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Supporting Life > Acute Confusion > Flashcards

Acute Confusion Flashcards

1
Q

What is delirium

A

Condition of acute brain failure - characterised by acute onset, fluctuating course, disorientation, reduced awareness of surroundings, and other disturbances

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2
Q

What is hyperactive delirium (20%)

A

Makes a person restless, agitated, aggressive

Increased confusion, hallucinations, sleep disturbance, less co-operative

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3
Q

What is hypoactive delirium (40%)

A

Makes a person withdrawn, quiet, sleep

Poor concentration, less aware, reduced mobility, reduced appetite

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4
Q

When should pharmacological interventions for delirium be used

A

should only be considered if all non-pharmacological interventions have failed
Treatments should be short term (<1 wk)

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5
Q

What drugs are used to treat delirium

A

Haloperiodol (do ECG first to check QTe interval)
Lorazepam (if antipsychotics contraindicated e..g. Parkinson’s)
Chlordiazepoxide usually used for alcohol withdrawal

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6
Q

What are anaethesias

A

render unconscious (propofol, etomidate)

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7
Q

What are sedatives

A

reduce anxiety (enzodiazepines, barbiturates)

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8
Q

What are analgesias

A

relief of pain (morphine, fentanyl, codeine, tramadol)

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9
Q

What is propofol

A

Anaesthetic induction, maintenance of anaesthesia, sedation ,anti-emesis

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10
Q

What is the mechanism of action of propofol

A

Enhances GABA-induced chloride currents (hyperpolarisation of post synaptic membrane) + inhibits NMDA glutamate receptors
Increases dopamine in nucleus accumbens (sense of well-being)
Decreases serotonin in area postrema (anti-emetic)

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11
Q

What are the effects of propofol

A

Neurological: loss of consciousness, seizure suppression, decrease ICP, decrease IOP/CPP, antiemesis
Resp: obtunds laryngeal reflexes, causes apnoea, decreases TV, increases RR
CV: decrease CO, SVR, BP. Baroreceptor reflex inhibition. Decrease O2 consumption

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12
Q

How is propofol metabolised

A

Oxidised and conjugated in liver (makes it more polar). Excreted by kidneys. Competitive inhibitor of CYP4A54, increases duration of action of midazolam.

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13
Q

What are barbiturates

A

Anxiolytic, anaesthetic induction, seizure suppression, sleeping aids

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14
Q

What is the mechanism of action of barbiturates

A

Low dose: positive allosteric modulator (enhances GABA-A receptor effect)
High dose: directly stimulates GABA-A receptors causing increased chloride current and hyperpolarisation

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15
Q

What are the effects of barbiturates

A

Neuro: loss of consciousness, decrease CMRO2, ICP, CBF, seizure suppression
Resp: decrease TV, RR. Causes apnoea, bronchoconstriction
CV: peripheral vasodilation, negative inotrope, increase HR, can prolong QT interval

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16
Q

How are barbiturates metabolised

A

Induce Cyt P450 enzymes. Much longer context sensitive half time than propofol

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17
Q

What is ketamine

A

Analgesia (acute), sedation (paeds), anaesthetic induction, bronchodilation

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18
Q

What is the mechanism of action of ketamine

A

Phencyclidine binds to NMDA (can potentiate pain) receptor (antagonist)
Racemic mixture of S and R ketamine (S isomer more potent)
Produces dissociative anaesthesia because px may not appear asleep

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19
Q

What are the effects of ketamine

A

Neuro: increase CMRO2, CBF, ICP, emergence reaction, vivid dreams, extracorporeal experiences, hallucinations
Resp: transient decrease in MV but rarely apnoea. Bronchial smooth muscle relaxant, increase salivation
CV: increase BP, HR, CO and myocardial O2 consumption. Increases sympathetic nervous system, can cause pulmonary hypertension

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20
Q

How is ketamine metabolised

A

Metabolised in liver to norketamine (less activity than ketamine) and hydroxynorketamine
Metabolites excreted in urine
Bioavailability orally less than intranasally

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21
Q

What is eomidate

A

GABA-A facilitation (lower dose of GABA required to activate receptor) - does not decrease BP

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22
Q

What are the effects of eomidates

A

Neuro: decrease CBF, CMRO2, CPP maintained, decrease ICP

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23
Q

What are benzodiazepines

A

Sedative, anticonvulsant, co-induction agent, sleeping aid

24
Q

What is the mechanism of action of benzos

A

Bind to GABA-A receptor, enhance response to GABA
Midazolam (short acting) - rapid onset, hepatically metabolised by CYP system including active metabolite 1-hydroxymidazolam
Lorazepam and temazepam (intermediate) - conjugated in liver to inactive compounds
Diazepam (long acting)
Flunitrazepam (Rohpnol)

25
Q

What are the effects of benzos

A

Neuro: anxiolysis, sedation, amnesia, anticonvulsant
Resp: decrease muscular tone in upper airway, response to increased CO2, hypoxic response (synergistic effect with opioids)
CV: decreased SVR leading to small drop in BP, preserved baroreceptor reflexes, CO maintained

26
Q

What are the endocrine effects of eomidates

A

Endocrine: dose dependent inhibition of 11B-hydroxlase (cannot produce cortisol or aldosterone)

27
Q

What is flumazenil

A

benzo receptor antagonist
Competitive antagonist
Short half-life- may get rebound effect of agonist
Rapid onset, 1-3 minutes
Can cause seizures in px on chronic benzos

28
Q

What is dexemetomidine

A

Sedation, withdrawal, delirium, opioids sparing analgesia
Alpha-2 receptor agonist (brain/spinal cord)
Useful for awake craniectomy (sedation without resp depression)

29
Q

How is dexemetomidien cleared

A

Almost complete biotransformation in liver with P450 system involvement
Clearance is impaired in liver failure but not renal impairment due to inactive metabolites

30
Q

What are the effects of dexemeomidine

A

CNS - sedation, analgesia, enhances neurological blockage (epidural), decrease CBF
CVS - bradycardia, reduced CO, initial increase BP (peripheral alpha1 receptor agonism)

31
Q

What are the ascending pain pathways

A

transmitting stimulus (C fibre is slow, A delta fast)

32
Q

What is the main receptor of opioid binding

A

Mu

Agonist binding -> decreased release of NT + pain transmissions

33
Q

What is morphine

A

Analgesia, palliation, perioperative
Can be given, oral, subcut, IV, intrathecal ,transdermal
Metabolised in liver (glucorinated)
Active metabolite (morphine 6 - glucuronide) - potent + longer lived
Excreted via urine
Low lipid solubility - slow BBB penetration and slow onset

34
Q

What are the effects of morphine

A

Neuro: sedation, analgesia, euphoria, cough suppression
Morphine stimulates CTZ (nausea, vomiting)
Edinger Westphal nucleus of III nerve - constriction of pupil

Resp: resp suppression and increased ventilator response to CO2

CV: vasomotor centre suppression, morphine can stimulate vagal centre (bradycardia), histamine release (vasodilatation)

Other: constipation (GI receptors), pruritis (histamine release)

35
Q

What is fentanyl

A 
Synthetic opioid
80-100x more potent than morphine
Few CV effects
Less histamine release
High lipid solubility, enters brain rapidly and produces peak analgesia in 5 minutes after IV
Short duration of action (30-40 minutes)
Transdermal fentanyl now available
36
Q

What does fentanyl target

A

Mu+delta

37
Q

What is codine

A

50% analgesia potency compared to morphine
Given orally
Pro-drug>active metabolites (only works by metabolism in the liver)
Metabolised by CPY2D6. Caution in ultra-rapid metabolisers. Lack of efficacy in poor metabolisers. Susceptible to drug-drug interactions
Risk to neonates (and breast feeding mother if rapid metaboliser)

38
Q

What is tramadol

A 
Atypical opioid (analogue of codeine)
Targets mu receptors + NA/5HT reuptake inhibition  
Has active metabolite
1/10 potency of oral morphine
Safer cardio-resp profile
Risk of serotonin syndrome
39
Q

What is naloxone

A

Competitive opioid receptor antagonist
Different route IV (2 mins onset), IM (5 mins onset), nasal
Short half life

40
Q

What is TIVA

A 
Propofol + remifentanil infusion IV
Avoids conventional anaesthetic gases
Improved CV profile
Less nausea and vomiting
Improved tube tolerance
41
Q

What is remifentanil

A 
Potent mu receptor agonist
Ultra-short acting drug
Rapid onset (1.3 minutes)
Rapid offset (metabolised by specific non tissue esterase)
42
Q

What is remifentanil used for

A

Sedation in ICU, PCA in obstetrics, pain relief during surgery, total intravenous anaesthesia

43
Q

What are the signs of alcohol withdrawal

A 
Increase pulse and BP
Sweating
Shaking
Agitation
May be confused
Hallucinating - tactile, auditory, visual
May develop seizures
Does not have to be BAC 0.00mg/l
Use the CIWA-Ar to assess
44
Q

What does alcohol do

A

Alcohol potentiates GABA as well as directly opening channel at high does
GABA is main inhibitory NT in the brain

45
Q

What does chronic drinking cause

A

fewer and less responsive GABA-A receptors
Alcohol is also an NMDA antagonist - inhibits CA2+ influx through NMDA glutamate receptors - reducing neuronal excitation
Chronic alcohol leads to receptor up-regulation - associated with impaired memory

46
Q

What is alcohol withrawl

A

Alcohol withdrawal results from sudden removal of alcohol in the presence of glutamate/GABA imbalance
Increased excitation of glutamate NMDA receptor
Decreased inhition of GABA-ergic activity
Leads to Ca2+ influx í neuronal hyperexcitablilty, seizures, cell death

47
Q

What is Wernicke-Korsakoff syndrome

A

(cerebral thymine deficiency) - alcohol inhibits thymine absorption and inhibits thymine storage. When px stops drinking, thymine reserves are depleted -> acute confusion state ->Irreversible brain damage and amnesia

48
Q

What are the signs of Wernicke-Korsakoff syndrome

A

Classic triad of ophthalmoplegia, ataxia, and confusion

Ask do you miss meals or suffer from pins and needles in hands or feet

49
Q

What is GHB/GBL

A

GHB is a GABA analogue -> can be metabolised to GABA

50
Q

What are the effects of GHB

A 
Acute effects:
Euphoria
Increased sexual arousal, stamina and pleasure
Reduce negative self-esteem
Altered perception of time
Impaired memory
Salivation
Slouching and unsteadiness 
Loss of consciousness
Bradycardia, hypotension
Respiratory depression 
Death
51
Q

What is the mechanism of action of GHB

A

Binds to GABA-B receptors and specific receptors
Effect is to decrease GABA release
GHB binds to presynaptic GHB receptors
Effect is to decrease GABA release
In high conc, binds to post-synaptic GABA-B receptors - inhibit post synaptic neuron

52
Q

What does GHB withdrawal cuase

A

Anxiety, agitation, sweating, shaking, increased HR and BP, visual and auditory hallucinations
Quicker onset than alcohol, fewer seizures and more DTs

53
Q

How to detox GHB

A

Use CIWA
Add benzodiazepines
Initially 20 mg diazepam then reassess every couple of hours
If not controlled, add baclofen

54
Q

How do opiods affect resp drive

A

Suppress resp via action on regions in the medulla and pons which control ventilation
Central control of resp occurs in the brainstem and medulla
Chemoreceptors detect pO2 and pCO2 which usually stimulates resp drive
There are mu opioid receptors in both resp centres in the brainstem and medulla and in chemoreceptors
Stimulation of these receptors slows resp

55
Q

What is the treatment for opioid OD

A

Give 400 mcg naloxone injection into outer thigh or upper arm muscle

Naloxone:
Antagonist
Competes with opioids for binding sites, blocking their action
Naloxone has high affinity for the mu opioid receptor
Rapidly redistributed from brain
Half-life is 60-90 minutes
Too much can send px into acute opioid withdrawal

56
Q

What is SCRA

A 
G protein coupled receptors - CB1 (brain) and CB2 (immune system)
Widely distributed in the brain
Endocannabinoids - anandamide and 2-AG
Rewards
Learning and memory
57
Q

How is SCRA withdrawal treated

A 
Cardiac monitoring
U&amp;Es, LFTs, CK
Fluids
Benzodiazepines
Anti-emetics
Antipsychotics - safe - no reports of increased seizures
Get liaison psychiatry involved

Supporting Life (14 decks)

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