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MS2 Unit3 Neurology > Week3 lectures (sans Dementia Day) > Flashcards

Week3 lectures (sans Dementia Day) Flashcards

1
Q

blocking this dopamine pathway, would result in worse negative sx (mesocortical/mesolimbic/nigrostriatal/tubuloinfundibular)

A

mesocortical

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2
Q

blocking this dopamine pathway, would result in ↓ positive sx (mesocortical/mesolimbic/nigrostriatal/tubuloinfundibular)

A

mesolimbic

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3
Q

blocking this dopamine pathway, would result in EPS or NMS (mesocortical/mesolimbic/nigrostriatal/tubuloinfundibular)

A

Nigrostriatal

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4
Q

blocking this dopamine pathway, would result in high prolactin (mesocortical/mesolimbic/nigrostriatal/tubuloinfundibular)

A

tubuloinfundibular

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5
Q

circuit for reward/motivation includes (3)?

A

ventromedial PFC, Nucleus Accumbens/Ventral Striatum, Thalamus

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6
Q

lesion in the reward/motivation circuit would cause (sx type)?

A

negative sx (apathy/amotivation)

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7
Q

Hallucination/Delusions from ↑DA can be improved with

A

dopamine blockers

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8
Q

Mania (euphoria/grandiosity) can be treated with

A

Antipsychotics (lithium + Valproic acid too, via other MOAs)

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9
Q

Antipsychotics mostly block ____ in the _____ DA pathway, EXCEPT pimvanserin

A

block D2 rcps; mesolimbic DA pathway

hint: useful for 1˚+ 2˚ psychosis and mood stabilziation; ↓DA –> ↓noise

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10
Q

D2 blocks in the nigrostriatal pathway lead to (2)

A
  1. extrapyramidal sx (EPS)
  2. tardive dyskinesia (TD)

hint: motor SE (invol movemnt)

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11
Q

Acute dysotnia (eg. torticollis), 2˚parkisnonism, akathisia are eg’s of _______ seen with what drugs?

A

extrapyramidal sx seen with antipsychotics (first gen)

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12
Q

toritcollis, oculogyric crisis (upwards eye deviation), and Opithotinus (arched back/neck) are eg’s of? How do you treat?

A

acute dystonia tw anticholinergic agentics (IV/IM benztropine)

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13
Q

why can’t anticholinergics be used in 1˚ parkinsons (older popn)?

A

adverse cognitive SEs; use DA agonists instead

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14
Q

steps for treating 2˚ parkinsonism (3)

A
  1. dc/↓ antipyschotics
  2. if not, switch to SGA w/lower D2 potency
  3. if not, tw with benztropune/amantidine to ↑DA
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15
Q

steps for treating Akathisia (1st line/2nd line)

A 
1st = propranolol (CNS β blocker)
2nd = benztropine (antiAch)
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16
Q

steps for treating tardive Dyskinesia (3)

A
  1. dc/↓ antipyschotics
  2. if not, switch to SGA w/lower D2 potency
  3. if not, tw with VMATi
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17
Q

Valbenzaine, tetrabenazine, deutetrabenazine are eg’s of (drug class)? MOA?

A

VMATi; block DA packaging and release into synapse

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18
Q

indications for VMATi (2)? what can it NEVER BE used for?

A
  1. TD
  2. HUntington’s CHorea

Never use for antipsychotic

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19
Q

Hyperthermia, unstable ANS/vitals, muscle rigidity, rhabdomyolysis + ↑CPK, confusions are all signs of (syndorme)?

A

NMS (Neuroleptic Malignant Syndrome

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20
Q

what 4 receptors do low pot FGA’s target, causing a mess?

A
  1. D2 dopamine rcp –> EPS
  2. H1 histamine rcp –> sedation + ↑appetite/wt
  3. AntiAch-M –> dry mouth, blurred vision, constipation
  4. Noradrenergic 𝛂1 rcp –> ortho hypotn
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21
Q

Haloperidol and FLuphenzaine are (high/low) potency FGAs?

A

high potency FGAs

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22
Q

Chlorpromazine + Thioridazine are (high/low) potency FGAs?

A

low potency FGAs

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23
Q

Atypicals/SGA mechanism of action?

A

lower affinity D2 blockade + 5HT2a rcp antags

hint: cant AUGMENT (not replace) anitD’s

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24
Q

SGA that cause severe metabolic SE (2)? zap

A

clozapine + olanzapine

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25
Q

SGA that cause intermediate metabolic SE (2)? PQR

A

Palepridone, Quetiapine, Risperidone

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26
Q

SGA that cause minimal metabolic SE (2)? (from LAZI + PIPs)

A

Aripirazole, Ziprasidone

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27
Q

dirty SGA that has activity on NDMA***, D1, nictoinic rcps; useful for refractory schizophrenia and suicide risk reduction

A

Clozapine

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28
Q

Dirty SGA that causes metab SE, agranulocytosis (watch WBCs), seizures, sedation, sialorrhea

A

Clozapine

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29
Q

This SGA is a partial D2 agonist/antag w/5HT1 agonism (antidepressant)? rips and pips

A

Aripirazole

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30
Q

DA is removed formt he sunapse by ____, destroyed in the neurons by _____, destroyed in the synapse by ______. (COMT, MAOab, DAT)

A

dat removes; MAOab internally destroys; COMT externally destroys

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31
Q

Valine substition for this genes –> agrresive DA breakdown –> too little DA

A

COMT

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32
Q 
Hyperfunctioning DA results in what in the following pathways?
Mesolimibic
Mesocortical
NIgrostriatal
Tuberoinfundibular
A

Mesolimibic - addiction
Mesocortical - hypervigilence
NIgrostriatal - dyskinetic movment
Tuberoinfundibular - hypoprolactinemia

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33
Q

This drug used for Parkinson’s Pyschosis is an inverse agonist (= below baseline) of 5HT2a glutamate neurons with no DA efx

A

Pimvanserin

hint: inh 5HT2a rcps on cortical glutamate neurons –> ↓stimulation –> ↓downstream mesolimbic*** DA firing

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34
Q

This drug blocks VMAT (↓DA) + used for htn (↓NE); causes depression, ↓ BP, ↓ psychosis. (Pimvanserins/Reseprine/Tetrabenazine)

A

Reserpine

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35
Q

Newer gen VMATi that ↓ choeric movemt + used for HD Chorea (Pimvanserins/Reseprine/Tetrabenazine)

A

Tetrabenazine

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36
Q

Valbenzaine and Deutetrabenzine block ____ (rcp type), ↓ synaptic DA?

A

VMAT2

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37
Q

Parkinson’s DA enhancing pro-drug that crosses BBB; high doeses cause dyskineisa + hallucinations/psychosis (Levadopa/Carbidopa)

A

Levodopa

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38
Q

Parkinson’s DA enhancing combo-drug that prevents peripheral DA activity; ↓fatigue, dizziness, nausea and hot flashes, etc (Levadopa/Carbidopa)

A

Carbidopa

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39
Q

Prescribe these 2 drugs to treat dperession caused by low DA state via the 1C pathway

A

l-methylfolate + s-adenosyl methionine

hint: ↑ 1C cycle –> ↑ neuronal DA prodn

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40
Q

Effectiveness and Purity are concnersn for _____

A

Complimnetary alternative Medicien

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41
Q

TT alleles for what enzyme results in lower DA prodn

A

MTHFR (methyl folate prodn)

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42
Q

ADHD stimulants that block and reverse DAT, ↑ VMAT2 DA ejection

A

Amphetamines (dextro-/lisdexam-phetamine + mixed salts)

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43
Q

ADHD stimulants that block DAT more aggresively than bupropion

A

Methylphenidate

stims have greater DA, NE, NRI SEs

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44
Q

Class IV stimulants for treating narcolepsy, apnea, shiftworks fatigue (but not ADHD) (2)

A

Modafinil + Armodafinil

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45
Q

Modafinil and Armodafinils may lower birth control effectiveness; cause addiction; or appetite + weight loss. How?

A

↑ p450-3A4 enzymes lower OCP;
↑DA in the mesolimbic pathways –> addiction (psychosis at hig doses);
↑ NE –> apetite and weight loss

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46
Q

stimulants that ↑ histamine activity in TMN (alertness) and ↑ orexine activity (wakefulness, requires DAT; may manipulate post-syn NE rcps (amphetamines/finils)

A

Modafinial + Armodafinil

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47
Q

Isocarboxid, phenelzine, tranycypromine, selgeine can all treat _____ (dz) viah ___ (mech)?

A

depression;

MAOa/b inh

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48
Q

low dose MAOb and high dose MAOa/b inh for Parkisnons + Depression

A

Selegiline

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49
Q

MAOb inh used for Parkinsons

A

Rasagaline

hint: MAOb more sgf for DA

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50
Q

MAOi SEs include hypotn, dizziness, insomnia, wt gain via antagonism of what 2 rcp’s

A

𝛂1 + histimine1 rcp antagonism

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51
Q

MAOi for depression primariy targets MAOa which interferes with ___ (2 NTs) breakdown.

A

5HT + NE

hint: basis for drug-drug interaction

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52
Q

how may a Hypertensive crisis leading to a heart attack/stroke occur

A

↑↑↑ NE –> ↑↑↑BP –> HC

eg ingesting tyramine or adding and NE agonist –> release NE –> HC

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53
Q

how may seratonin syndrome occur?

A

adding aggressive 5HT drug (antiD, narc, antiH1) –> toxic 5HT levels in CNS –> SS

hint: tremor, muscle spasm, unstable vitals, hyperthermia, delirium, coma and death

54
Q

2 COMTi drugs for Parkinsons and SEs

A

Entacapone (nausea + fatigue)
Tolcapone (liver failure/∆lfTs)

hint: ↑synaptic DA

55
Q

Bromocriptine, Pramipexole, Ropinerole, and Apomorphine injections treat Parkinsons and RLS via____ (MOA)

A

phasic D2 agonism** to ↑DA activity

hint: common SEs = nausea, fatigue, dizziness, and mania

56
Q

Aripiprazole and the pips treat Schizophrenia and Depression via____ (MOA)

A

tonic D3 partial* agonism to ↑ alertness and energy

57
Q

Used to treat Parkinson’s and Influenza* by releasing DA, blocking DAT and stimulating D2

A

Amantidine

hint: SE = pyschosis, insomnia, seizures

58
Q

DSM5 insomnia criteria (4)

A
  1. CC of dissatification with sleep quality or qty
  2. causes distress or impairs life/functioning
  3. 3+ nights/wk for 3+ mo
  4. not due to substance/meds/mental disorder
59
Q

Excess of NTs at night can lead to insomnia (4)

A
  1. NE (locus ceruleus)
  2. 5HT (raphe nucleus)
  3. DA (vent tegmental area)
  4. Histamine (tuberomamillary nucleus)
60
Q

Defc of NTs at night can lead to insomnia (3)

A
  1. GABA
  2. melatonergic tone
  3. adenosinergic tone
61
Q

Psych cause for insomnia where short REM sleep latency, repeated nightime awakenings, and wkaing too early occurs?

A

MDD

62
Q

Psych cause for insomnia where manic and hypomanic have problems falling/staying asleep (and usually don’t feel tired) occurs?

A

Bipolar Disorder

63
Q

Psych cause for insomnia dt nightmares/trouble falling asleep occurs?

A

Generalized anxiety disorder/PTSD

64
Q

Sleep deprivation hits what 3 areas of the brain the hardest?

A

ant cingulate gyrus, prefontal Cortex, thalamus

65
Q

steps to tx insomnia (3)

A
  1. dx, consent, education
  2. behavioral counseling (sleep hygiene)
  3. Meds
  4. Mgt (risk of addiction)
66
Q

Pharmocodynamic MOA of BZRAs and BZs

A

positive allosteric modulation of GABAa rcp –> sensitized Cl- pores (↑opening duration + frequency) –> ↑hyperpolz

67
Q

___(drug class) stimulate wake cts where NE, 5HT, DA, and ACh are made. These are targets for ↓ arousal

A

orexins

68
Q

antagonizing 5HT2a creates ____(effect)

A

deeper sleep patterns

69
Q

antagonizing 5HT1d and 7 promotes ____(effect)

A

more accurate circadian clock

70
Q

antiD’s can also target ____(rcp), to ↓arousal –> sedation –> sleep initiation

A

H1 rcp (histamine)

71
Q

how would you dx and tx the following: xs datyime sleepiness/cant maint wakefulness; not dt medical/substance issues; affecting daily life.

A

hypersomnia;

tw stimulants (cafeine, methylphenidate, amphetamine, modafinil/armodafinl)

tw hygeine (morning- light/excercise/meal or strategic naps)

72
Q

how would you dx and tx the following: abrupt sleep attacks; cataplexy; hyno-pompic/gogic hallucination; ↓↓REM latency; sleep paralysis

A

narcolepsy

tw stimulants or armodafinil (if defc orexin rcps)

73
Q

how would you dx and tx the following: partner complains of snoring/gasping/coughing; obese/overwt pt; yields insomnia/hypersomnia

A

sleep apnea

tw CPAP, dental devices, surgery, impantable device for hypoglossal stim.

74
Q

how would you dx and tx the following: yields in-/hypersomnia dt sleep wake cycle mistmatch/shift/syncrhony advanced (elderly) vs delayed (jetlag/shiftwork)

A

CRSD (circ rhythm sleep disorder)

tw benzos, melatonin, exercise, stimulants, or light tx

75
Q

how would you dx and tx the following: 1) unconscious leg movements 2) creeping sensations, conscious movements occurs

A

1) nocturnal myoclonus
2) RLS

tw D2 rcp agonists (pramipexole, ropinirole)

76
Q

how would you dx and tx the following: long frightening dreams where pt is awake, alert, oriented and remembers dreams vividly; occurs during REM

A

Nightmare Disorder

tx: Self-limiting

77
Q

how would you dx and tx the following: Pt is awake disoriented, not consolable, has no emmory, dreams are vague if remembered; happens in 1st 1/3 of the night in NREM stage (3 or 4)

A

Sleep Terror disorder

tx: self limiting

78
Q

how would you dx and tx the following: teeth frinding in stage 2 of sleep

A

Sleep rel bruxism

tw mouth guard/bite plate

79
Q

how would you dx and tx the following: occurs during sleep, pt can awaken confused but orients; but will not remember the event

A

sleeptalking/walking (somn-iloquy/ambulism)

tx: self limiting

80
Q

how would you dx and tx the following: 1) atonia during REM –> violently act out dreams
2) rocking head back and forth /left and right while asleep

A

1) REM sleep behaviro disorder tw D2 agonists

2) Jactatio capitis nocturna/sleep related head banging; tx = self limiting

81
Q

hyperthyroidism and pheochromocytoma are organic causes of anxiety disordrs dt increased ___(NT)

A

↑NE levels

82
Q

neurogbio factors contributing anxiety ↑ ____(2 NTs) and ↓ ____ (2NTs)

A

↑NE + Glutamate;

↓5HT + GABA

83
Q
  1. xs worry about 1+ event, for 6+ months
  2. can’t control worry
  3. 3/6 sx
  4. sgf impairments
  5. no other explanation
A

list the DSMV criteria for GAD (5)

84
Q

AntiD’s for GAD + MOA

A

SSRis: escitalopram/Paraoxteine;
SNRis: Venlafaxine/Duloxetine;

MOA: ↑NE/5HT –> desentiize rcps

85
Q

5HT agonist for GAD + MOA

A

Buspirone;

MOA: 5HT1a ag –> ↓5HT actiivty –> downregn –> ↑5HT output

hint: ↓sex/wt gain SEs

86
Q

2nd line Rx for GAD dt addiction/fall/apnea risk + MOA

A

BZs;

MOA: GABAa PAM –> ↑Cl+ channel openings

87
Q

Abrupt, unexpected surge of intense fear/discomfort (minutes) with 4/12 sx

A

Panick Attack (DSMV)

88
Q
  1. Recurrent, unexpected attacks
  2. 1+ attack –> 1+ mo of (concern of attacks + maladaptive behavior change)
  3. no other sx explanation
A

Panic Disorder (DSMV )

89
Q
  1. fear/anxiety abt 2/5 situations
  2. fear of inability to escape situation
  3. situation always produces fear
  4. Avoids situations
  5. fear out of propn to actual danger
  6. 6+ mo
  7. sgf impairment
  8. øother explanation
A

Agoraphobia (DSMV)

90
Q

Therapy tx for Panic Disorder (2)

A

CBT (flooding/desnesitizn) + Psychodynamic Tx

91
Q

Meds for Panic Disorder (3)

A
  1. Fast BZs like alprazolam (emergency)
  2. SS/NRis (1st line long term)
  3. intermediate/long BZ’s (2nd line long term dt addiction)
92
Q
  1. 6+ mo’s
  2. sgf impairment
  3. marked fear for specific obj/situation
  4. obj/situ always provokes fear
  5. actively avoids obj/situ
  6. fear out of propn
  7. øother sx explanation

Tx?

A

Specific phobia (DSMV)

93
Q

vocal tics, motor tics, ± OCD

A

Tourrette’s Disorder

94
Q

repetitive motor movements ≠compulsion

A

temporal lobe epilepsy

95
Q

rigid, moralisitc workaholic pt who is list/pattern oriented w/ no insight into behavior. Wont’s have discret, repetitive behaviors to undo anxiety

A

OC Personality D (OCPD)

96
Q

Comorbidt’s of OCD (3)

A

MDD (1/3)
Tourrettes (2/3)
high suicide risk

97
Q

OCD PsychoTx (2)

A
  • CBT (exposure + response)

- ACT (acceptance + commitment)

98
Q

OCD PharmaTx (4)

A

1st line = high dose/duration SSRi
2nd = CLimpriamine (TCA for OCD)
3rd = AntiPsy’s/antiD’s

hint: BZ don’t work!!!

99
Q

Tx for Social ANxiety Disorder (social Phobia)

A

PsychoTx: CBt, ACT

1st line: SS/NRis’s (Paroxetine/Venafaxine ER)
2nd: MAOi’s (Phenelzine, Tranylcypromine)

100
Q

1st line Rx for performance social anxiety (public speaking) ONLY?

A

Beta Blockers (propranolol)

101
Q

3 chrs of local anesthetic?

A
  1. reversible
  2. blocks nerve impuslse transmission
  3. ø efx on consciousness
102
Q

first lcoal anesthetic?

A

Cocaine

hint: Incan use –> eye surgery –> jaw nerve block –> brach plex –> spinal anesthia

103
Q

Cocaine was followed by ____ in 1901 and ____ in 1928

A

Procaine (unstable/allergy inducing);

Tetracaine (high vol tox)

104
Q

This anesthetic, mde in 1942, was more effective/longerlasting/lower risk than its predecessors, and could be diluted/stored with Epi

A

Lidocaine

105
Q

Why is the inside of the neuron negative? (3)

A
  1. ↑ ⊖ cytoplsamic proteins
  2. K+ efflux thru leak channels/impermb to Na+ ions
  3. Active Na/K pumps (3 Na+ out/2 K+ in)
106
Q

preemptive analgesia

A

nerve block before incision

107
Q

Local anesthetics bind reversibly to the ____ part of the Na+ channel to inactivate it

A

intracellular

hint: ↑excitation threshold/↓impulse conduction

108
Q

critical length in myelinated nerves is

A

2-3 Nodes of ranvier

109
Q

name the state of the Na+ channel:

ø stimulus

A

resting (closed but modifiable)

110
Q

name the state of the Na+ channel:

immediately on depolz

A

active

111
Q

name the state of the Na+ channel:
refractory to repeat stimulus
transitions ms’s after opening

A

inactivated (closed + non modifiable)

112
Q

Na+ Blockade deps on (2)

A

voltage and time

hint: ↑ during active state + rapid fire axons

113
Q

name the 3 parts of local anesthetic mol

A
  • aromatic rign (lipophilic; potency)
  • intermediate link (ester/amide)
  • terminal 3˚amine (hydrophilic wk base; on/off switch)
114
Q

Cocaine, Procaine, Tetracaine, Chlorprocaine, and Benzocaine are all eg’s of

A

esters broken down by esterases

hint: “one eyed esther has allergies”

115
Q

Lidocaine, Bupivacaine, Ropicaine, Mepivacaine are all eg’s of

A

Amides

hint: amides have two I’s

116
Q

how does a LA repond to infected tissue; when bicarbonate is added

A
  • ↓effectiveness dt acidic/infected env;

- ↑potency/faster onset bc less ionized form can cross CM –> activate

117
Q

onset of action depends on (2)

A

pKa + lipid solb

118
Q

duration of action deps on

A

plasma protien binding to 𝛂1 GP

hint: rel to lipid solb

119
Q

list the order of Nerve block sensitivity by nerve type: A𝛂, Aβ, A𝛅, C

A

C(pain w/chem) > A𝛅 (pain) > Aɣ (muscle tone) > Aβ (touch) > A𝛂 (propio/P) > motor

120
Q

what is more senstive than C fibers?

A

B fibers (pregangiolonic SNS)

hint: vasomotor for viscero-/sudo-/pilo-motor

121
Q

Epi (↑/↓) absorbtion?

A

epi decreases abs

hint: ↑HR after epi = probable bv insertion

122
Q

rapid* metabolism to water solb metabolites is impaired by abnormal ____(gene/enz)

A

psuedocholinesterase that break down esters

hint: occurs in plasma

123
Q

How are intrathecal esters metabz?

A

abs into blood bc CSF lacks pseudocholinesterase

124
Q

slow metabolizm by _____ (enz)may be impaired by liver dz (liver tox); or prolongd by ↓hepatic flow/CHF/Vasopressor use

A

Carboxyl esterases or CYP450 enz’s that break down amides

125
Q

COntinuous spinal catheter use results in pt reporting severe back pain, loss of motor control, sensory deficits (saddle anesthesia). Bladder and bowel control is also lost. what happened?

A

Cauda Equina syndrome

hint: also occurs with high dose lidocaine (neurotoxic acc’m of LA in caudal space after admin to a restricted subarachnoid space) –> conduction failure, membrane/cytosk/axonal transport dmg, ↑intracell Ca+, apoptosis

126
Q

Pt in surgery for lithotomy reports brief, severe pain (dysesthesia). Dx? what 3 drugs were most likely used? (lidocaine, Bupivicaine, Procaine, Chlorprocaine, Mepivacaine)

A

Transient Neurologic Sx;

lidocaine, Procaine, Mepivacaine

127
Q

circumoral numbness, dizziness, tinnitus, blurred vision, and CNS excitation are all early signs of

A

systemic toxicity

128
Q

how does bupivicaine cause cardiotox

A

binds Na+ channels in the heart –> ↓myocard contractn + refractory period

129
Q

intrinsic props that ↑ potential for CNS tox (2)

A

↓prot binding + clearance

130
Q

extrinsic props that ↑ potential for CNS tox

A

metabolic acidosis

hint: ↑CBF + ↓plasma prot binding –> ↑PCO2

131
Q

all LAs are vasodilators (± cardiac arrest) except (2)

A

Cocaine + Ropivacaine

MS2 Unit3 Neurology (10 decks)

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