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ACEM Viva > Pharmacology - CNS & Autonomic > Flashcards

Pharmacology - CNS & Autonomic Flashcards

1
Q

What is the mechanism of action and clinical uses of carbamazapine

A
  • mechanism: blocks Na+ channels and inhibits high frequency firing
  • uses: anticonvulsant (partial and generalised tonic clonic seizures), bipolar mood disorder, trigeminal neuralgia
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2
Q

What is the metabolism, side effects and drug interactions of carbamazapine

A

-pharmacokinetics: well absorbed, slowed by meal, peak level 6-8 hours, 70% protein bound
metabolised by liver enzymes, induces itself, active metabolites

-adverse effects: diplopia and ataxia are most common, sedation, seizure, gi upset, agranulocytosis

-drug interactions: carbamazapine is a enzyme inducer
causes increased clearance of: warfarin, OCP phenytoin, valproate, lamotrigine

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3
Q

What is the mechanism of action, pharmacokinetics and side effects of phenytoin

A

-mechanism: blocks Na+ channel (preferentially binds to inactivated state), decreases glutamate, increases GABA

-pharmacokinetics: high bioavailability, highly protein bound, low VD, CSF concentration proportional to blood plasma
metabolised to inactive metabolites in liver, excreted by kidney
first order kinetics at low level, zero order kinetics at high level

-side effects: early nystagmus, diplopia, ataxia, sedation, gingival hyperplasia, megaloblastic anaemia

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4
Q

Describe how phenytoin is administered in status epilepticus, why loading dose and risks of IV administration

A
  • IV loading dose of 10-15 mg/kg, diluted in saline (precipitates in glucose), then 100mg 6-8 hourly as maintenance
  • loading dose is used to reach target concentration more rapidly, otherwise would need 4 half lives to get to steady state
  • risks of IV administration: hypotension and bradycardia with rapid infusion; as a vesicant = phlebitis, extravasation -> tissue damage
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5
Q

What is the mechanism of action, pharmacokinetics and adverse effects of sodium valproate

A

-mechanism: blocks high frequency firing Na+ channels, blocks NMDA, enhances GABA

-pharmacokinetics: well absorbed, good bioavailability, food delays absorption, 90% protein bound, peak level in 2 hours
95% hepatic metabolism, 5% unchanged in urine, clearance is dose dependant

-adverse effects: nausea, vomiting, reflux, weight gain, hair loss, hepatotoxic

-drug interactions: enzyme inhibitor, also inhibits its own metabolism
increased levels of = phenytoin, carbamazepine, phenobarbitone
displaces phenytoin from plasma proteins

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6
Q

What are the pharmacodynamics and pharmacokinetics of ethanol

A

-pharmacodynamics:
cns = sedation, relief of anxiety, disinhibition, slurred speech, ataxia
cvs = depression of myocardial contractility
smooth muscle = vasodilation and relaxation of uterus

-pharmacokinetics: rapid absorption from the GI tract, food delays absorption by slowing gastric emptying
peak concentration in 30 minutes, volume of distribution approximates total body water, readily crosses BBB
90% metabolised in liver by alcohol dehydrogenase, rest by Microsomal Ethanol Oxidizing System (MEOS)
follows zero order kinetics, excreted through lungs and urine

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7
Q

What does zero order kinetics mean

A

elimination occurs at a constant rate independent of drug concentration, also known as saturable elimination kinetics

E.g. alcohol, warfarin, heparin, aspirin, phenytoin

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8
Q

What classes of local anaesthetics are used in ED and what is the mechanism of action and which ones are used topically

A

classes:
amides: lidocaine, prilocaine, bupivacaine
metabolised by liver P450 enzymes
esters: procaine, tetracaine, benzocaine
very short half lives, metabolised by plasma cholinesterase

Mechanism: blockade of voltage-gated Na+ channels, preventing depolarisation

-topical: co-phenylcaine (spray with lignocaine), EMLA (cream with lignocaine and prilocaine)

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9
Q

What is the mechanism of action, pharmacokinetics and toxic effects of bupivacaine?

A

-mechanism: amide, weak base, block voltage-gated Na+ channel (higher affinity for activated/inactivated state)
prevents depolarisation

-pharmacokinetics: biphasic distribution, metabolised by liver P450, duration of action 4-8 hours (longer than others)
renal excretion

  • use: nerve blocks (femoral, digital, intercostal), local infiltration, epidurals
  • toxicity: lip and tongue numbness, metallic taste, nystagmus, twitching, seizures, arrhythmia, more cardiotoxic than lidocaine
  • safe dose: <2mg/kg
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10
Q

What is the mechanism, factors affecting absorption, maximum dose and toxic effect of lidocaine

A
  • mechanism: Na+ channel blocker, class 1b
  • factors affecting absorption: dose, site, tissue blood flow, use of adrenaline

-doses: plain 3mg/kg (maximum 300mg), with adrenaline 5mg/kg (maximum 500mg)

-toxic effects: early lip and tongue numbness, metallic taste, nystagmus, muscle twitching, seizures, hypotension, arrhythmia
transient neurological symptoms = severe pain, highest rate with lidocaine

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11
Q

Why do you get tachyphylaxis with local anaesthetic use

A

due to increased ionisation

(actually mechanisms remain unclear and inconclusive, a few suggested mechanisms: local pH change altering ionisation, increased clearance due to local flow or metabolism, increased afferent input from local nociceptors, sodium channel down regulation)

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12
Q

Give some examples of drugs used as anaesthetic agents

A

thiopentone, propofol, ketamine, fentanyl, midazolam, etomidate

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13
Q

Describe the onset and recovery of propofol and ketamine

A
  • propofol: rapid onset/recovery due to redistribution rather than metabolism, rapidly metabolised by liver (also in lungs)
  • ketamine: rapid onset, recovery due to redistribution but is slower and is more associated with emergence phenomena
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14
Q

Describe the cardiovascular effects of propofol and ketamine

A
  • propofol: reduction in BP during induction due to vasodilation of arterial/venous circulations, inhibition of baroreceptor reflex
  • ketamine: transient increase in BP/HR/CO via SNS stimulation
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15
Q

Describe the pharmacodynamics and pharmacokinetics of ketamine

A

Pharmacodynamics: NMDA receptor antagonist, blocking glutamate, inhibit reuptake of catecholamine and serotonin

Pharmacokinetics: highly lipid soluble/rapid onset, low protein binding, effect terminated by redistribution to inactive tissue sites, metabolised by liver (CYP450), excreted in urine

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16
Q

Describe the pharmacodynamics and pharmacokinetics of propofol

A

Pharmacodynamics: potentiation of glycine and chloride current mediated through GABAa receptor complex

Pharmacokinetics: large VOD, high protein bind, rapid onset, distribution t1/2 2-4 min, elimination t1/2 4-23 min, doa 3-8 min
rapid onset/recovery due to redistribution rather than metabolism
rapidly metabolised in liver, extra-hepatic metabolism in lungs, excreted in urine

-dosing: induction 1-2.5 mg/kg, procedural sedation 0.5-1 mg/kg

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17
Q

Describe the pharmacodynamics, pharmacokinetics and side effects of thiopentone (describe the distribution)

A

-pharmacodynamics: enhances effect of GABA on GABAa receptors, causing neural inhibition
action determined by redistribution rather than metabolism
-pharmacokinetics: highly lipid soluble, distributes to highly vascular tissue, rapidly crosses the BBB then distributes to fat
t1/2 9 hours, hepatic metabolism
-advantages: rapid, controllable, amnesic, reduces ICP, anticonvulsant, neuroprotection
-disadvantages: hypotension, venous irritant, myocardial depression, contraindicated in acute intermittent porphyria

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18
Q

Describe the solubility characteristics of nitrous oxide

A

-relatively insoluble in blood, thus few molecules needed to increase the partial pressure = low partition coefficient = fast onset

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19
Q

What is the mechanism of action, organ effects and metabolism of nitrous oxide

A

-mechanism: inhibition of NMDA receptors and activation of opioid/GABAa receptors

-organ effects:
cns = analgesia, amnesic, increased CBF
cvs = dose dependent myocardial depression
respiratory = respiratory depression, no real change in tidal volume (unlike other volatiles)
renal = decreased GFR, increased filtration fraction, increased renal vascular resistance

-pharmacokinetics: not metabolised and excreted unchanged through lungs and skin

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20
Q

List the classes of drugs used in ED for procedural sedation

A
  • benzodiazepines: midazolam, diazepam
  • dissociative anaesthetics: ketamine
  • intravenous anaesthetics: propofol (no analgesic properties)
  • inhaled anaesthetics: nitrous oxide, volatiles
  • opiates: morphine, fentanyl
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21
Q

What is the mechanism of action of benzodiazepine - effects and uses?

A

-mechanism: agonist at the GABAa receptor in the CNS and causes increased frequency of Cl- channel opening
binds to subunit different than GABA binding site, does not activate the channel, enhances GABA effect on the receptor
-effects: sedation, hypnosis, anaesthesia, anticonvulsant, muscle relaxation, respiratory and cardiovascular depression
-uses: anticonvulsant, sedation in agitated patient, alcohol withdrawal, toxidromes
-commonly used: diazepam, midazolam, lorazepam, clonazepam, temazepam

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22
Q

Explain the rationale to use benzodiazepines in alcohol withdrawal

A
  • alcohol dependant people exhibit down regulation of neuro-inhibitory GABA receptors
  • this leads to GABA deficiency in withdrawal
  • benzodiazepine facilitate GABA binding to GABAa receptor, enhancing Cl- activation
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23
Q

What is Flumazenil and how does it work (adverse effects)

A
  • competitive antagonist at the benzodiazepine binding site on GABAa
  • blocks actions of benzodiazepines
  • adverse effects: agitation, confusion, dizziness, nausea, abstinence syndrome, seizure
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24
Q

What is the mechanism, clinical use and anticonvulsants properties of clonazepam

A
  • mechanism: binds to GABAa receptors, potentiating opening of Cl- channels causing inhibition by hyperpolarisation
  • uses: anticonvulsant, anxiolytic, sedative
  • why effective anticonvulsant: lipid soluble, crosses BBB, potentiates inhibitory interneurons
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25
Q

What is the mechanism, clinical effects and pharmacokinetics of midazolam

A
  • mechanism: binds to GABAa receptor subunit, potentiating GABA inhibition by assisting in opening of Cl- channels
  • clinical effect: amnesia, anticonvulsant, anxiolytic, sedative-hypnotic, antiemetic
  • pharmacokinetics: PO/IV/IM/buccal/PR/IN, poor oral bioavailability, lipid soluble, highly protein bound, crosses BBB, hepatic metabolism with active metabolites, short elimination half life (oral bioavailability of diazepam is 100%)
  • adverse effects: excess sedation, respiratory depression, decreased motor skills, impaired judgement, hypotension
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26
Q

Draw the arterial anaesthetic tension vs time for N2O, halothane and methoxyflurane

A
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27
Q

Describe the systemic and adverse effects of Ketamine.

A

Sedative-hypnotic

  • systemic effects:
    cns = dissociative amnesia, analgesia, preserves reflexes, cerebral vasodilator (increased ICP)
    cvs = transient increase in BP/HR/CO via SNS stimulation
    respiratory = relaxes bronchial smooth muscle, no significant respiratory depression
  • indications: analgesia, bronchodilator in asthma, procedural sedation, intubation, acute behavioural disturbance, depression
  • side effects: emergence phenomena and laryngospasm in children, vomiting, salivation/lacrimation, hypertension, tachycardia
  • reasons to avoid: allergy, raised intracranial pressure, raised intraocular pressure
  • dose for procedural sedation in a child: 1-2 mg/kg IV
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28
Q

What is the mechanism of action, pharmacokinetics and side effects of levitaracetem

A

MOA: binds to synaptic vesicular protein SV2A, modify release of GABA and glutamate, inhibits N-type Ca+2 channels

Use: partial seizures, primary tonic clonic seizures, myoclonic seizures

Pharmacokinetics: BD dosing, complete oral absorption, rapid and unaffected by food, peak plasma concentration 1.3 hours -linear kinetics, low protein binding, t1/2 6-8 hours, 2/3 excreted unchanged in urine, no active metabolites

Adverse effects: depression, asthenia, ataxia, dizziness, minimal drug interactions

29
Q

Why is elimination kinetics important clinically with Phenytoin?

A

small dose increases may cause toxicity

30
Q

Describe the cinical effects, side effects and interactions of propofol

A

Clinical effects:
cns = hypnotic, no analgesic properties, reduced cerebral perfusion
cvs = reduced BP, inhibition of baroreceptor reflexes
respiratory = depression, reduced upper airway reflexes
other = antiemetic

Uses: induction agent, procedural sedation (rapid onset/offset), maintaining anaesthesia

Side effects: decreased cerebral perfusion, decreased BP, respiratory depressant, reduced upper airway reflexes
cross-reactivity with egg allergy, pain on injection

Drug interactions: opioids enhance respiratory depression, benzodiazepines enhance sedation

How to limit side effects: small titrated doses, no opiates at same time, iv fluid bolus or metaraminol pre-administration

31
Q

Describe pancruronium

A

-mechanism: non-depolarising neuromuscular blocking medication, competitive antagonist at nicotinic receptor

prevent depolarisation at the neuromuscular junction

-pharmacokinetics: highly polar (no oral absorption), long acting (doa >35 minutes)

80% renal elimination unchanged, rest by hepatic metabolism with biliary excretion

-adverse effects: minor tachycardia, hypertension, anaphylaxis

32
Q

Describe Rocuronium

A

Paralytic agent

  • pharmacodynamics: non-depolarising neuromuscular blocking medication, competitive Ach antagonist at the nicotinic receptor
  • pharmacokinetics:
    highly ionised with small vd (IV only), rapid distribution, onset 45-60 seconds (within a minute), intermediate acting (doa 20-35 minutes, half an hour), metabolised in liver,
    75-90% eliminated by the liver, rest by the kidney
  • reversal agent: sugammadex
  • c.f. suxamethonium: suxamethonium has a much shorted doa (5-10 minutes) and is depolarising
33
Q

Describe Vecuronium

A

-mechanism: non-depolarising neuromuscular blocking medication, competitive antagonist at the nicotinic receptor

prevent depolarisation at the neuromuscular junction

-pharmacokinetics: highly polar (no oral absorption), onset within 60 seconds, intermediate acting (doa 20-35 minutes)

75-90% eliminated by liver, rest by kidney

34
Q

Describe Suxamethonium

A

-mechanism: depolarising neuromuscular blocking medication, agonist at the nicotinic receptor

phase 1 block = depolarising, reaction with receptor opens channels and causes depolarisation of motor end plate

phase 2 block = desensitising, membrane becomes repolarised and cannot become depolarised by desensitisation

-pharmacokinetics: rapid onset 30-60 seconds, doa 5-10 minutes

rapid hydrolysis in liver and plasma by pseudocholinesterase

-adverse effects: pain from fasciculation, hyperkalaemia (worse with burns), raised IOP, malignant hyperthermia, bradycardia

prolonged paralysis if genetic low levels of plasma pseudocholinesterase

35
Q

What are the actions of dantrolene

A

Skeletal muscle relaxant
- antagonist at the RYR1 receptor in sarcoplasmic reticulum membrane, preventing the release of calcium
- uses: malignant hyperthermia (1mg/kg IV), spasms

36
Q

Why is levodopa given with carbidopa and what are the adverse effects of levodopa

A
  • levodopa can cross the BBB but dopamine cannot
  • when levodopa is ingested, it is rapidly metabolised by decarboxylation to dopamine
  • carbidopa is a dopa-decarboxylase inhibitor that does not cross the BBB and increases amount of levodopa that does
  • side effects: cardiac arrhythmia, postural hypotension, depression, anxiety, hallucinations, nausea and vomiting

dyskinesia - commonly choreoathetosis or face and distal extremities

response fluctuations - end of dose akinesia and on-off phenomena

37
Q

What drug classes are used in the management of acute agitation in ED

A
  • benzodiazepines: diazepam, midazolam
  • antipsychotics: droperidol (typical), olanzapine (atypical)
  • barbiturates: phenobarbital
38
Q

What is the predominant mechanism of action of typical and atypical antipsychotics

A
  • typical (droperidol, haloperidol, prochlorperazine): mostly act as dopamine D2 blockers
  • atypical (quetiapine, risperidone, olanzapine): mostly act as serotonin antagonists with less affect on D2
39
Q

What are the adverse effects of antipsychotics and what receptors are involved?

A

Side effects:

- neurologic: extrapyramidal effects (tremor, bradykinesia, rigidity, restlessness, dystonic) less common with atypicals
- ans: antimuscarinic effects (dry mouth, constipation, urine retention, blurred vision)
- cardiac: orthostatic hypotension, arrhythmia, wide QRS, myocarditis
- endocrine: weight gain, hyperglycaemia, amenorrhoea, galactorrhea, infertility
- haematologic: agranylocytosis
- other: NMS (bradykinesia, fevers, autonomic instability) more common with typicals

Receptors: antimuscarinic, alpha block, D2 antagonism, serotonin antagonism, anti-histamine

40
Q

How are extrapyramidal side effects managed

A
  • lower the dose, switch to an atypical
  • reversal agents: benztropine = centrally acting antimuscarinic that causes an increase in dopamine (restore cholinergic-dopaminergic balance, does not treat tardive dyskinesia)
  • symptomatic relief: benzodiazepines for akathisia and agitation
  • supportive care: close monitoring, hydration, manage hyperthermia, rhabdomyolysis
41
Q

What is the general pharmacokinetic principles of most antipsychotic drugs

A
  • most are readily but not completely absorbed, highly lipid soluble and protein-bound with large VOD
  • undergo significant first pass metabolism
42
Q

What are the uses, mechanism and side effects of chlorpromazine (largactil)

A
  • chlorpromazine (largactil) is a typical antipsychotic with other receptor effects
  • uses: antipsychotic (schizophrenia), sedative, antiemetic
  • mechanism and side effects:

dopamine (D2) blockade - antipsychotic, extra-pyramidal side effects, lactation

serotonin blockade - depression

antimuscarinic - anticholinergic effects

alpha blockade - hypotension

histamine blockade - antiemetic, sedation

43
Q

Compare olanzapine to haloperidol in terms of sedation, hypotensive effect and extrapyramidal toxicity

A

-olanzapine: atypical, mostly blocks serotonin, also blocks alpha 1, histamine and D4

high sedation, low postural hypotension, medium anticholinergic, low extrapyramidal effect, high weight gain

-haloperidol: typical, mostly blocks dopamine (D2), also blocks alpha 1, histamine, serotonin

low sedation, low postural hypotension, low anticholinergic, high extrapyramidal, medium weight gain

44
Q

By what routes can olanzapine be administered and what are the advantages over typical class

A
  • oral (tablet or wafer), parenteral (IM), dose of 5-20mg
  • uses: autism, delirium, behavioural emergencies, dementia, schizophrenia
  • advantages: less hypotension, less tachycardia, less extrapyramidal side effects
  • disadvantages: anticholinergic effects, lowered seizure threshold, weight gain, diabetes, hyperlipidaemia
45
Q

How does metoclopramide cause a dystonic reaction

A

metoclopramide is a dopamine antagonist, causing imbalance of dopamine in basal ganglia

46
Q

How does benztropine help extrapyramidal side effects and what are its side effects?

A

Mechanism:

  • centrally acting antimuscarinic: blocks CNS excitation in M1 receptors
  • indirectly causes an increased in dopamine

Side effects: tachycardia, sedation, mydriasis, urine retention, dry mouth

47
Q

How do antidepressants exert their action

A
  • monoamine hypothesis: depression is associated with decreased amine transmission of serotonin, NA and dopamine
  • enhance serotonin, noradrenaline and dopamine by:

inhibition of serotonin reuptake by inhibiting SERT = ssri, snri, tca

inhibition of NET (also has some affinity for dopamine re-uptake) = snri

inhibition of breakdown by monoamine by blocking MAO = maoi

increased release of serotonin = mirtazapine

48
Q

What are advantages of some antidepressants over others

A

-SSRI:

advantage = effective with minimal effect on other neurotransmitters

disadvantage = can cause enzyme inhibition, serious interaction with MAOI to cause serotonin syndrome

-SNRI:

advantage = NET also has a moderate affinity for dopamine

disadvantage = can cause increased BP and HR due to increased NA, levels affected by hepatic impairment

-TCA:

advantage = may be useful in refractory depression

disadvantage = high side effect profile, including anticholinergic syndrome and wide QRS

49
Q

What is the mechanism, pharmacokinetics and adverse effects of tricyclic antidepressants (amitriptyline)

A

-mechanism: tricyclic antidepressant

blocks SERT, NET, ACh muscarinic, alpha-1, H1 and Na+ channels

-pharmacokinetics: well absorbed, long half life, large VOD, high tissue concentration, high protein binding, lipid soluble

high first pass metabolism, active metabolites

-adverse effects (seen in overdose):

anticholinergic syndrome = blurred vision, dry mouth, tachycardia, urine retention, delirium

cardiac = wide QRS, bradycardia, hypotension

others = seizure, sexual side effects, weight gain, sedation

-treatment of toxicity: supportive, dopamine/NA for hypotension, sodium bicarbonate for cardiac toxicity, intralipid

50
Q

Describe the volume of distribution of TCAs and what therapies for TCA toxicity may reduce their tissue distribution

A
  • TCAs have a large VOD, tissue concentrations are high, lipid soluble, high protein binding
  • plasma alkalinisation increases plasma protein binding of free drug, removing it from tissues
  • barbiturates increase rate of hepatic metabolism of TCA
51
Q

What is the mechanism of action, pharmacokinetics and side effects of lithium

A
  • mechanism: not entirely understood, closely related to Na+ and can stimulate Na+ in generating action potentials
  • pharmacokinetics: 100% bioavailability, peak level within 30 minutes, no protein binding, distributes in total body water. excreted unchanged in urine, long t1/2 20 hours, steady state not reached for 5-7 days
  • adverse effects:
    neuro: tremor (earliest sign of toxicity), ataxia, confusion
    cardiac: flat T waves, T wave inversion, heart block, SSS
    thyroid: hypothyroidism
    endocrine: nephrogenic diabetes insipidous
    other: vomiting, acne, weight gain
  • signs of toxicity: tremors, confusion, slurred speech, ataxia, drowsiness, blurred vision, seizures
  • how to assess toxicity: measure levels 10-12 hours post last dose, toxic if >2mmol/L
  • factors that increase plasma levels:

drugs = thiazides and nsaid

post partum = due to increased clearance during pregnancy

other = dehydration, hyponatraemia, renal failure

52
Q

What is the mechanism of serotonin syndrome and what causes it? What are signs?

A
  • excessive stimulation of serotonin receptors in the CNS
  • due to overdose of single drug (ssri) or combination of certain drugs (MAOI + SSRI)
  • causes:

inhibition of reuptake of serotonin = SSRI (fluoxetine), SNRI (venlafaxine), TCA (amitriptyline)
inhibition of serotonin metabolism = MAOI (moclobemide)
S-shivering
H-hyperreflexia
I-Increased temp/sweating
V-Vital sign instability
E-encephalopathy
R-restlessness

53
Q

Why are SSRI safer than TCA

A

SSRI are very specific for serotonin receptors and have little affect on other neurotransmitters

54
Q

What is the effect of adrenaline on blood vessels in different tissues

A
  • cutaneous: vasoconstriction (alpha 1)
  • mucous membranes: vasoconstriction (alpha 1)
  • skeletal muscle: vasodilation (beta 2)
  • renal: vasodilation (D 1)
55
Q

Describe the effects of adrenaline on organs other than the heart

A
  • respiratory: bronchodilation (beta 2)
  • ocular: pupillary dilation (alpha 1), decrease aqueous humour (alpha 2), increase aqueous humour (beta 2)
  • genitourinary: contraction of bladder (alpha 1)
  • salivary glands: decrease secretion
  • liver: enhanced glycogenolysis (beta 2)
    pancreas: inhibits (alpha 2) or stimulates (beta 2) insulin secretion
56
Q

What are the effects of IV adrenaline on the cardiovascular system

A

-low does beta > alpha = increased cardiac output, vasodilation with widened pulse pressure

beta 1: increased force of contraction and increased HR, beta 2: skeletal vasodilation

-high dose has alpha effects = vasoconstriction with narrowed pulse pressure

alpha 1: constriction of skin arterioles causing increased PVR, alpha 2: central vasodilation (reduced SNS discharge)

57
Q

What are the cardiovascular effects of infused noradrenaline

A

-increased PVR, increased SBP and DBP, little chronotropy, positive inotropy

58
Q

What are the side effects of an adrenaline infusion

A
  • general = anxiety, tremor, nausea, vomiting, pallor
  • cvs = palpitations, arrhythymia, myocardial ischaemia, hypertension
  • metabolic = metabolic acidosis, hypokalaemia, hyperglycaemia
59
Q

How does the affect of adrenaline differ from noradrenaline

A
  • adrenaline profile: beta 1 = beta 2 >> alpha 1 = alpha 2
  • noradrenaline profile: alpha 1 = alpha 2 >> beta 1 >> beta 2
60
Q

How does noradrenaline increase BP

A
  • activation of alpha 1 receptor causes vasoconstriction, which increases total peripheral resistance and increases DBP
  • activation of beta 1 receptor causes increase in myocardial contractility, which increases SBP
61
Q

How does noradrenaline affect HR

A
  • activation of beta 1 receptor causes increase in HR
  • compensatory baroreflex from increased BP from other effects causes reflex bradycardia, so only minimal change in HR
62
Q

What is the cellular mechanism of beta agonists

A
  • beta agonists bind to g protein coupled receptors, stimulating adenylyl cyclase and causing increased cAMP
  • this causes activation of protein kinase A
63
Q

Compare cardiovascular effects of adrenaline and dobutamine

A
  • adrenaline profile: beta 1 = beta 2 >> alpha 1 = alpha 2
  • dobutamine profile: beta 1 > beta 2 >>>>> alpha

Adrenaline: non selective adrenergic, more beta than alpha

Dobutamine: selective beta-1 adrenergic

64
Q

What is the mechanism of action of amphetamines

A
  • indirectly cause increase in catecholamines at synapses and inhibits dopamine transport
  • effects: increases HR and BP, euphoria, appetite suppression
65
Q

What is the mechanism of action of metaraminol

A

Vasopressor, synthetic sympathomimetic
- direct acting alpha 1 receptor agonist, indirect via NA release
- effects: vasoconstriction via activation of vascular smc, causing increased BP

66
Q

What role do sympathomimetics have in management of shock

A

temporising only

67
Q

What is the mechanism of action, organ effects and uses of atropine

A
  • mechanism: highly selective reversible muscarinic receptor competitive antagonist
  • organ effects of atropine: eye = pupil dilation (M3), ciliary muscle relaxation (M3)

cns = delirium, decrease tremor in parkinsons disease (M1)

respiratory = bronchodilation (M3)

genitourinary = bladder relaxation (M3)

gastrointestinal = decreased gastric acid secretion (M1)

cvs = tachycardia (M2)

  • uses: bradycardia by vagal stimulation, eye exam, dry secretions in palliative care, bladder spasms, travellers diarrhoea
  • pharmacokinetics: well absorbed, widely distributed, crosses BBB, rapid and slow phase of elimination, t1/2 2 hours
  • toxic effects: anticholinergic syndrome (blurred vision, hyperthermia, dry skin, tachycardia, urine retention, hallucinations)
68
Q

What is the mechanism of action of indirectly acting cholinomimetics

A
  • medications that activate the cholinergic system but do not directly activate receptors
  • produce their effect by inhibiting acetylcholinesterase enzyme and thus increase concentration of endogenous acetylcholine
  • will have an effect on both nicotinic and muscarinic receptors -
    examples: reversible = neostigmine - does not cross BBB, used in myasthenia gravis and to reverse NM block

physostigmine - crosses BBB, used in anticholingergic poisoning

irreversible = organophosphates - treat poisoning with pralidoxime (regenerates cholinesterase) -cardiovascular effects: bradycardia, decreased CO, decreased contractility, minimal change in BP

ACEM Viva (39 decks)

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