|
|
|
What are the tumorous cells in PCNSL?
|
large B-cell (CD 20+),
|
|
|
What are the most common presenting features of PCNSL?
|
cognitive impairment or behavioral changes NOTE: not B symptoms
|
|
|
Why should steroids not be given to a patient with suspected PCNSL?
|
the PCNSL can transiently disappear delaying the diagnosis, after Dx they make a good treatment
|
|
|
What treatments are used for PCNSL?
|
radiation, steroids, methotrexate
|
|
|
What kind of brain tumors are the most likely to present with seizures?
|
meningioma, low grade glioma
|
|
|
What kind of brain tumors are the most likely to present with cognitive impairment?
|
PCNSL
|
|
|
What kind of brain tumors are most likely to present with focal neurological dysfunction?
|
High grade glioma
|
|
|
What is the immunostain that can be used to detect gliomas, there is more of it the higher the grade of tumor?
|
Ki67 (MIB1)
|
|
|
What are the histological signs of ependymoma?
|
ependymal rosettes or perivascular pseudo rosettes
|
|
|
What is the "small blue cell" tumor?
|
Medulloblastoma
|
|
|
What virus genome is sometimes present in Primary CNS Lymphoma?
|
Epstein-Barr of course
|
|
|
Loss of what chromosome is associated with meningiomas?
|
22q
|
|
|
What is contained in an Antoni A area?
|
sclerotic vessels, areas of palisading nuclei, Verocay bodies,
|
|
|
What is contained in an Antoni B area?
|
loosely cellular and microcytic
|
|
|
What are the phakomatoses?
|
neurofibromatosis I
neurofibromatosis II tuberous sclerosis von Hippel-Lindau disease |
|
|
What is the inheritance of NF1 and NF2
|
AD
|
|
|
What are the Signs and Sx of NF1?
|
gliomas of optic nerve, lisch nodules of iris, cafe au lait spots, neurofibromas, gene 17q11.2
|
|
|
What are the Signs and Sx of NF2?
|
bilateral acoustic schwannomas
multiple meningiomas ependymomas of spinal cord gene: 22q12 merlin |
|
|
What are the signs and Sx of tuberous sclerosis?
|
AD with relationship to 9q34 and 16p13.3
angiofibromas, hypopigmented areas, renal angiomyolipomas, cortical "tubers", subependymal hamartomas (candlestick drippings in ventricles) |
|
|
What are the signs and Sx of von Hippel-Lindau disease?
|
autosomal dominant: 3p25-26
hemangioblastomas, cerebellum, retinal hemangioblastomas, renal cell carcinoma, polycythemia |
|
|
What is Wallerian degenerations?
|
degeneration of an axon that takes place distal to the site of injury--> loss in 24-48 hrs
|
|
|
Is muscle loss typical of axonal loss or demyelination?
|
axonal loss
|
|
|
Which axons tend to be lost first in disease? What diseases are typical culprits?
|
the longer ones, DM, uremia, vitamin deficiency, alcohol, heavy metal toxicity, medications, organic solvents
|
|
|
What are typical causes of segmental demyelination?
|
entrapment from arthritis, tenosynovitis, mucopolysaccharide deposition, amyloid deposition
|
|
|
What is the cause of damage in Guillan Barre Syndrome?
|
autoimmune demyelination ascending in motor nerves
|
|
|
What formation appears in poor remyelination?
|
onion bulb
|
|
|
What is the histology in the muscle of neurogenic atrophy?
|
angular atrophy or hypertrophy, loss of mosaicism, internally placed nuclei,
|
|
|
What is the genetic profile of Myotonic Muscular Dystrophy?
|
AD, DM-1 CTG repeat, DM-2 CCTG repeat
|
|
|
What is the cause of muscular dystrophy?
|
messed up dystrophin causes a flimsy lipid bilayer which ruptures allowing Ca+2 to flow down concentration gradient and activate proteases
|
|
|
What are diseases that effect the Dystrophin Associated Glycoproteins (DAG)?
|
SCARMD (severe childhood autosomal recessive muscular dystrophy),
|
|
|
What is the storage disease of myophospharylase that results in the storage of glycogen?
|
McArdle's Disease
|
|
|
What causes "ragged red" fibers?
|
The body attempting to make up for crappy mitochondria or ETC by making more mitochondria
|
|
|
Where are most of the missense mutations that cause AD?
|
regions that flank the endoproteolysis beta and gamma secretase processing sites, beta first then gamma, messes with notch as well
|
|
|
What are the three genes and gene products that have been described as causing FAD?
|
21-betaAPP, 14-presenilin 1, 1-presenilin 2
|
|
|
What is the best known kind of polymorphism that can cause FAD?
|
chromosome 19 mutation of apoE
|
|
|
What is the common phenotype when these mutations (AD type)?
|
increased creation and deposition of amyloid (bad)
|
|
|
What is the bad amyloid called?
|
Abeta42
|
|
|
What processing is rate limiting for amyloid formation?
|
beta-secretase, getting rid of extracellular domain, it is done by BACE from chromosome 11
|
|
|
What is the excellent potential therapeutic target for AD?
|
BACE-1
|
|
|
What do you see in animals with APPmut expressed in them?
|
if you express a human APP mutation in transgenic mice the animals will develop amyloid deposits that look like plaque in 9-10 months but in animals
|
|
|
What do you see in animals with PS-1 mutation expressed?
|
increase in secreted Abeta42
|
|
|
What do you see in animals with both APPmut and PS-1 mut?
|
amyloid plaques in just 10-12 weeks
|
|
|
What happens to an animal with BACE1 knocked out and strong APPmut?
|
there will not be a whole lot of amyloid produced
|
|
|
What is the expression in bigenic mice?
|
ALS picture (tauopathy)+augmented neurofibrillary pathology which means that Tau and APP/Abeta are linked in formation of NFTs in limbic system
|
|
|
What are the characteristics of partial seizures?
|
focal onset by semiology, sterotyped aura, structural lesion
|
|
|
What are teh characteristics of genralized seizures?
|
generalized at onset, genetic syndrome, no aura, no structural lesion, epilepsy syndrome
|
|
|
What are the characteristics of Juvenile Myoclonic Epilepsy?
|
8-12 years at onset (otherwise healthy)
Starring spells, morning myoclonus, convulsions Fast (3-4 Hz) generalized spike wave discharges No remission (life long treatment) Valproic Acid (Depekote) Carbamazepine / Phenytoin may exacerbate Non- surgical |
|
|
What are the characteristics of Benign Rolandic Epilepsy?
|
Nocturnal events
Classic central/temporal spikes (BECTS) on EEG Drooling, Dysarthria Rare motor convulsions “Benign” outcome with remission +/- treatment (gabapentin, carbamazepine) Non- surgical |
|
|
What are the characteristics of Childhood Absence Epilepsy?
|
4-10 years old
Healthy normally developing children Multiple starring spells per day 3 hz generalized discharges Induction by hyperventilation Resolves by adolescence Usually easily treated with remission Ethosuximide, Valproic Acid, Lamotragine Non- surgical |
|
|
What are the characteristics of West Syndrome/Infantile Spasms?
|
4-10 months of age
Normal or delayed children May have prior seizures Idiopathic vs. symptomatic spasms Flurries of periodic spells Sleep changes Hypsarhythmic EEG ACTH, vigabatrin May be surgical |
