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Imperial > 24. Higher Cerebral Functions > Flashcards

24. Higher Cerebral Functions Flashcards

1
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A
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2
Q

What are the five clinically desirable effects of general anaesthetics? State which two effects are caused by ALL general anaesthetics.

A

Loss of consciousness (ALL) Suppression of reflex responses (ALL) Relief of pain Muscle relaxation Amnesia

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3
Q

Name 4 inhalational general anaesthetics.

A

Nitric oxide Diethyl ether Halothane Enflurane

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4
Q

Name 2 IV general anaesthetics.

A

Propofol Etomidate

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5
Q

What is the Meyer/Overton correlation?

A

For a long time it was believed that anaesthetic potency increases in direct proportion with the oil/gas partition coefficient In other words: anaesthetic potency is directly correlated with lipid solubility

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6
Q

hat was the explanation for the Meyer/Overton correlation?

A

The drugs disturbed the lipid bilayer

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7
Q

What were the problems with this explanation?

A

At therapeutic doses, the changes to the lipid bilayer were minute How would the change in membrane impact on membrane proteins anyway?

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8
Q

What are the two real mechanisms of action of general anaesthetics?

A

Reduced neuronal excitability Altered synaptic function

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9
Q

Describe the difference in the selectivity of IV and inhalational agents.

A

IV agents are more selective for GABA-A Inhalational agents are far less selective

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10
Q

Which specific subunits of the GABA-A receptor do IV agents thatalter synaptic function target and what are their effects?

A

Beta 3 – important in suppression of reflex responses Alpha 5 – important in amnesia

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11
Q

What are the two main targets of inhalational agents that alter synaptic function?

A

GABA-A receptors Glycine receptors

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12
Q

Which subunit of the GABA-A receptor do inhalational agents seem to be more selective for?

A

Alpha 1 – important in suppression of reflex responses

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13
Q

Explain how nitrous oxide induces its anaesthetic effect.

A

Nitrous oxide competes for the glycine-binding site on NMDA receptors (glutamate receptors) Glycine is an important coagonist of NMDA receptors – it allows the full receptor response to be transduced

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14
Q

What is the effect of blocking neuronal nicotinic acetylcholinereceptors with regards to general anaesthesia?

A

Blocking nAChR leads to reduced nerve conduction This is important for amnesia and relief of pain

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15
Q

Which channels are important in reducing neuronal excitability via the action of inhalational agents?

A

TREK – background leak K+ channels These lead to hyperpolarisation of neurones and inhalational agents facilitate the opening of these channels

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16
Q

Inhalational agents are less selective than IV agents. What effect does this have on the dose needed to induce general anaesthesia?

A

Generally speaking, a higher dose of inhalational agents is required

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17
Q

Explain how general anaesthetics cause a loss of consciousness.

A

Loss of consciousness is caused by depressing the excitability of thalamocortical neurones This is mediated by TREK channels and GABA-A NOTE: the reticular activating system is also involved

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18
Q

Explain how general anaesthetics suppress reflex responses.

A

Depression of reflex pathways in the dorsal horn of the spinal cord This is done by anaesthetics that enhance GABA-A and glycine function

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19
Q

Explain how general anaesthetics cause amnesia.

A

There are a lot of GABA-A receptors in the hippocampus that have the alpha 5 subunit General anaesthetics stimulate these receptors to decrease synaptic transmission in the hippocampus

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20
Q

Explain how blood: gas partition coefficient affects the speed at which the general anaesthetic penetrates the brain.

A

If you have a GA that dissolves really well in the blood, then there is less GA in the gas phase in blood and hence less GA penetrates the blood-brain barrier and reaches the brain It is only anaesthetic that remains in the gas phase that diffuses easily into the brain

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21
Q

Would a general anaesthetics with a high or low blood: gas partition coefficient be useful for anaesthetics and why?

A

LOW This means that less of the GA will dissolve in the blood so more will be left in the gas phase Hence more of the drug will penetrate the blood-brain barrier and reach the brain

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22
Q

What are the benefits of inhalation anaesthetics?

A

Rapidly eliminated Good control of the depth of anaesthesia

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23
Q

What are the benefits of IV anaesthetics?

A

Fast induction Less coughing/excitatory phenomena

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24
Q

What types of drugs can be used to achieve: a. Relief of pain b. Muscle relaxation c. Amnesia

A

a. Relief of pain Opioids b. Muscle relaxation Neuromuscular blockers c. Amnesia Benzodiazepines

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25
Q

What three techniques are used to monitor activity during sleep?

A

Electroencephalography (EEG) Electromyography (EMG) Electrooculography (EOG)

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26
Q

Describe the EEG and EMG activity in wakefulness.

A

EEG – fast brain rhythm – beta waves (~30 Hz) EMG – reasonable amount of muscle tone because you are maintaining posture and ready for action

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27
Q

Describe the EEG, EMG and EOG activity in non-REM sleep.

A

Stage 1+2  Light sleep  EEG – theta (4-8 Hz) waves – gradually becoming more and more drowsy  EOG – NO eye movements  EMG – muscle activity reduced considerably Stage 3+4  Very deep sleep  EEG - Delta activity (< 4 Hz)  EOG – minimal eye movement  EMG – continued relaxation of muscles

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28
Q

Describe the EEG, EMG and EOG activity in REM sleep.

A

EEG – brain shifts abruptly back to fast rhythm (similar to wakefulness) EOG – rapid eye movement EMG – muscle activity at its lowest – subject is basically paralysed

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29
Q

How long is a normal sleep cycle?

A

1-1.5 hours

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30
Q

Compare the relative amounts of NREM and REM sleep in a sleep cycle at the start of a night’s sleep and at the end.

A

Start of the night – more NREM sleep End of the night – more REM sleep

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31
Q

Describe how heart rate and respiratory rate change during sleep.

A

SLOW during NREM FAST during REM sleep

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32
Q

Which system is responsible for maintaining consciousness?

A

Reticular activating system

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33
Q

How does the reticular activating system control the activity of the cortex?

A

Either via direct connections Or via indirect connections through the intralaminar nuclei of the thalamus

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34
Q

What are the two important nuclei in the hypothalamus that are responsible for influencing the reticular activating system and, hence, regulating the sleep-wake cycle?

A

Lateral Hypothalamus – excitatory Ventrolateral Preoptic Nucleus – promotes sleep NOTE: they have an antagonistic relationship

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35
Q

Describe the circadian synchronisation of the sleep-wake cycle.

A

The suprachiasmatic nucleus is responsible for synchronising the sleep-wake cycle with falling light level It receives an input from the retina (not from the usual photogenic cells) and as light level falls the suprachiasmatic nucleus becomes more active

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36
Q

Describe the effect of the suprachiasmatic nucleus on the nuclei within the hypothalamus.

A

Falling light level –> increased activity of suprachiasmatic nucleus This leads to activation of ventrolateral preoptic nucleus and inhibition of lateral hypothalamus so you become sleepier

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37
Q

What other important projection does the suprachiasmatic nucleus have and what is the importance of this projection?

A

Projection to the pineal gland Increase in suprachiasmatic nucleus activity leads to activation of pineal gland so that it releases melatonin Melatonin adjusts various physiological processes in the body that fit with sleep

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38
Q

What are some consequences of sleep deprivation?

A

Sleepiness/irritability Performance decrements Concentration difficulties Glucose intolerance – risk of diabetes Reduced leptin Hallucinations

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39
Q

Describe three ways in which sleep is regulated after sleep deprivation.

A

Reduced latency of sleep onset (fall asleep faster) Increased NREM sleep (sleep for longer) Increased REM sleep (after selective REM sleep deprivation)

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40
Q

During what stages of sleep can you dream?

A

Both NREM and REM but you tend to dream more and are able to recall dreams better during REM sleep

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41
Q

Describe the brain activity of the limbic system compared to the frontal lobe in sleep.

A

Brain activity in the limbic system is higher than in the frontal lobe This is because the content of dreams tends to be more emotional thanin real life

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42
Q

Sleep is important in memory consolidation. What is the difference in memory consolidation between NREM and REM sleep?

A

NREM – declarative = facts and events REM – procedural = learning skills

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43
Q

State some causes of insomnia that are physiological or due tobrain dysfunction.

A

Physiological – sleep apnoea, chronic pain Brain Dysfunction – depression, fatal familial insomnia

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44
Q

Hypnotics can be used to treat insomnia. How do they work?

A

They enhance the inhibitory (GABAergic) circuits in the brain

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45
Q

What is narcolepsy?

A

A condition characterised by an extreme tendency to fall asleep whenever in relaxing surroundings

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46
Q

What is cataplexy?

A

Sudden onset of muscle weakness that may be precipitated by excitement or emotion

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47
Q

Explain narcolepsy with regards to the sleep cycle.

A

It tends to be due to a dysfunction of control of REM sleep Patients go straight to REM sleep without going through NREM sleep so they become paralysed

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48
Q

What is narcolepsy caused by?

A

Orexin deficiency Orexin is a neuropeptide, which is the neurotransmitter in the lateral hypothalamus Orexin deficiency could be autoimmune or genetic Manage with tight control of sleep

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49
Q

What are the potential consequences of working night shifts?

A

Physiological processes could become desynchronised This can lead to sleep disorders, fatigue and increased risk of some conditions such as obesity, diabetes and cancer

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50
Q

Pathophys of sleep disorders?

A
  • sleep-wake cycle governed by complex group of biologic processes that serve as internal clocks - suprachiasmatic nucleus - pineal gland - other NTs involved: serotonin (arousal) NE (arousal) acetylcholine dopamine GABA (sleep promoting)
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51
Q

2 diff sleep stages?

A
  • REM sleep - non-REM (NREM) sleep: 4 progressive categories
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52
Q

How does breathing change during sleep?

A
  • stages 1&2 of NREM show cylcic waning and waxing of tidal volume and RR, which can include brief periods of apnea called periodic breathing - in stages 3&4 of NREM breathing becomes more regular - ventilation is 1-2 L/min less than awake: CO2 2-8 mm Hg greater, O2 5-10 mmHg les, pH decreases 0.03-0.05 - resp control mechanisms are intact during NREM sleep - REM sleep respirations become irregular (not periodic) and may include short periods of apnea
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53
Q

Epidemiology of sleep disorders?

A
  • 1/3 of Americans have sleep disorders at some pt - 20-40% adults report difficulty, but only 17% report that it is serious problem - 20% report chronic insomnia - elderly - more common in women: menstrual cycle and menopause - OSA - more common in men
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54
Q

RFs of sleep disorders?

A
  • sleep deprivation exists when sleep is insufficient to support adequate alertness, performance and health - stress, depression, anxiety, jet lag
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55
Q

Types of sleep disorders?

A
  • insomnia - hypersomnolence - narcolepsy - breathing related sleep disorders - circadian rhythm sleep-wake disorders - non-rapid eye movement sleep arousal disorders - REM sleep behavior disorder - movement disorder
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56
Q

What is insomnia? More common in women or men? What can insomnia cause?

A
  • difficulty initiating, maintaining sleep, or waking up early in the AM w/o ability to return to sleep - prevalence of the complaint of insomsnia higher in women: 40% to 30% - insomnia causes: impaired ability to concentrate, and poor memory
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57
Q

Common factors assoc with insomnia?

A
  • stress, caffeine, physical discomfort, daytime napping, early bedtimes - depression and manic disorders
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58
Q

3 major causes of insomnia?

A

-medical conditions - psych conditions - enviro problems

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59
Q

Medical conditions that can cause insomnia?

A
  • cardiac: CHF - neuro - pulmonary: COPD, asthma - GI: acid reflux - substances: stimulants, corticosteroids
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60
Q

Pysch conditions that can cause insomnia?

A
  • depression - anxiety - PTSD - panic disorder - psychotropic meds
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61
Q

Enviro conditions that can cause insomnia?

A
  • bereavement - shift work - jet lag - changes in altitude - temperature
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62
Q

Effects of sleep deprivation on the body?

A
  • impaired brain activity - cognitive dysfxn - moodiness - depression - accident prone - cold and flu - DM II - heart disease - HTN - wt gain - weakened immune response - micro sleep - hallucinations - memory problems - yawning - accidental death
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63
Q

Sxs of insomnia?

A
  • difficulty falling asleep and staying asleep - daytime sleepiness - irritability - fatigue/malaise - increased errors or accidents
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64
Q

Dx insomnia?

A

sleep hx: - number of awakening - duration of awakening - duration of the problem sleep log: - bedtime - duration until sleep onset - final awakening time

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65
Q

Tx of insomnia?

A

-b/f instituting therapy, most pts are asked to maintain a sleep log for 2-4 weeks sleep hygiene: -optimal sleep enviro -optimal temp, light and ambient noise -use bedroom only for sleep - wind down b/f sleep - avoid caffeine, nicotine, beer, wine and liquor in 6-8 hrs b/f bedtime - go to bed only when sleepy

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66
Q

What else should you think of b/f tx pt with insomnia?

A
  • eval pts for other primary sleep disorders (sleep apnea) - impact of Rx meds - underlying medical, psych and substance abuse disorders - consultation for medical causes: psychiatrist neurologist pulmonologist sleep medicine specialist
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67
Q

Med consideration for tx of insomnia? What is typically used?

A
  • many agents are helpful - short term therapy is preferred to restore normal sleep pattern - hypnotic drugs are approved for 2 weeks or less of continuous use - in chronic insomnia, longer courses may be indicated which require long term monitoring
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68
Q

What are the meds used in insomnia when the pt has trouble getting to sleep?

A
  • zolpidem (ambien): 1st line - zalepon (sonata): alt
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69
Q

Zolpidem (Ambien) use? MOA? Preg? SEs?

A
  • 1st line for insomnia - trouble getting to sleep - MOA: interacts with GABA- benzodiazepine receptor complexes - dose: 5-15 mg PO hs - preg: B - SEs: abdominal pain, rebound tenderness, HA half life: 1.5-2.4 hrs
70
Q

Zaleplon (sonata) use? MOA? Preg? SEs?

A
  • alt use in trouble getting to sleep (insomnia) - MOA: interacts with GABA-benzodiazepine receptor complexes - dose 5-10 mg PO qhs - preg C - SEs: HA, dizziness, nausea - half life: 1 hr
71
Q

First line med for trouble maintaining sleep (insomnia)? MOA Preg SEs?

A
  • Eszopiclone (lunesta) - MOA: interacts with GABA-benzodiazepine receptor complexes - dose: 1-3 mg PO qhs - SEs: unpleasant taste, amnesia, hallucinations - Half life: 5-7 hrs
72
Q

Benzodiazepines use? MOA SEs What pts should use caution while on this drug?

A
  • insomnia - traizolam, lorazepam, estazolam - MOA: bind to several GABA type A receptor subtypes - SEs: daytime sedation, lightheadedness, dependence * depresses breathing - be careful in COPD, other breathing disorders
73
Q

Melatonin agonists use? MOA? SEs CI

A
  • insomnia - ramelteon - MOA: binds to melatonin receptors expressed in suprachiasmatic nucleus - SE: somnolence - CI: with fluvoxamine (Luvox) - half life: 1.5-5 hrs
74
Q

Use of orexin receptor antagonists?

A
  • used for sleep onset or maintenance in insomnia - Suvorexant (belsomra) - MOA: blocks binding of wake promoting neuropeptides orexin A and orexin B to receptors OZ1R and OX2R - Preg C - SE: drowsiness HA abnorm dreams LE weakness cough
75
Q

What is hypersomnolence disorder? Sxs?

A
  • charact. by recurrent episodes of excessive daytime sleepiness or prolonged nighttime sleep - typically affects adolescents and young adults - have difficulty waking from a long sleep and may feel disoriented - other sxs: anxiety increased irritation decreased energy restlessness trouble fxning
76
Q

Dx criteria for hypersomnolence?

A
  • predominant feature is excessive sleepiness for at least 1 month (acute) or at least 3 months (persistent) as evidence by either prolonged sleep episodes or daytime sleep episodes that occur at least 3x/week: -excessive sleepiness causes distress or impairment -not caused by insomnia or any other sleep disorder - sleepiness isn’t due to getting enough sleep - drugs, meds, and medical conditions can’t cause sleepiness
77
Q

Non-pharm txs of hyper somnolence?

A
  • take naps whenever possible - maintain regular sleep schedule - avoid alcohol and meds that cause drowsiness
78
Q

Rx tx for hypersomnolence? First line? MOA? Preg? SEs?

A
  • Modafinil (provigil) - MOA: not well understood, but may increase dopaminergic signaling - dose: 200 mg qAM, up to 300-400 mg - Preg C - common SEs: HA Nausea nervousness dry mouth
79
Q

2nd line tx for hyper somnolence? MOA preg? SEs? BBW?

A
  • dextroamphetamine - MOA: not well understood, stimulates CNS activity, blocks reuptake and increases release of NE and dopamine in extraneuronal space (sympathomimetic) - dose: 5 mg bid - preg C - SEs: HTN, anorexia, and addiction BBW: high abuse potential!!
80
Q

What is narcolepsy? etiology?

A
  • syndrome of daytime sleepiness with cataplexy (transient muscle weakness resulting in sudden loss of postural tone - result in falls to floor), hypnagogic hallucinations, and sleep paralysis - 2nd most common cause of disabling daytime sleepiness - typically begins in teens and early 20s - etiology: loss or orexin (hypocretin) signaling genetic factors brain lesions (rare)
81
Q

Signs and sxs of narcolepsy?

A

-periods of extreme drowsiness during the day, may feel strong urge to sleep, often followed by short nap (sleep attack) -tetrad of sxs: lasts for about 15 min each, can be longer may happen after eating, driving, talking to someone most often - person wakes feeling refreshed - sudden brief (15 min) sleep attacks may occur during any type of activity - sleep paralysis: generalized flaccidity of muscles with full consciousness in transition zone b/t sleep and wakening - cataplexy: sudden loss of muscle tone in small muscles or generalized muscle weakness while awake that makes them slump to floor unable to move, strong emotions can trigger this - attacks lasts shorter than 30 sec, in severe cases - person may fall and stay paralyzed for as long as several minutes - hypnagogic hallucinations, visual or auditory, whichmay precede sleep or occur during sleep attack

82
Q

dx of narcolepsy?

A
  • hx of daytime sleepiness - absence of underlying nocturnal sleep disorders - epworth sleepiness scale - polysomnogram (PSG): recording of biophysiological changes during sleep: EEG, eye movements (EOG), muscle activity (EMG), and heart rhythm (ECG) - mult sleep latency test
83
Q

non-pharm tx for narcolepsy?

A
  • good sleep hygiene - take 1 to 3 planned 15-20 min naps/day - avoid certain drugs
84
Q

First line Rx tx for narcolepsy? What else is this used for? MOA? preg? SEs?

A
  • modafinil (provigil) - also used 1st line for hypersomnolence = MOA: may increase dopaminergic signaling - preg C - Ses: HA, Nausea, nervousness, dry mouth
85
Q

2nd line therapy for narcolepsy?

A
  • dextroamphetamine - also used 2nd line for hyper somnolence - MOA: stim CNS activity, blocks reuptake and increases release of NE and dopamine in extraneuronal space (symp) - preg C - SEs: HTN, anorexia, addiction - BBW: high abuse potential
86
Q

How common is OSA? Who does ic commmonly affect?

A
  • 2-5% of adults in US - primarily middle aged or elderly men
87
Q

Classic presentation of OSA?

A
  • obese pt - loud snoring - multiple arousals or awakenings during the night - gasping for breath
88
Q

What does OSA result in?

A
  • sleep fragmentation - daytime sleepiness - morning HA - impaired occupational performances - exacerbated by alcohol use at bedtime and sedative hypnotic drugs
89
Q

RFs for OSA?

A
  • obesity (BMI greater than 30) - neck circum greater than 17 in - narrow airway - large tongue
90
Q

Screeninga nd dx for OSA?

A
  • pt complaints - sleep partner complaints - epworth sleepiness scale - sleep studies
91
Q

What is included in the polysomnography (PSG)?

A
  • EOG: electrooculogram (recording eye movements) - EMG - EEG - EKG - tracheal noise - nasal and oral airflow - thoracic and abdominal resp effort - leg movement - pulse Ox, capnography, end tidal CO2
92
Q

Tx of OSA?

A
  • wt loss - smoking cessation CPAP: -air pressure mask -keeps upper airway passages open -Delivers O2 -cumbersome but getting better other options: oral appliances surgery - mandibular advancement, UPPP
93
Q

What is Central sleep apnea? How is it ID? causes?

A
  • defined by repetitive cessation or decrease of both airflow and ventilatory effort during sleep - primary CSA is rare, usually mixed with OSA - presents similar to OSA and ID on polysomnography - causes: stroke or brain tumor a-fib or CHF neuromuscular disorders
94
Q

Tx for CSA?

A

-tx underlying cause -if pt is sx with no apneic SEs then monitor - CPAP - 1st line therapy, BiPAP may be used if no response to CPAP - meds: acetazolamide (diamox), or theophylin

95
Q

What is Pickwickian syndrome? Dx? Tx?

A
  • obesity hypoventilation syndrome: -combo of brain’s control over breathing and obesity. -Often tired due to sleep loss, poor sleep quality, and chronic low blood O2 levels -alveoloar hypoventilation results from combo of blunted vent drive and increase mechanical load imposed on chest by obesity -most pts suffer from OSA -dx: polysomnogram -tx: wt loss (diet and surgery) Bipap resp stimulants: theophylline, acetazolamide, and medroxyprogesterone acetate, O2, tracheostomy (severe cases)
96
Q

What is a circadian rhythm disorder? What disorders are included?

A
  • disruption in person’s internal body clock that regulates 24 hr cycle of biological procees - disruption results from either malfxn in internal body clock or mismatch b/t internal body clock and external enviro regarding timing and duration of sleep - includes: delayed sleep phase disorder (DSPD) advanced sleep phase disorder (ASPD) non-24-hr-sleep wake disorder (NON-24) irregular sleep-wake disorder (ISWD) shift work disorder
97
Q

What is delayed sleep phase disorder? (DSPD) Most common in?

A
  • most common in adolescents/young adults - night owl tendencies delay sleep onset - if allowed to sleep in (around 3 pm) person ok - causes daytime sleepiness - most are often alert, productive and creative late at night
98
Q

WHat is ASPD? Seen in what pop?

A
  • usually seen in elderly - person has early bedtimes (6-9) and early morning waking (2-5 am) - usually sleep in late afternoon or early evening - morning larks
99
Q

NON-24? Common in what pops? Sxs? Tx?

A
  • condition in which a person’s day length is longer than 24 hrs - commonly seen in blind - impairs ability to fxn at school, work, or at their social lives - sxs: cog dysfxn, confusion, extreme fatigue, HA tx: bright light therapy and melatonin - hetlioz (tasimelteon): first drug for NON-24 in blind pts moa: binds to melatonin MT1 and 2 receptors - preg C, SEs: HA, and abnormal dreams
100
Q

ISWD? Sxs?

A
  • irregular sleep wake syndrome is sleeping w/o any real schedule - usually occurs in person who has problem with brain fxn and who doesn’t have a regular routine during the day - sxs: sleeping or napping more than usual during the day. Trouble falling asleep or staying asleep at noc Waking up often during the noc
101
Q

What is shift work disorder?

A
  • people who rotate shifts or work at noc - work schedule conflicts with circadian rhythm - results in insomnia or excessive sleepiness
102
Q

Tx of CRD?

A
  • light therapy - combo of planned sleep scheduling, timed light exposure, and timed melatonin - hetlioz for non-24 pts who are blind - good sleep hygiene
103
Q

What are NREM sleep arousal disorders?

A
  • sleepwalking - sleep terrors - enuresis
104
Q

What part of sleep stage does sleepwalking (somnambulism) occur? What occurs during sleepwalking? Causes?

A
  • occurs during stage 3 & 4 - usually 8-12 yo - during first few hours of sleep and in REM sleep in later hours - includes ambulation or other intricate behaviors while sleeping - can be agitated or aggressie when aroused - no recollection of event - causes: idiosycratic drugs (marijuana, ETOH), medical conditions (seizures)
105
Q

What are night terrors? when do they occur, and in who are they most common in? Sxs?

A
  • (pavor nocturnus) - abrupt terrifying arousal from sleep - stages 3 & 4 - usually in preadolescent boys - marked vocalization and movement - hard to wake person during episode - unable to recall the event - sxs: fear, sweating, tachycardia
106
Q

Tx of NREM sleep arousal disorders?

A
  • improving sleep first line tx - setting a regular bedtime - practicing relaxation - limit food or drink b/f sleeping - est a bedtime routine - scheduled awakenings
107
Q

Enuresis? When does it occur? Tx?

A
  • involuntary micturition during sleep in person with voluntary control - more common in kids - usually 3-4th hr of bedtime - not limited to stages of sleep - amnesia for event is common - difficult to awake -tx: simple behavioral interventions first line approaches, DDAVP, oxybutynin, imipramine,alarm systems (parents have to take active role)
108
Q

REM sleep behavior disorder? Common in? Dx? Tx?

A
  • chracterized by dream-enactment that happens during a loss of REM sleep atonia - ranges from hand gestures to violent thrashing, punching, and kicking - among young adults who take antidepressants, narcoplepsy, or alpha-synyclein neurodegeneration (elderly) - dx: polysomnography - tx: est safe sleep enviro melatonin: 1st line, moa: prepares body for sleep, SEs: abnorm heartbeat, dizziness, and fatigue clonazepam
109
Q

What is RLS?

A
  • disorder in which there is an urge or need to move legs to stop unpleasant sensations - C/O sensation of wanting to move legs while awake, “heebie jeebies”, or “creepy crawler” sensations - occurs while awake as well as when sleeping - makes falling asleep difficult - sleep partner complaints
110
Q

Causes of RLS?

A
  • CKD - diabetes - Fe deficiency - parkinson’s disease - peripheral neuropathy - pregnancy - use of certain meds such as caffeine, CCBs, lithium or neuroleptics - withdrawal from sedative - chronic venous insufficiency (varicose veins)
111
Q

Tx for RLS?

A
  • stretching, massage, warm baths - avoid caffeine: chocolate, coffee, tea and pop - tx or control underlying disease - meds: Fe supp: try first with non-pharm options 1st line after above has been tried: dopamine agonist - ropinirole (requip) alpha-2-delta calcium channel ligands: gabapentin
112
Q

For what other disease do we use ropinirole (requip)?

A
  • parkinson’s
113
Q

What is bruxism? pts hx? tx?

A
  • teeth gnashing/grinding - hx: pt c/o of jaw soreness, flattening of teeth and radiating AM headaches -tx: clonazepam botox referral to be custom fitted for nocturnal oral appliances relaxation and behavioral therapy
114
Q

What is periodic limb movement disorder? Dx? Tx?

A
  • pt moves limbs involuntarily during sleep and has sxs or problems related to the movement - pt is often unaware - unknown etiology but may be related to other medical problems sich as PD or narcolepsy -dx with aid of PSG - tx: 1st line: dopamine agonist anticonvulsants benzodiazepines
115
Q

EEG? Uses?

A
  • measures and records the electrical activity of the brain - electrodes placed and connected to a computer -uses: study sleep disorders Dx epilepsy and type of seizure Check for problems with LOC or dementia
116
Q

Other dxs used in sleep disorders?

A
  • sleep hx - sleep diary - outpt: overnight oximetry, actigraphy (measures gross motor activity) - inpt: PSG, mult sleep latency test
117
Q

What should be included in your pt hx?

A
  • psch, medical or med changes - impairment of sleep onset - trouble staying asleep: mult awakenings, early awakenings - partial arousal - breathing abnorm - involuntary movements - normal but non refreshing sleep - epworth sleepiness scale
118
Q

Another name for a concussion? What is it caused by? What does it result in?

A
  • TBI trauma induced alteration in mental status may or may not involve loss of consciousness - caused by direct blow to head, face, neck or body - result in neuropathological changes: fxnl not structural - resolution of clinical and cognitive sx follows a sequential course - assoc with grossly normal neuroimaging studies
119
Q

Eye opening - Glasgow scale?

A
  • spontaneous 4 - response to verbal command 3 - response to pain 2 - no eye opening 1
120
Q

Best verbal response - glasgow scale?

A
  • oriented 5 - confused 4 - inappropriate words 3 - incomprehensible sounds 2 - no verbal response 1
121
Q

Best motor response - glasgow scale?

A
  • obeys commands 6 - localizing response to pain 5 - withdrawal response to pain 4 - flexion to pain 3 - extension to pain 2 - no motor response 1
122
Q

What is a TBI? pts at highest risk? Rating on GCS?

A
  • head injury due to contact and/or acceleration and/or deceleration forces - 1.5 mill reported incidents/yr in US - TBI leading cause of death for persons age 1-45 in north america, males greater than females, 5 mill people suffer TBI disability - pts at higher risk: less than 5 and older than 60 (fall prone) - mild: GCS 13-15 measured 30 min after injury - moderate: GCS 9-12 - severe: GCS less than 8
123
Q

Etiologies of TBI?

A
  • MVAs (20-45%) - falls (30-38%, increasing in older pt) - occupational accidents (10%) - assaults (5-17% - increasing) - contact sports - soldiers in combat
124
Q

Primary injury phase - cortical contusion (direct trauma)

A
  • coup-direct blow to brain - contrecoup injury to brain on opp side of head - severe: axonal rupture - mild: diffuse axonal injury: disruption of axonal neurofilament organization, impairs axonal transport and leads to axonal swelling
125
Q

Secondary brain injury pathophys?

A
  • begins quickly after primary phase - continues for hours to days - cascade of molecular injury mechanisms: -NT mediated excitotoxicity causing glutamate, free radical injury to cell membranes -electrolyte imbalances -mitochondria dysfxn -apoptosis -secondary ischemia from vasospasm, focal microvascular occlusion and vascular injury
126
Q

Clinical features of TBI? Assoc sxs?

A
    • or - LOC, confusion, stupor, amnesia: impt to know presence and length of any of these sxs - assoc sxs: HA, dizziness, disorientation, N/V
127
Q

TBI signs?

A
  • vacant stare - inabilty to focus - gross incoordination - memory difficulties - delayed verbal expression - slurred or incoherent speech - emotionality out of proportion to events
128
Q

Complicated TBI? assoc signs and sxs?

A
  • indicates more serious brain injury or rising ICP: seizures focal neuro signs worsening HA, confusion, lethargy protracted N/V other injuries to head/neck decreasing GCS (keep on repeating GCS - is it deteriorating?)
129
Q

Management of TBI?

A
  • examine - look at pupils, do neuro exam: CNs, reflexes, strength, touch, movements - amnesia almost always involves loss of memory of traumatic event and frequently includes loss of recall for events immediately before and after trauma - longer the frame of amnesia - more serious the injury
130
Q

What are the guidelines for CT scan in ER?

A
  • GCS less than 15 - open or depressed skull fracture - any sign of basilar skull fracture: CSF leak - 2 or more episodes of vomiting - 65 yo or older - amnesia b/f impact of 3 or more minutes - dangerous mech (ejected from vehicle, fall from more than 3 ft) - bleeding diathesis or an oral anticoagulant (increased chance of brain bleed) - seizure or focal neuro sign - intoxication (drunk or brain injury - have to rule it out)
131
Q

What are signs of a basilar skull fracture?

A
  • raccoon eyes - hematoma behind ears (battle sign) - hemotympani - CSF draining out of ears or nose - fracture is hard to detect on CT - do MRI
132
Q

CT scan abnormalities?

A
  • subdural hematoma - intracranial bleeding - cerebral edema - skull fracture
133
Q

What TBI pts should be hospitalized?

A
  • hospitalization for those at risk: GCS less than 15 or deteriorating abnorm CT seizures abnormal bleeding parameters
134
Q

Criteria for TBI pts who can be observed as outpt?

A

GCS=13-15, normal CT scan outpt: must have responsible companion!!! - somnolence or confusion - diff w/ vision, severe or worsening HA - urinary or bowel incont. - weakness or numbness involving any body part - unsteadiness or seizures - N/V more than 2 episodes - allow the pt to rest as needed but check on pt if any of the above occur return to ED

135
Q

Sequela from TBI?

A
  • post-concussion syndrome - post-traumatic HAs - post-traumatic seizures/epilepsy - post-traumatic vertigo - other CN injuries - second impact syndrome - cumulative neuropsych impairment: boxers - dementia pugilistica (20%),, football players - CTE
136
Q

Sxs of post-concussion syndrome (PCS)? RFs?

A
  • HA - dizziness - neuropyschiatric - cog impairment including noise sensitivity - PP: direct brain injury, psychogenic - female gender and increasing age: RFs
137
Q

Dx and Tx of PCS?

A
  • Dx: clinically and w/ hx - if severe sx and pt hasn’t had MRI - get one! - Tx: education!!!! minimize meds, but use appropriately, low dose - typically resolves by 3 months 90% of the time - may need more extensive neurocognitive rehab
138
Q

How can we prevent TBIs?

A
  • sport-specific helmets: used in baseball, hockey, alpine sports found to reduce injuries - helmets used in soccer haven’t been found to reduce rate of head injury - in some cases use of protective equipment may encourage risky behavior - Bicycle and motorcycle helmets do reduce accident related head injuries!!
139
Q

Definition of coma? common etiologies?

A
  • unarousable and unresponsive (lasts longer than 1 hr) - common etiologies: TBI hypoxic ischemic encephalopathy (HIE) drug overdose intracranial hemorrhage CNS infections brain tumors
140
Q

etiologies of coma? Systematically?

A
  • primary cerebral: bilateral, unilateral - brain stem disorders (pons, midbrain) - systemic (toxins: meds, drug overdoses) - endocrine
141
Q

What is the ARAS?

A
  • ascending reticular activating system (ARAS): originates upper pons and midbrain, the neurons project to thalamus and hypothalamus then to cerebral cortex - focal lesions to upper brainstem can alter alertness by damaging ARAS - in coma with toxic, metabolic and infectious etiologies mecahnism less well understood
142
Q

What information do you want from the pt’s hx?

A

obtained from family, witnesses, medical personnel: -time course of LOC -focal signs or sxs precede? -pt have previous neuro episode? -recent illness, fever, HA, falls, confusion? - Rx drugs, illicit drugs or alcohol?

143
Q

What should you focus on during PE?

A
  • complete with special attention to: LOC brainstem reflexes pupillary light, EOM and corneal reflexes - motor exam: assess muscle tone, spontaneous and elicited movements - note if asymmetric, reflexes
144
Q

Coma posturing and meaning?

A
  • decorticate: UE adduction with LE extension - dysfxn of cerebral cortex or thalamic damage (has better prognosis) - decerebrate posturing: UE extension, adduction and pronation with LE extension - injury to caudal diencephalon, midbrain or pons
145
Q

Different respiratory patterns seen with coma?

A
  • cheyne-stokes: cyclic pattern, hypernea, apnea: seen in pts with bilateral hemispheric or diencephalic insults - hyperventilation - injury to pontine or midbrain tegmentum - apneustic breathing: prolonged pause end of inspiration- indicates lesion to mid- and caudal pons - ataxic breathing: irregular in rate and tidal volume- damge to medulla
146
Q

Dx goal in coma?

A

ID tx causes: - infection, metabolic abnorm, seizures, intoxications/overdoses, surgical lesions - give O2, thiamin, fluids, narcan, glucose - papilledema/focal neuro findings suggest structural etiology - urgent brain CT - neuorimaging and coag test BEFORE lumbar puncture - IICP - LP: don’t delay tx if LP is delayed, get blood cultures - EEG: used primarily to detect seizures

147
Q

Labs to order in coma pts?

A
  • CBC - CMP (w/ Ca and magnesium) - TSH - Tox screenings - UA - adrenal fxn tests - carboxy hemoglobin - specific drug concentrations
148
Q

Management of coma pt?

A
  • ID tx causes - supportive: protect airway, hydrate, monitor blood glucose and electrolytes
149
Q

What are the four different forms of cocaine and how are theymade?

A

Cocaine paste –this is simply the plant (erythroxylum coca) mushed up in a solvent Cocaine HCl – therapeutic form of cocaine: you take the cocaine paste and dissolve it in an acidic solution Crack – cocaine is precipitated with an alkaline solution (e.g. baking soda) Freebase – slightly purer form of crack: you take crack and dissolve it in a non-polar solvent (e.g. ammonia and ether)

150
Q

Which route of administration of cocaine gives the fastest absorption?

A

Smoking (though IV gives a higher bioavailability)

151
Q

Why is cocaine very slowly absorbed in the GI tract?

A

Cocaine has a pKa of 8.7 so it is mainly ionised in the stomach meaning that it isn’t very lipid soluble and it isn’t very easily absorbed This does, however, mean that the cocaine has a prolonged action

152
Q

What is the half-life of cocaine?

A

20-90 mins

153
Q

Where is cocaine metabolised and what is it metabolised into?

A

Liver – inactive metabolites: ecgonine methyl ester+ benzoylecgonine Plasma – it can be metabolised by plasma cholinesterases so it doesn’t last long in the plasma

154
Q

Which factors affect the addictive potential of a drug?

A

The speed at which you associate the euphoria with taking the drug and the speed with which the effects are lost

155
Q

Explain how cocaine can act as a local anaesthetic.

A

Cocaine blocks sodium channels and hence inhibits nerve transmission

156
Q

By what mechanism does cocaine exert its most profound effects?

A

Inhibition of monoamine transporters – leads to an accumulation of monoamines (e.g. dopamine) at the synapse

157
Q

How does cocaine cause euphoria?

A

Cocaine blocks the monoamine transporters at the end of the dopaminergic neurones projecting to the nucleus accumbens – this leads to an accumulation of dopamine in the synapse at the nucleus accumbens –> EUPHORIA

158
Q

What are the differences between the effects of low dose cocaine and high dose/chronic cocaine use?

A

Low dose – positive reinforcement – more energetic, need less sleep, more sociable, more talkative High dose – negative/stereotypical effects – exhaustion, irritability, hostility, insomnia

159
Q

Describe how cocaine is associated with a significantly increased cardiovascular risk.

A

Cocaine causes an increase in sympathetic output (NOTE: noradrenaline is also a monoamine) This leads to vasoconstriction, thus causing an increase in cardiac work It will also activate platelets and promote atherosclerosis, leading to thenarrowing of vessels and decreased oxygen supply to the heart This could lead to myocardial infarction

160
Q

How can cocaine prompt seizures?

A

It causes vasoconstriction in various arteries of the brain and it also causes an increase in temperature, which can prompt seizures It is linked to the development of epilepsy

161
Q

What percentage of a cigarette is particulate and what percentage is volatile?

A

5% particulate 95% volatile

162
Q

Why is the nicotine delivery via a cigarette so effective?

A

Heating the cigarette melts the tar so that it forms lipid droplets The alkaloids dissolve in the lipid droplets, which are then widely distributed across the lungs and can be easily absorbed

163
Q

Which matter contains most carcinogenic elements?

A

Volatile

164
Q

Why is the cigarette not particularly efficient in delivering nicotine to the body?

A

Cigarette smoke is acidic whereas the pKa of nicotine prefers a more alkaline environment This means that the nicotine in cigarette smoke becomes ionised and, hence, it is less easily absorbed

165
Q

Describe the metabolism of nicotine. What is the product?

A

Nicotine is metabolised by CYP2A6 in the liver This produces COTININE, which is then excreted in the urine

166
Q

What is the half-life of nicotine?

A

1-4 hours

167
Q

Describe how nicotine causes euphoria.

A

Nicotine binds to nicotinic acetylcholine receptors on the cell bodies of dopaminergic neurones in the ventral tegmental area and stimulates sodium influx This leads to an increase in the firing rate of the dopaminergic neurones, hence, more dopamine secretion

168
Q

How does nicotine increase cardiovascular disease risk?

A

Nicotine causes an increase in sympathetic drive – increased heart rate and stroke volume, so more cardiac work Vasoconstriction of coronary arterioles – reduces oxygen delivery to the myocardium In addition it also promotes atherosclerosis and increases thromboxane A2 (hence increases platelet activity) All of these factors increase oxygen demand and decrease oxygen supply

169
Q

What effect does nicotine have on metabolism?

A

It increases metabolism So chronic smokers often find that they gain weight after quitting

170
Q

Explain how nicotine reduces the risk of Parkinson’s disease.

A

Nicotine increases the activity of the CYP450 enzymes in the brain, so it is better able at removing neurotoxins that have the potential to contribute to the onset of Parkinson’s disease

171
Q

Explain how nicotine reduces the risk of Alzheimer’s disease.

A

Chronic nicotine diminishes some of the proteins that contribute to Alzheimer’s disease (decrease in beta-amyloid toxicity, decrease in amyloid precursor protein)

172
Q

Explain how caffeine can cause mild euphoria.

A

Adenosine acts via adenosine receptors to decrease dopamine release and decrease D1 receptor function Caffeine is an adenosine receptor antagonist so it will remove the inhibitory effect of adenosine However, the inhibitory effect of adenosine is very minimal so caffeine will not cause a significant rise in dopamine release

Imperial (23 decks)

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