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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Makes a person withdrawn, quiet, sleep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
What are the effects of benzos
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
What are the endocrine effects of eomidates
Endocrine: dose dependent inhibition of 11B-hydroxlase (cannot produce cortisol or aldosterone)
27
What is flumazenil
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
What is dexemetomidine
Sedation, withdrawal, delirium, opioids sparing analgesia Alpha-2 receptor agonist (brain/spinal cord) Useful for awake craniectomy (sedation without resp depression)
29
How is dexemetomidien cleared
Almost complete biotransformation in liver with P450 system involvement Clearance is impaired in liver failure but not renal impairment due to inactive metabolites
30
What are the effects of dexemeomidine
CNS - sedation, analgesia, enhances neurological blockage (epidural), decrease CBF CVS - bradycardia, reduced CO, initial increase BP (peripheral alpha1 receptor agonism)
31
What are the ascending pain pathways
transmitting stimulus (C fibre is slow, A delta fast)
32
What is the main receptor of opioid binding
Mu | Agonist binding -> decreased release of NT + pain transmissions
33
What is morphine
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
What are the effects of morphine
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
What is fentanyl
``` 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
What does fentanyl target
Mu+delta
37
What is codine
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
What is tramadol
``` 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
What is naloxone
Competitive opioid receptor antagonist Different route IV (2 mins onset), IM (5 mins onset), nasal Short half life
40
What is TIVA
``` Propofol + remifentanil infusion IV Avoids conventional anaesthetic gases Improved CV profile Less nausea and vomiting Improved tube tolerance ```
41
What is remifentanil
``` Potent mu receptor agonist Ultra-short acting drug Rapid onset (1.3 minutes) Rapid offset (metabolised by specific non tissue esterase) ```
42
What is remifentanil used for
Sedation in ICU, PCA in obstetrics, pain relief during surgery, total intravenous anaesthesia
43
What are the signs of alcohol withdrawal
``` 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
What does alcohol do
Alcohol potentiates GABA as well as directly opening channel at high does GABA is main inhibitory NT in the brain
45
What does chronic drinking cause
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
What is alcohol withrawl
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
What is Wernicke-Korsakoff syndrome
(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
What are the signs of Wernicke-Korsakoff syndrome
Classic triad of ophthalmoplegia, ataxia, and confusion | Ask do you miss meals or suffer from pins and needles in hands or feet
49
What is GHB/GBL
GHB is a GABA analogue -> can be metabolised to GABA
50
What are the effects of GHB
``` 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
What is the mechanism of action of GHB
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
What does GHB withdrawal cuase
Anxiety, agitation, sweating, shaking, increased HR and BP, visual and auditory hallucinations Quicker onset than alcohol, fewer seizures and more DTs
53
How to detox GHB
Use CIWA Add benzodiazepines Initially 20 mg diazepam then reassess every couple of hours If not controlled, add baclofen
54
How do opiods affect resp drive
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
What is the treatment for opioid OD
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
What is SCRA
``` 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
How is SCRA withdrawal treated
``` Cardiac monitoring U&Es, LFTs, CK Fluids Benzodiazepines Anti-emetics Antipsychotics - safe - no reports of increased seizures Get liaison psychiatry involved ```

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