Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Mind > Test 1 > Flashcards

Test 1 Flashcards

1
Q

Differentiate Psychosis, delusions, hallucinations, and illusions

A

Psychosis: inability to distinguish reality from fantasy, creates new realities, greatly varied sxs
Delusions: disturbances about perception of reality
Hallucinations: disturbances about perceptions in 5 senses
Illusion: misperception of real external sensory stimuli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are 11 common meds implicated w/psychotic reactions

A

1) anticonvulsant
2) cardiovascular
3) antiparkinson (Levodopa, carbidopa)
* 4) dopamine over activity
5) amphetamine/cocaine
6) general anesthetics (ketamine, PCP)
7) glutamate
* 8) NMDA receptor antagonists
* 9) anticholinesterase drugs (nerve gases, organophosphates, insecticides
* 10) cannabis & EtOH
* 11) cocaine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the 4 NTs affected by Acute Alcohol Intoxication?

A

AAI NTs

1) more dopamine (excitability)
2) more endorphins
3) GABA (CNS depressant, calm, sleepy)
4) glutamate disruption (inhibits NMDA, decreased coordination, memory formation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the 3 areas of the brain affected by Acute Alcohol Intoxication?

A

AAI brain areas

1) frontal
2) thalamus
3) middle cerebellar peduncle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe Delirium Tremens?

A

Delirium Tremens: acute delirium episode d/t alcohol withdrawal in alcoholic
sxs: nightmares, agitation, global confusion, disorientation, hallucinations (visual and auditory), hypertension, febrility, diaphoresis, autonomic hyperactivity (tachycardia, hypertension), severe tremors, paranoia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Differentiate Cocaine’s acute intoxication sxs and psychosis sxs

A

Cocaine
Acute: tachy, HTN, agitation, mydriasis, euphoria, fever
Psychosis: paranoia, auspiciousness, violence, delirium/delusions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q 
What are common withdrawal sxs of
Alcohol/Benzo's
Caffeine
Opiates
Nicotine
Cocaine
A

withdrawal sxs
Alcohol/Benzo’s: seizures, agitation, irritability, insomnia, delirium
Caffeine: HA, fatigue, depression
Opiates: vomiting, diaphoresis, myalgias, agitation, anxiety, insomnia
Nicotine: depression, wt gain, cravings, nausea
Cocaine: depression, insomnia, physical slowing, agitation, body aches

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe ICU psychosis/syndrome

A

ICU psychosis/syndrome:

d/t environmental causes of sensory and sleep deprivation, OR medical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What can cause neuropsychiatric manifestations in SLE? how often?

A

SLE tx drugs (steroids) can cause NeuroPsychiatric SLE, occurring in 2/3 of SLE pts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the 3 common subtypes of Porphyria?

A

3 Porphyrias:

1) acute intermittent
2) variegate porphyria
3) coproporphyria?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Differentiate Schizophrenia, Schizophreniform, Schizoaffective, and Delusional disorders

A

Schizophrenia: >6mo of behavior changes, delusions, hallucinations
Schizophreniform: 1-6mo of schizophrenic changes
Schizoaffective Disorder: uninterrupted period of illness of (+)/(-) sxs w/Mood Disorder sxs too, and 2w of sxs w/o Mood sxs
Delusional: personality preserved, disturbances

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are (+) and (-) sxs that define schizophrenia?

A

Schizophrenia
(+): Delusions (esp Referential delusions and bizarre delusions, thought insertion, delusions of loss of control d/t outside forces), hallucinations, disorganized speech, bizarre/disorganized behavior, inappropriate affect
(-): diminution or loss of normal functions, 5As Alogia (poverty of speech), Affective blunting, Avolition/Apathy, Anhedonia (can’t achieve pleasure), Attentional impairment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q 
What are main characteristics of schizophrenia subtypes?
Paranoid
Disorganized
Catatonic
Undifferentitaed
Residual
A

Paranoid: prominent, persecutory/grandiose delusions, hallucinations, may predispose to suicidal behavior
Catatonic Type I: oscilates b/w Catatonic Stupor and Catatonic Excitement
Disorganized: disorganized speech and behavior
Residual: at least 1 schizophrenic episode, but clinical picture w/o strong (+) sxs
Undifferentiated: 90% of dxs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are Psychotic Disorder tx options?

ADEs?

A

Dopamine D2 receptor antagonists
1st gentypicals : chlorpramazine, haloperidol

D4, D4, 5HT, alpha, H1 receptor antagonists
2nd gen atypicals: risperidone, clozapine

  • can cause tardive dyskinesia aka upregulation of D2 receptors
  • *plus HAM Dope

Lithium, Benzos, anticonvulsants (carbamazepine, valproate, gabapentin),

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are types of delusional disorders, and differentiate

A

Erotomanic Type: delusions that another person, usually of higher status, is in love with them. (women > men)

Grandiose Type: delusions of inflated worth, power, knowledge, identity, or special relationship to a deity or famous person.

Jealous Type: delusions that the individual’s sexual partner is unfaithful. (paranoia, men> women)

Persecutory Type: delusions that the person has some physical defect or general medical condition (three main types are, parasitosis, dysmorphophobia, foul body odors, or halitosis).

Mixed Type: delusions characteristic of >1 of above with no predominance.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are genetic and non-genetic factors in Schizophrenia?

A

Genetic: Glutamate pathways, heterogenous

plus environment, social, psychological, neurodevelopmental (PI3K-PKB-GSK3 cascade), Dopamine, neurodegeneration…

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are Schizphrenia assoc CNS structural changes?

A

Neuron disorganization (hippocampus) and migration failure,
Cortical pyramidal cells: in schizophrenics there can be smaller cell body (soma) size; decreased spine density, decreased dendritic length and lesser # of presynaptic terminals.
Possible accelerated synaptic pruning
frontal, medial, lateral, parietal, occipital, temporal lobes, corpus callosum, thalamus, cerebellum, basal ganglion, limbic system, hippocampus… esp DorsoLateral Prefrontal Cortex is underactive and dopamine deficient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What’s the CNS neurochemistry of Schizophrenia?

A

Overactivaton of subcortical D2 receptors, leads to (+) sxs

Deficit of Dopamine receptors in prefrontal cortex, leads to (-) sxs and cognitive deficits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are Schizophrenia assoc functional changes?

A

Overactivation of D2 receptors, deficit of Dopamine receptors… maybe d/t Glutamatergic NMDA dysfunction, that allows excessive Dopamine stimulation that ends up killing the D2 receptors/neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the typical and atypical antipsychotics?

A

Typical = 1st gen, neuroleptics, conventional
-D2 receptor antagonist

Atypical = 2nd gen
-D3, 4 antagonist AND 5HT2a antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the typical and atypical antipsychotics?

A 
Typical antipsychotics TI:
-Phenothiazines = Chlorpromazine, Thioridazine, Perphenazine, Trifluoperazine, Fluphenazine
-Haloperidol
-Pimozide
-Molidone
-Loxapine
-Thiothixene
Atypical Antipsychotics TI:
-Aripiprazole, Brexipiprazole
--Cariprazine
-Asenapine, Clozapine, Olanzapine, Quetiapine
-Iloperidone, Lurasidone, Paliperidone, Risperidone, Ziprasidone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the ADEs of typical antipsychotics? (hate HAM and Dope)

A

typical ADEs: worsens (-) sxs, early onset extrapyramidal sxs (tx w/anticholinergics or Propranolol for akathisia), *neuroleptic malignant syndrome, hyperprolactinemia (assoc breast enlargement, irregular periods, galactorrhea)

Atypicals: wt gain, metabolic syndrome (*esp Olanzapine)

both: anticholinergic, orthostatic, long QT, sedation, cognition, lens opacities, priapism, seizures, gambling/high-risk behaviors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what are drug-drug and drug-disease interactions of antipsychotics

A

antipsychotics interacts w/
-cytochrome P450, esp CYP3A4 and 2D6

smoking induces CYP1A2
additive/contradicting effects w/long QT, CNS depressants (benzos), amphetamines and pressors, antiHTNs, AChE inhibitors, Levodopa, Metoclopramide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are Clozapine’s unique adverse and good effects?

A

Clozapine:
constipation, higher risk seizures, agranulocytosis, sialorrhea
*agranulocytosis, seizures, myocarditis, other cardiopulmonary effects
use with refractory mood disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are Antipsychotics prescribing general rules?

A

Antipsychotics:

  • Clozapine preferred in tx refractory pts
  • only use 2 simultaneously during cross-titration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the 4 main types of anxiety disorders

A 
anxiety
1 substance
2 associations (trauma, OCD)
3 generalized = GAD
4 intermittent acute (agoraphobia, other phobias, panic attacks)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are anxiety related brain changes? structure and function

A

Anxiety brain:
loss of brain volume
loss of synapses in hippocampus/prefrontal cortex (memory/selfcontrol)
increased amygdala activity (fear)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are generalized anxiety tx options?

A

GAD tx:
SSRIs
CBT
Relaxation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Describe panic attacks/disorder, and tx?

A

Panic attack/disorder:
sudden irrational attacks of fear causing tremors, nausea, shortness of breath, dizziness, hyperventilation, chest constriction, tachycardia, agitation.
Intense worry about experiencing further panic attacks or fear of going where prior stressful event occurred (PTSD).

tx: CBT, SSRIs, TCAs, psychotherapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Describe social anxiety disorder, and tx?

A

Social anxiety disorder:
irrational fear to event/someone that poses no/minimal threat, avoiding social situations, and actual physical sxs of anxiety while in social situations (sweaty palms, SOB, dizziness, nausea, diaphoresis, speech difficulties)
tx: CBT, counseling, meds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is Agoraphobia? tx?

A

extreme irrational fear of being in public places, crowds, open areas, often starts with panic or anticipatory anxiety, leads to strict avoidance.
tx: desensitizaton, flooding (provoking exposure in controlled environment), graded exposure, support groups

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are substances that can start and exacerbate anxiety/panic?
what withdrawal of substances does the same?
Tx?

A 
CNS stimulants:
marijuana
amphetamines (Adderil, Ritalin)
Caffeine, Ephedrine
MDMA (ecstasy), Mephedrone, MDPV (bath salts)
Cocaine
Methamphetamine

Withdrawal of EtOH and CNS depressants

Tx: SSRIs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Diseases that can cause anxiety related sxs?

A 
Hyperthyroidism
Chronic obstructive pulmonary disease
Asthma
Drug abuse and withdrawal
Chronic pain 
Irritable bowel syndrome
Rare tumors (ex., pheochromocytoma)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

other diseases assoc w/anxiety?

A 
Cardiac disorders
Cerebrovascular disorders
Minor and Major Cognitive Disorders
Hypertension
Gastrointestinal problems
Genitourinary difficulties
Immune deficiencies/opportunistic infections
Headache and other pain syndromes.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Differentiate OCD Obsessions from Compulsions

A

OCD
Obsessions: recurrent or pressistent obtrusive ideas, impulses, images causing anxiety
Compulsions: excessive repetitive behaviors or mental acts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are features of OCD spectrum? tx?

A 
OCD Spectrum:
Obsessive-compulsive disorder
Body dysmorphic disorder
Hoarding disorder
Trichotillomania (hair-pulling disorder)
Excoriation (skin- picking disorder)
Often an overlap

Tx: SSRI, esp Clomipramine (TCA)+ Fluvoxamine, antipsychotics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

How is amygdala involved in fear conditioning? structures and functions or
dorsal PAG
ventral PAG
lateral nucleus

A

Amygdala responds to innate and conditioned fears:
Innate fears goes through dorsal PAG (periaqueductal gray)
Conditioned fears goes through ventral PAG
Lateral nucleus receives input from thalamus and indirectly from cortex, where unconditioned stimulus and conditioned stimulus converge, and CS can be strengthened

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Differentiate hippocampus vs amygdala in fear conditioning

A

Amygdala has Implicit, Pavlovian fear conditioning, where if it detects danger it initiates responses through hypothalamus or brainstem

Hippocampus is Explicit learning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

How would a pt w/o amygdala behave?

A

w/o amygdala, inability to have implicit learning or experience fear

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What’s found in amygdala vs prefrontal cortex activity in anxiety pts?

A

Anxiety has increased Amygdala activity
Decreased Prefrontal cortex activity (esp VentroMedial PFC, area related to extinction learning and inhibiting emotional responses)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are changes in Hippocampus w/PTSD?

A

Hippocampus is smaller in PTSD pts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What are changes in amygdala w/PTSD

A

Left Amygdala and anterior cingulate cortex are smaller in PTSD pts, w/INCREASED activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What are changes in vmPFC w/PTSD

A

Reduced vmPFC in PTSD pts in response to emotional or threatening cues (area related to extinction learning and inhibiting emotional responses)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What are changes in ACC w/PTSD

A

Reduced rostral ACC activity in response to emotional or threatening cues, BUT
Increased activity in dorsal ACC during fear conditioning, extinction learning recall, and response selection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What are possible risk factors for PTSD

A

Genetic predisposition w/reduced hippocampal volume
abnormal medial prefrontal cortex activity
greater amygdala activation in response to (-) emotional stimuli, and greater amygdala activity in general

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What are defining features of PTSD?

A

1) Direct recipient/witness/knowledge of catastrophic trauma w/intense response of fear/helplessness/horror
2) persistent avoidance/numbing, Feelings of intense fear, dreadfulness or helplessness, psychological numbness, interpersonal, social, educational, and vocational dysfunctions
3) relive the traumatic events
4) hyperarousal
5) **>1mo
6) resulting in life impairment
7) blaming self/others
8) reckless behavior

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are causes of PTSD?

biological

A

Biology: hypersensitivity of HPA axis, increased activity in amygdala, hypothalamus, locus ceruleus, and PAG (periaquaductal gray), and dysregulation of stress hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

establish ddx of PTSD

A

Acute stress disorder: Symptoms last minimum 2 days and maximum 4 weeks (< 1 mo.)
Depression: May occur following traumatic event; disturbances in energy, sleep, appetite, loss of interest, suicidal ideation and intention.
Specific phobias: Symptoms of fear and avoidance triggered by situations,but not re-experiencing spontaneously.
Panic disorder: Recurrent, unexpected panic attacks, not triggered by recall of trauma
Generalized anxiety disorder: Constant worrying or obsession about small or large concerns, trouble concentrating, trembling, but not occur due to traumatic event.
Adjustment disorders: Specific stressors leading to mood, anxiety, worry, sleep disturbances, inability to cope.
Dissociative disorders:Persistent or recurrent feelings of detachment, and estrangement from oneself (depersonalization). Absence of re-experiencing and hyper arousal symptoms.
Obsessive compulsive disorder: Recurrent intrusive thoughts, leading to anxiety, may be accompanied by compulsions, rituals, or activities to counteract the anxiety and not related to a traumatic experience.
Substance abuse or medically: Medical history, symptoms onset and resolution induced symptoms are associated with medical condition(s) and/or abuse of substances.
Malingering: inconsistency in symptom presentation, poor work record, discrepancies in the capacity for working vs. ability to participat in recreation and entertainment activities are common.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What are PTSD tx?

A

1st line: SSRIs (Fluoxetine, Paroxetine, CItalopram) or Venlaflaxine (SNRI)
2nd line: SNRI
3rd line: TCA or Mertazapine (atypical antipsychotic)

If response, tx for 1yr. If no response, try next line

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Which neural circuits are affected in OCD?

A

Circuit dysfunctions in striatum

Increased activity in basal ganglia (esp caudate nucleus head), anterior cingulate cortex (ACC), and orbitofrontal cortex activity and gray matter

Less striatal gray matter

Larger thalamic volumes, Left amygdala, Larger corpus callosum, Larger Lt orbital frontal cortex, white matter fiber density, axonal diameter and myelination in certain white matter tracks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Differentiate OCD to Tourette syndrome pathophysiology

A

Tourette syndrome also has striatum circuit dysfunctions, and 50% of Tourette pts exhibit OCD tendencies
more OCD-Tourette overlap than other anxiety disorders

52
Q

Differentiate OCD to Sydenham chorea pathophysiology

A

Sydenham chorea: Antibodies to streptococcal infection bind to neurons in the striatum.

53
Q

What are OCD txs?

A

OCD tx:

SSRIs, esp Clomipramine (TCA)+ Fluvoxamine, antipsychotics

54
Q 
What's the MOA of Anxiolytic Benzodiazepines?
What're other FDA approved indications?
ADEs?
drug-drug interactions?
drug-disease interactions?
A

MOA: binds to GABA(A) receptors, leading to increased GABA channel opening frequency
other TI: seizures, sedation
ADEs: CNS depression, memory impairment, rarely disorientation, depression, confusion, irritability, aggression, excitement
drug-drug: additive ADEs, CYP interactions but Lorazepam and Oxazepam do NOT go through Phase I hepatic metabolism
drug-disease: pregnancy

55
Q

What’s the MOA of Antidepressants?

ADEs?

A

MOA: UNK, maybe 5HT +/- NE (SSRIs, SNRIs, some TCAs and MAOIs)
ADEs: HAM/triC’s

56
Q

What’s the MOA of Buspirone?
What’re other FDA approved indications?
ADEs?

A

MOA: UNK, maybe 5HT partial agonism
TI: Generalized Anxiety Disorder
ADEs: better tolerated than benzos bc no seizures or dependency or sedation or interactions or withdrawal rxns, but still dizzy, nausea, HA

57
Q

What’s the MOA of Anticonvulsants?
What’re other FDA approved indications?
ADEs?
drug-drug interactions?

A

MOA: UNK, maybe GABA augmentation (gabapentin, tigabine, pregabalin)
other TI:?
ADEs: somnolence, dry mouth, wt gain, cognitive impairment
drug-drug: depends

58
Q

What’s the MOA of Antihistamines?
What’re other FDA approved indications?
ADEs?

A

MOA: unk in anxiety (diphenhydramine, vistaril)
other TI:?
ADEs: sedation, anticholinergic

59
Q

What’s the MOA of Antiadrenergics?
What’re other FDA approved indications?
ADEs?
drug-drug interactions?

A

MOA: related to decreased physical response to anxiety from NE release (clonidine alpha2, prazosin alpha1, propranolol)
other TI:?
ADEs: decreased BP,
drug-drug: depends

60
Q

What’s the “antidote” to anxiolytic benzodiazepine OD?

A

Anxiolytic Benzo OD antidote = Flumazenil

61
Q

What are the 1st and 2nd line treatments for most anxiety disorders?
What’s general tx strategy? except for?

A

Acute Anxiety tx
1st line: anxiolytic benzodiazepines, Antidepressants
2nd line: Buspirone

In general acute benzo’s until chronic SSRIs take effect,

except PTSD acutely needs anti-adrenergics not benzos,

and OCD nothing works acutely

62
Q

What are the acute and chronic tx for Generalized anxiety disorder?

A

GAD tx
Acute: Benzodiazepine, antihistamine, anti-adrenergic
Chronic: Antidepressants (SSRIs, or SNRI Venlafaxine), Buspirone, anticonvulsants

63
Q

What are the acute and chronic tx for Panic disorder?

What’s not effective?

A

Panic disorder tx
Acute: Benzodiazepine, Clonidine
Chronic: antidepressants (SSRIs, or SNRI Venlafaxine)

Not: Buspirone, antihistamines, betablockers

64
Q

What are the acute and chronic tx for Social Anxiety Disorder?
Situational?

A

Social anxiety disorder tx
Acute: Benzodiazepines, beta blockers
Chronic: antidepressants (SSRI, SNRI Venlafaxine), phenelzine, mirtazapine, gabapentin, pregabalin
Situational: Propranolol or benzodiazepine prn

65
Q

What are the acute and chronic tx for PTSD?

A

PTSD tx:
Acute: anti-adrenergics (Clonidine, Prazosin, Propranolo) NOT benzodiazepine
chronic: SSRIs (Fluoxetine, Paroxetine, CItalopram) or Venlaflaxine (SNRI), then TCAs or Mertazapine

66
Q

What are the acute and chronic tx for OCD

A

OCD tx
Acute: none
Chronic: SSRI, esp Clomipramine (TCA)+ Fluvoxamine, antipsychotics

67
Q

What are the names of 4 SSRIs?

A

Fluoxetine, Paroxetine, CItalopram, Fluvoxamine

68
Q

Differentiate Somatic Symptom Disorder and Illness Anxiety Disorder

A

SSD: Excessive thoughts, feelings, or behaviors related to the somatic symptoms, authentic suffering, health concerns may assume a central role in the individual’s life, becoming a feature of his or her identity and dominating interpersonal relationship >6mo
IAD: Preoccupation with having or acquiring a serious illness, Somatic symptoms are not present or, if present are only mild in intensity. If another medical condition is present or there is a high risk for developing a medical condition (e.g. a strong family history) the preoccupation is clearly excessive or disproportionate, >6mo

69
Q

Describe Microbiome-gut-grain axis (NTs)

A

gut microbiome creates lots of NTs:
NE (lactobacillus, bifidobacterium)
DA (EColi, Bacillus, Saccharomyces)
5HT (Candida, Streptococcus, Escherichia, enterococcus)

70
Q

how to manage mind-body syndromes?

A

Schedule regular outpatient visits
Establish a collaborative, therapeutic alliance w/ patient
Acknowledge and legitimize somatic symptoms or worry of symptoms
Set goals of treatment as functional improvement (avoiding excessive rest and disability)
Communicate with specialists who are treating the patient
Evaluate and treat diagnosable general medical diseases
Exercise, PT, OMM
Medications: modulators of pain perception (e.g. gabapentin, pregabalin), pain medications (avoid opioids when possible), anti-depressants, beta-blockers for situational anxiety (avoid benzodiazepines when possible)
Cognitive behavioral therapy & Psychotherapy
Mindfulness meditation
Journaling and writing exercises

71
Q

Differentiate Somatoform disorders from fictitious and malingering disorders from primary medical conditions

A

Somatoform Disorders: no obvious gains or incentives from being ill, not willfully adopting or faking sxs, no general medical explanation/mental disorder/substance use, and causes significant impairment of life fx
Fictitious Disorder: faking sxs for unconscious internal gain
Malingering Disorder: faking sxs for external gain (money)

72
Q

What are Somatoform Disorder txs?

A

Somatoform Disorder Tx:
Pharm: not helpful
CBT

73
Q

Differentiate Conversion Disorder from Somatoform Disorder?

A

Conversion Disorder: 1 single dramatic symptom, not medically explained, related to voluntary motor/sensory fx, doesn’t conform to known anatomic/physiologic mechanisms, and pts don’t seen to care, usually spontaneous resolution

Not diffuse sxs like Somatoform Disorder

Undifferentiated Somatoform: 1 unexplained sxs for< 6mo

74
Q

Define Pain Disorder

A

Pain disorder: Pain assoc w/underlying psychological stress, onset/exacerbation may have medical reason, can lead to med OD and dependency

75
Q

Define Hypochondriasis?

A

Hypochondriasis: pts who misinterpret/fixate on/exaggerate physical sxs, fear life threatening conditions despite reassurance >6mo

76
Q

Define Somatization Disorder

A

1) Different pain sites
2) GI sxs other than pain
3) sexual or reproductive sxs other than pain
4) 1 pseudoneurological sxs

77
Q

Define Reflex Sympathetic Dystrophy?

A

Reflex Sympathetic Dystrophy:
Past injury site presenting w/painful swelling, decreased skin temperature, cyanosis, delayed capillary refill, limitation of functioning, often w/anxiety and depression, Pain with autonomic dysfunction, edema, movement problems, and atrophy if severe enough

78
Q

Differentiate b/w Dissociate Identify Disorder, Dissociative Amnesia, and Depersonalization/Derealization

A

Dissociative Identity Disorder: split personalities, recurrent episodes of amnesia
Dissociative Amnesia: inability to recall autobiographical info
-selective (specific aspect of an event)
-localized (an event or period of time)
-generalized (identify and life hx)
Depersonalization/Derealization: out of body experience, or experience w/unreality like in a dream, but reality testing is intact

79
Q

What’s relationship b/w dissociative disorders and stress/trauma-related disorders?

A

Both acute stress disorder and PTSD contain dissociative symptoms, such as amnesia, flashbacks, numbing, and depersonalization/derealization
BUT PTSD amnesia extends beyond immediate time of trauma

80
Q

What’s the fx of the primary motor cortex?

What are the inputs?

A

Primary motor cortex controls movement

Receives input from Ventral Lateral Nucleus of Thalamus (VL)

81
Q

What’s the fx of the Somatosensory Cortex?

What are the inputs?

A

Somatosensory cortex processes sensory input from dorsal ganglion roots
Receives input from Ventral Posterior Lateral and Medial nuclei (VPL and VPM) of Thalamus

82
Q

What’s the fx of the Primary visual cortex?

What are the inputs?

A

Receives input from Lateral Geniculate Nucleus (LGN, L = light) of Thalamus

83
Q

What’s the fx of the basal ganglia?
What are the inputs?
Where does it output?

A

fx: action selection
Receives input from cerebral cortex
Outputs to thalamus

84
Q

What’s the fx of the Hippocampus?

What are the inputs?

A

Receives inputs from Association Areas (frontal/temporal/parietal)

85
Q

What’s the fx of the prefrontal cortex?
What are the inputs?
Where does it output?

A

Prefrontal cortex: Restraint, Initiative, Order… connects w/parietal, occipital, and temporal assoc cortices, with motor assoc cortices in frontal lobes
Receives input from Mediodorsal nucleus and VA in thalamus
Projects output to basal ganglia through caudate nucleus head

86
Q

What’s the fx of the parietal association cortex?

What happens when there’s a lesion?

A

Parietal Assoc Cortex:
related to motor cortex, involved w/motor planning
Lesion: hemineglect syndrome, ignoring information that comes in from lesioned side, most severe when lesion’s on nondominant side

87
Q

What’s the fx of the inferior association temporal cortex?
What are the inputs?
What occurs w/lesions?

A

Inferior Temporal Assoc Cortex:
processes visual understanding
Input from Primary visual cortex
Lesions: inability to match/copy complex visual shapes/objects, ID objects, or people (prosopagnosia)

88
Q

What’s the fx of the amygdala?
What are the inputs?
Where does it output?

A

Basolateral side Receives input from thalamus, assoc cortices, and sensory structures
Central side projects out to emotional response structures
Corticomedial nucleus, related to olfaction and appetite
Projects output to orbital and medial frontal lobes through Uncinate Fasciculus

89
Q

What structures are involved with consciousness (alertness, attention, awareness)?

A

Alertness: subcortical arousal system, PontoMesencephalic Reticular formation
Attention: non-dominant hemisphere
Awareness: horizontal connections in cortical layers

90
Q

Where are the 5HT projection systems? where does it originate?

A

Raphe nuclei in midbrain, pons, and medulla project to entire forebrain (cortex, thalamus, basal ganglia)

Caudal raphe nuclei of caudal pons and medulla project to cerebellum, medulla, and spinal cord

91
Q

Where are the Ach projection systems? where does it originate?

A

Nucleus Basalis of Meynert projects to entire cortex

92
Q

Where are the NE projection systems? where does it originate?

A

Locus ceruleus and lateral tegmental area
Projections are generally excitatory to thalamic neurons.
Projections to cortex can be excitatory or inhibitory.

93
Q

Where are the DA projection systems? where does it originate?

A

Mesostriatal (from SNc)
Mesolimbic (from VTA)
Mesocortical (from VTA and scattered DA neurons around SN)

94
Q

Where are the histamine projection systems? where does it originate?

A

Neurons of the posterior hypothalamus in the tuberomammillary nucleus
The histamine excites thalamic neurons
In the cortex, the effects are both inhibitory and excitatory effects

95
Q

Differentiate ADHD from Disruptive (Behavior) Disorder

A

ADHD: inability to conform to societal rules d/t inattention, hyperactivity, and impulsivity

Disruptive: precipitated by stressful life event, includes Oppositional Defiant Disorder and Intermittent Explosive Disorder

96
Q

Differentiate Oppositional Defiant Disorder and Antisocial Disorder?
From Conduct Disorder?

A

Oppositional Defiant: >6mo, can develop → Conduct → Antisocial Personality if starts early and sxs are severe, argumentative, angry, and loses temper w/authority figures

Antisocial Personality: >17yo impulsive, disregard for rights/boundaries of others, impoverished moral sense or conscience

Conduct: bridge b/w Oppositional Defiant and Antisocial Personality, violates others’ rights, physical harm, property damage, deceitful, violation of rules

97
Q

How does ASD and Intermittent Explosive Disorder fit into the Psychosis scheme?

A

ASD: deficits in social communication and social interaction, restricted repetitive behaviors, interests, activities

Intermittent Explosive: repeating/persistent sudden violent episodes of impulsive, aggressive, angry verbal outbursts out of proportion to inciting event, at least 2x/week for 3mo

98
Q

How to dx Autism spectrum disorder?

A

ASD Dx:

  1. persistent defects in social communication and social interactions
  2. Restricted, reptitive patterns of behavior, interests, or activities
  3. Sxs present in early developmental period
  4. Sxs cause clinically significant impairment in social, occupational, or other important areas of current functioning
  5. Disturbances not better explained by intellectual disability or global developmental delay
99
Q

What’re the structural and functional changes in brain w/Autism spectrum disorder?

A

ASD brain initially has overgrowth, followed by slow/arrested growth
Abnormal connectivity in amygdala, superior temporal sulcus, prefrontal, and inferior temporal cortices, temporoparietal areas, Lt medial prefrontal cortex
Reduced in-network integration in default mode and visual, and structural connectivity in sensorimotor network

100
Q

What’re the molecular and genetic factors related to etiology of Autism spectrum disorder?

A

ASD etiologies

  • Increased Copy Number Variants
  • synaptic plasticity proteins like FMRP (fragilex mental retardation protein) and TSR (tuberous sclerosis complex)
101
Q

What’s the importance of autoimmune factors and microbiome in Autism spectrum disorder?

A

Maternal IL6 may be responsible for maternal immune activity gene transcriptional changes in infants frontal cortex
ASD have distinct microbiomes

102
Q

Which meds can be used to treat ASD?

*Which are FDA approved?

A

ASD tx:
*atypical antipsychotics = Risperidone, Aripiprazole
antidepressants = SSRIs, TCAs,
typical antipsychotics = Chlorpromazine, Haloperidol

103
Q

For atypical antipsychotics, what’s the
MOA
TI
ADEs

A

atypical antipsychotics = Risperidone, Aripiprazole
MOA: D2 and 5HT receptor antagonists
TI: irritability assoc w/ASD
ADEs: drowsy, wt gain, orthostatic HTN (RIsperidone)

104
Q 
For antidepressants, what's the
MOA
TI
ADEs
drug interactions
A 
Antidepressants = SSRIs, TCAs
MOA
TI
ADEs
drug interactions
105
Q

For typical antipsychotics, what’s the
MOA
TI
ADEs

A

typical antipsychotics = Chlorpromazine, Haloperidol
MOA: C unk, H D2 receptor block
TI: severe behavior problems in kids, not ASD specific
ADEs: significant

106
Q

Differentiate Learning Disability from mental retardation?

A

LD is average or above average intelligence, LD not due to other disabilities or extrinsic influences

107
Q

How to dx ADHD?

A

ADHD dx:
<17yo: 6+ sxs of hyperactivity or 6+ sxs of inattention
>17yo: 5+ sxs of hyperactivity, or 6+ sxs of inattention
and sxs must have started <12yo, interfere w/life fx, occuring in 2 separate locations

108
Q

What are pathogenic changes in ADHD?

A

ADHD pathology:
strong genetic factor
neuroanatomy:
-smaller/thinner anterior cortex/*prefrontal volume, cerebrum, *cerebellum, white tracts, *basal ganglia
-decreased global and anterior frontal activation (responsible for inhibition and executive fx)
-decreased DA (inhibitory), increased NE (stimulating)

109
Q

What’s tx protocol for ADHD? kids vs adult

A

kids ADHD tx
1) Methylphenidate, DNRI

adult ADHD tx
1) Atomoxetine, SNRI

110
Q

Which receptors are most involved with ADHD, and what do they bind?

A

ADHD receptors implicated:

  • D4 receptor, binds DA and NE
  • alpha2, binds NE and Epi
111
Q

What’s tx protocol for ADHD?

A 
ADHD tx:
1) Synthetic stimulants (dex(methylphenidate)) or
Amphetamines
2) Atomoxetine (SNRI)
3) Bupropion (DNRI)
4) combo/adjunct alpha2agonists
112
Q 
For synthetic and amphetamines, what's: 
MOA
TI
ADEs
drug interactions
A

(dex)methylphenidate, amphetamines:
MOA: DNRI
TI: ADHD, narcolepsy (not preschool kids)
ADEs: methylphenidate has wt loss/decreased appetite, insomnia, growth suppression, slight increased risk of seizures, increased BP/HR, risk dependence
drug interactions: MAOIs

113
Q

What’s first line drug for ADHD w/person hx drug abuse?

A

ADHD + hx drug abuse

use Lisdexamfeatmine = lysine prodrug

114
Q 
For Atomoxetine, what's: 
MOA
TI
ADEs
drug interactions
A 
Atomoxetine:
MOA: SNRI
TI: ADHD
ADEs: nausea, anorexia, insomnia, fatigue, high BP/HR, hepatotoxicity
Drug interactions: MAOIs
115
Q 
For Bupropion, what's: 
MOA
TI
*ADEs
drug interactions
A

Bupropion
MOA: DNSRI (D>N=S)
TI: depression, smoking cessation, seasonal affective disorder, NOT ADHD!
ADEs: agitation, increased HR/BP, HA, dizziness, GI, *OD toxicity, *decreased seizure threshold

116
Q 
For alpha2 agonists, what's: 
MOA
TI
ADEs
drug interactions
A

Clonidine, Guanfacine
MOA: alpha2 agonists
TI: ADHD, HTN
ADEs: sedation, hypotension, bradycardia, syncope, rebound HTN (Guanfacine better than Clonidine)

117
Q 
For TCAs, what's: 
MOA
TI
ADEs
drug interactions
A

TCAs
MOA: SNRI
TI depression, NOT ADHD
ADEs: anticholinergic, sedation, cardiac conduction changes

118
Q

Defining characteristics of Intermittent Explosive disorder?

Tx?

A

Intermittent Explosive: recurrent behavioral outbursts representing failure to control aggressive impulses, disproportionate to provocation, not premediated or to achieve tangible objective, >6yo
Tx: prefer CBT, can use Fluoxetine (SSRI)

119
Q

Defining characteristics of Oppositional Defiant disorder?

A

Oppositional Defiant: >6mo, angry/irritable mood, argumentative/defiant behavior or vindictiveness w/4+ sxs and directed at someone other than a sibling

120
Q 
Defining characteristics of Conduct disorder?
What are the ages of onset for
Childhood onset
adolescent onset
>18yo
A

Conduct: repetitive persistent behavior where basic rights of others or major age-appropriate societal norms or rules are violated, aggressive to people and animals

Childhood onset <10yo
Adolescent onset >10yo, <18yo
>18yo, it’s Antisocial Personality Disorder

121
Q

What are Conduct Disorder tx options?

A

Conduct disorder tx:

1) D2/NE stimulant = methylphenidate
2) antidepressants = Fluoxetine
3) anticonvulsants = lithium
4) alpha2 agonists = Clonidine
5) atypical antipsychotics = Risperiodone

122
Q

Differentiate non-psychotic disorder and Psychotic Disorder?

A

Non-psychotic disorder: brief episode >1, <1mo, substance induced and/or medical condition
Psychotic disorder: Schizoprenia >6mo, Schizophreniform <6mo, Schizoaffective, Delusional Disorder

123
Q

What is Capgras Syndrome?

A

Capgras: imposter syndrome, loses ability to recognize faces that were important, thinks it’s someone pretending to be close friend/family
maybe d/t neural misfiring in fusiform gyrus and amygdala, or lesions of Rt parietal lobe

124
Q

What is Cotard syndrome

A

Cotard syndrome: bizarre delusions, like they’re already dead or they’re decaying
maybe d/t neural misfiring in fusiform gyrus and amygdala, or lesions of Rt parietal lobe

125
Q

What is Fregoli delusion

A

Fregoli delusion = delusion of doubles, breakdown in normal facial recognition, sees faces but thinks they’re someone famous

Mind (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions