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Clinical Pharmacology, Therapeutics & Principles of Prescribing > Session 12 > Flashcards

Session 12 Flashcards

1
Q
  1. Definition of Epilepsy
  2. Diagnosis requires evidence of ?
A
  1. Episodic discharge of abnormal high frequency electrical activity in brain leading to seizure
  2. recurrent seizures unprovoked by other identifiable causes
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2
Q

What causes Epilepsy? (4)

A

Increased Excitatory Activity

Decreased Inhibitory Activity

Loss of Homeostatic Control

Spread of Neuronal Hyperactivity

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3
Q

Classification of Epilepsy

Two main types:

A
  • Partial seizures
  • Generalised seizures
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4
Q

Classification of Epilepsy

Partial (or focal) seizures

Simple (conscious)

Complex partial seizures (impaired consciousness)

Secondary generalised seizures

Loss of local excitatory/inhibitory homeostasis

Increased discharges in focal cortical area

A
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5
Q

Partial (or focal) seizures

Symptoms reflect area affected eg

A
  • Involuntary motor disturbance
  • Behavioural change
  • Impending focal spread accompanied by ‘Aura’ eg unusual smell or taste, déjà vu / jamais vu
  • May become secondarily generalised
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6
Q
  1. What are Generalised seizures?
  2. Give examples
A
  1. Generated centrally spread through both hemispheres with loss of consciousness
  2. Tonic-clonic seizures (Grand mal) – 60%

Absence seizures (Petit mal) – 5%

Many other types /sub types recognised

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7
Q
  1. Most seizures are short lived ( up to ?)
  2. Some seizures prolonged beyond this or experienced as series of seizures without recovery interval. Referred to as ?
  3. What type of epilepsy can SE occur in?
  4. Prolonged seizure treated as a Medical Emergency. Untreated Status Epilepticus can lead to ?
A
  1. 5 mins
  2. Status Epilepticus
  3. Any
  4. brain damage or death (SUDEP)
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8
Q

Dangers in Severe Epilepsy

Uncontrolled epilepsy is not a benign condition: what general effects does it have?

A
  • Physical injury relating to fall/crash
  • Hypoxia
  • SUDEP – sudden death in epilepsy
  • Varying degrees of brain dysfunction/damage
  • Cognitive impairment
  • Serious psychiatric disease
  • Significant adverse reactions to medication
  • Stigma / Loss of livelihood
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9
Q

Etiology of Epilepsy

  1. What do we mean by this is primary epilepsy?
  2. What do we mean by this is secondary epilepsy?
  3. What is the likely etiology of epilepsy in the elderly?
A
  1. No identifiable cause – idiopathic (65-70%)

Channelopathies ?

  1. Secondary Medical conditions affecting brain (30-35%)

Vascular disease

Tumours

  1. In the elderly (60+) secondary responsible for 60% of seizures – important diagnostic
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10
Q

Precipitants

A

MIST B

Sensory stimuli: eg flashing lights/strobes or other periodic sensory stimuli

Brain Disease/ Trauma: Brain Injury Stroke / Haemorrhage Drugs/Alcohol Structural abnormality/Lesion

Metabolic disturbances: Hypo - glycaemia/calcaemia /natraemia

Infections Febrile convulsions in infants

Therapeutics Some drugs can lower fit threshold AEDs + Polypharmacy: PKs lower levels

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11
Q

Therapeutic Targets for AEDs (2)

A
  • Voltage Gated Sodium Channel Blockers
  • Enhancing GABA Mediated Inhibition

​

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12
Q

VGSC blockers - mechanism of action

A

Bind to domain 4

VGSC Blockers reduce probability of high abnormal spiking activity

  • Local loss of membrane potential homeostasis starts at focal point
  • Relatively small number of neurones form generator site
  • Neurones heavily depolarise
  • Hyperactivity spreads via synaptic transmission to other neurones
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13
Q

Where/when do VGSC blockers bind?

Effect of binding?

When does it detach?

A

With VGSC Blocker – gets access to binding site only during depolarisation - hence voltage dependent!

Prolongs inactivation state – firing rate back to normal

Once neurone membrane potential back to normal VGSC. Blocker detaches from binding site.

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14
Q

VGSC blockers 1: Carbamezepine

  1. Pharmacology/ Mechanism of action: ?
  2. Pharmokinetics:
  3. ADRs
  4. DDIs
  5. Why must we monitor?
  6. Epilepsy types treated with Carbamezepine
A
  1. Carbamezepine prolongs VGSC inactivation state
  2. Well absorbed 75% protein bound – Linear PK

Initial t 1/2 = 30 hrs but strong inducer of CYP450.

Affects its own Phase 1 metabolism

Repeated use t 1/2 = 15hrs

  1. Wide ranging Type As:

CNS - dizziness drowsy ataxia motor disturbance numbness tingling

GI - upset vomiting

CV – can cause variation in BP Contraindicated with AV conduction problems

Others: Rashes Hyponatraemia

Rarely Severe bone marrow depression – neutropenia

  1. Because CYP450 inducer can affect many other drugs

Phenytoin (AED) decrease + PK binding - CBZ plasma conc increase

Warfarin decrease

Systemic Corticosteroids decrease

Oral contraceptives decrease​

Antidepressants - SSRIs MAOIs TCAs & TCA interfere with action of Carbamezepine

  1. Dosing to effect and adjust dosing as t1/2 decrease

Check BNF with any other drugs given

  1. Generalised Tonic - Clonic

Partial - All Not Absence Seizures

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15
Q

VGSC blockers 2: Phenytoin

  1. Pharmacology/mechanism of action:
  2. Pharmacokinetics:
  3. ADRs:
  4. DDIs
  5. How to monitor the drugs
  6. Epilepsy types treated with Phenytoin
A
  1. Phenytoin prolongs VGSC inactivation state
  2. Well absorbed – but 90% bound in plasma competitive binding can increases levels (see DDIs) Also CYP450 inducer (CYP3A4 - not CYP2C9 & CYP2C19 which metabolise Phenytoin)

Sub-therapeutic concs linear PK but NON-LINEAR PK at therapeutic concns - very variable t 1/2 = 6-24hrs

  1. Very wide ranging Type A’s: CNS – dizziness ataxia headache nystagmus nervousness

Gingival Hyperplasia (20%)

Rashes - Hypersensitivity + Stevens Johnson (2-5%)

  1. Competitive binding eg with Valproate (AED) NSAIDs/ salicylate increases plasma levels- exacerbates Non-Linear PKs

Very wide range of interactions including Oral Contraceptives decrease

Cimetidine - Phenytoin increase

Must check BNF for any other drugs given in combination

  1. Drug Monitoring

Close monitoring of free concn plasma

Can use salivary levels as indicator of free plasma

  1. Generalised Tonic-Clonic

Partial - All Not

Absence Seizures

​

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16
Q
A

Plots from five patients showing highly non linear PKs and variability in dose necessary to get to therapeutic levels.

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17
Q

VGSC blockers 3: Lamotrigine

  1. Pharmacology:
  2. Pharmacokinetics:
  3. ADRs
  4. DDIs
  5. Epilepsy types treated with LTG
A
  1. Lamotrigine (LTG) prolongs VGSC inactivation state Ca2+ channel blocker ? Glu release decrease ?
  2. Well absorbed – Linear PK t1/2= 24hrs (Phase II)

No CYP450 induction -> fewer DDIs

  1. Less marked CNS Dizziness ataxia somnolence Nausea. Still some mild (10%) and serious (0.5%) skin rashes
  2. Adjunct therapy with other AEDs.

Oral Contraceptives reduce LTG plasma level

Valproate increase LTG in plasma (competitive binding)

  1. Partial Seizures

Generalised - Tonic-clonic and Absence Seizures and other subtypes
LTG increasingly first line AED for Epilepsy

Not first line paediatric use as ADRs increase

Appears safer in pregnancy ?

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18
Q

Enhancing GABA Mediated Inhibition

  1. Fucntion?
  2. Distinct pharmacological targets I

Binding with GABAA receptor

Direct GABA agonists e.g.

A
  1. Major role in post synaptic inhibition – 40% synapses in brain are GABA-ergic
    GABA (Increase) is natural anticonvulsant or excitatory ‘brake’
  2. Benzodiazepine Site – Enhance GABA action

Barbiturate Site – Enhance GABA action

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19
Q

General Mechanism for GABA Mediated Inhibition Enhancement

A
  • Increased Chloride current into neurone - increases threshold for action potential generation
  • Reduces likelihood of epileptic neuronal hyper – activity

Makes memb. potential more negative

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20
Q

Enhancing GABA Mediated Inhibition

Distinct pharmacological targets II GABA Metabolism

Which target sites enhance action of GABA

A

Inhibition of GABA inactivation ( GABA inc)

Inhibition of GABA re-uptake (GABA inc)

Increase rate of GABA synthesis (GABA inc)

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21
Q

Enhancing GABA Mediated Inhibition 1

Valproate

  1. Pharmacology:

2. Pharmacokinetics:

  1. ADRs
  2. DDIs
  3. How would we monitor the drug
  4. Epilepsy types treated with Valproate
A
  1. Evidence in vitro for mixed sites of action - pleiotropic

Weak Inhibition of GABA inactivation enzymes - GABA increase

Weak Stimulus of GABA synthesising enzymes - GABA increase

VGSC blocker + Weak Ca2+ channel blocker - Discharge decrease

  1. Absorbed 100% - then 90% plasma bound

Linear PK t 1/2 = 15 hrs

  1. Generally less severe than with other AEDs

CNS sedation ataxia tremor - weight gain

Hepatic function Transaminases ​increase in 40% patients

Rarely - hepatic failure

  1. Adjunct therapy with other AEDs –

Care needed with adjunct therapy. Both Valproate and adjunct PKs affected. Always check BNF.

Antidepressants - SSRIs MAOIs TCAs & TCA inhibit action of Valproate

Antipsychotics - antagonise Valproate by lowering convulsive threshold.

Aspirin - competitive binding in plasma Valproate increase

  1. Close monitoring of free concn plasma

Can use salivary levels as indicator of free plasma

Plasma Valproate not closely associated with efficacy

Monitor for blood, metabolic and hepatic disorder.

  1. Partial Seizures

Generalised: Tonic-clonic + Absence Seizures

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22
Q

Enhancing GABA Mediated Inhibition 2

Benzodiazepines

  1. Pharmacology:
  2. Pharmacokinetics:
  3. ADRs
  4. DDIs
  5. Epilepsy types treated with BZDs

Side effects limit first line use

A
  1. Benzodiazepines (BZDs) act at distinct receptor site on GABA Chloride channel (see earlier slide)

Binding of GABA or BZD enhance each others binding

Act as positive allosteric effectors

Increases Chloride current into neurone - increases threshold for action potential generation

  1. Well absorbed 90-100% highly plasma bound 85-100% Linear PK t 1/2 vary 5-45hrs
  2. Sedation

Tolerance with chronic use

Confusion impaired co-ordination

Agression

Dependence/Withdrawal with chronic use

Abrupt withdrawal seizure trigger

Respiratory and CNS Depression

  1. Some adjunctive use

Overdose reversed by IV flumazenil but its use may precipitate seizure/arrhythmia.

  1. Lorazepam / Diazepam – Status Epilepeticus

Clonazepam – Absence seizure short term use

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23
Q

AEDs and Pregnancy

  • Balance of Risk
  • Epilepsy vs AED Teratogenicity
  1. If Mild disease you may decide?
  2. Severe disease/ Status Epilepticus you may decide?

Need to consider each patient individually and stage of pregnancy

A
  1. Stop treatment
  2. Harm to both mother and baby if treatment is stopped? Severe fits prolonged hypoxia bad for mother and baby
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24
Q
  1. What are the three effects AED have on pregnancy?
A

Failure of Contraception

Failure rate x 4 with Carbamazepine/Phenytoin increase to between = 4-8%

Dangers to foetus during Pregnancy

  • Congenital malformations ( All AEDs ?)
  • Valproate - neural tube defects
  • Facial and digit hypoplasia

Following birth

• Learning difficulties / mild neurological dysfunction?

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25
Q

AED risk of birth defects =?% vs =2% normally

A

8

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26
Q

AEDs and Pregnancy

  1. Solution of severe or status epilepticus?
  2. Treatment best avoided and why?
  3. Treat best used and why
A
  1. With multiple AED Teratogenic Risk increase, use single AED agent if possible at lowest dose
  2. Valproate best avoided - neural tube defect increase
  3. Lamotrigine may be safest - birth defect rate = 2 %
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27
Q

Valproate and Pregnancy – 2017

  • Recent studies highlighting risks of Valproate
  • Revised estimates of birth defect = 10%
  • Neurodevelopmental disorders - e.g.? risk may be as high as 30-40%
  • 1 in 5 pregnant women on valproate unaware of risk meaning?
A

learning/autism

Risks known for 40 yrs – doctor/patient communication issue

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28
Q

AEDs and Pregnancy and Dietary supplements

Which supplements should you give and why.

A
  • Folate supplement high does (1-5mgB) - reduce risk of neural tube defects - start prior to conception
  • AEDs associated with Vitamin K deficiency in new born - coagulopathy and cerebral haemorrhage
  • Vitamin K supplement 10 mg/day in last trimester.
29
Q

Status Epilepticus Status Epilepticus is a Medical Emergency

Adult mortality = 20% Risk increases with length of SE

(Controlled with 30 mins - only a few
Longer than half an hr tends to be higher = 20%
Damage sustained to brain = death)

first line of action?

A

Priorities are ABC

Exclude hypoglycaemia

Hypoventilation may result with high AED doses

ITU for paralysis & ventilation if failing

30
Q

Status Epilepticus treatment

A

Benzodiazepines

Lorazepam (0.1 mg/kg) preferred - longer pharmacodynamic half life than diazepam (0.2 mg/kg) IV route (rectal if difficult iv access)

Phenytoin

Zero order kinetics – (15-20 mg/kg) Rapidly reaches therapeutic levels IV Cardiac monitoring – arrhythmias + hypotension

Other drugs

Midazolam Pentobarbital Propofol

31
Q

• Understand the clinical presentation of PD and course LO

  1. Clinical presentation
  2. Non motor manifestations
A
  1. • Tremor* (rest)
    • Rigidity* (Lead pipe rigidity - flex extend at elbow- resistance whole way through
    Cogwheeling)
    • Bradykinesia**
    • Postural instability

*low dopamine and disturbance other neurotransmitter levels

**low dopamine

  1. • Mood changes (Depression & anxiety)
  • Pain (Generally side not working)
  • Cognitive change
  • Urinary symptoms

• Sleep disorder (Poor sleep
REM sleep behavior disorder
No REM sleep Atonia
Violent vivid
Punching, kicking etc)

• Sweating

  • Constipation
  • Loss of olfactory function
32
Q

Prognosis in PD (15 year follow up) (Course LO)

A
  • 94% Dyskinesia (Related to L dopa treatment. Involunatary abnormal writhing movements)
  • 81% Falls (Early parkinsons don’t usually have falls)
  • 84% Cognitive decline (50% hallucinations) (Can be made worse by drugs e.g. dopamine agonists)
  • 80% Somnolence (Impacts on driving, strong desire to sleep. Sleep attacks -> secondary narcolepsy. Should not drive)
  • 50% Swallowing difficulty
  • 27% Severe speech problems
33
Q

Diagnosis of IPD

A
34
Q

What is a DAT scan

A
  • Labelled tracer
  • Presynaptic uptake
  • Abnormal in PD
  • Not diagnostic
  • Tremor
  • Neuroleptic
  • Vascular
35
Q

Pathology of IPD (4)

A

• Neurodegeneration

• Lewy bodies

– synucleinopathy

• Loss of pigment

– 50% loss->symptoms

– Increased turnover

– Upregulate receptors

• Reduced dopamine

36
Q
A
37
Q

Basal Ganglia Circuit

A
38
Q

Catecholamine Synthesis

A
39
Q

Dopamine Degradation

A
40
Q

• Know the basis for treating PD LO

Namely ?

A
  • Symptomatic (• Movement disorder • Non-motor features)
  • Neuroprotection
  • Surgery
41
Q

• Understand the range of drug classes that are commonly used to treat PD. [You do not have to learn all the names]. LO

Drug Classes in IPD

A
  • Levodopa (L-DOPA)
  • Dopamine receptor agonists
  • MAOI type B inhibitors
  • COMT inhibitors
  • Anticholinergics
  • Amantidine
42
Q

Why not use dopamine?

A
43
Q

Why is levodopa less effective in progressive PD

A
44
Q

• Know the basic pharmacology of PD drug therapy as outline in the lecture and in particular, appreciate the range of ADRs with these agents and how this may limit their scope. LO

Levodopa (L-DOPA)

  1. Administration?
  2. How is it absorbed?
  3. How much is inactivated in the intestinal wall?
  4. Half life
  5. What happens to the dopamine which is not inactivated in the intestinal wall?
A
  1. Oral administration
  2. Absorbed by active transport (In competition with amino acids (NB high protein meals))
  3. 90% inactivated in intestinal wall (monoamine oxidase & DOPA decarboxylase 1/2)
  4. 2 hours
    • short dose interval
    • fluctuations in blood levels and symptoms
    • (physiologically dopamine is produced tonically)
  5. 9% converted to dopamine in peripheral tissues (DOPA decarboxylase)

<1% enters CNS (Again competes with amino acids for active transport across blood brain barrier)

45
Q

Formulations of L-DOPA

  1. L-DOPA is used in combination with a ?
  2. Benefits
A
  1. peripheral DOPA decarboxylase inhibitor :
  • Co-careldopa Sinemet
  • Co-beneldopa Madopar
  1. • Reduced dose required
  • Reduced side effects
  • Increased L-DOPA reaching brain
46
Q

What enzyme metabolises L- DOPA & what drug can prevent L - DOPAs metabolism. Where is most of L- DOPA metabolised.

A
47
Q

Formulations of L-DOPA

A

• Tablet formulations only
– Standard dosage – variable strengths
– Controlled release preparations (CR)
– Dispersible Madopar (not soluble)

48
Q

L-DOPA advantages

A
  • Highly efficacious
  • Low side effects

Nausea/ anorexia
– Vomiting centres

Hypotension
– central and peripheral

Psychosis
– Schizophrenia-like effects. Hallucination/ delusion/ paranoia

Tachycardia

49
Q

Disadvantages of L-DOPA

A
  • Precursor (needs enzyme conversion)
  • Long term
  • Loss of efficacy (Only effective in presence of dopaminergic neurones)
  • Involuntary movements
  • Motor Complications
    (On / off, Wearing off, Dyskinesias, Dystonia, Freezing)
50
Q

What drugs effect L-DOPA & explain how they effect it?

A

• Pyridoxine (vitamin B6) increases peripheral breakdown of L-DOPA

• MAOIs risk hypertensive crisis
(not MOABIs at normal dose-lose specificity at high dose)

• Many antipsychotic drugs block dopamine receptors and parkinsonism is a side effect (newer, ‘atypical’ antipsychotics less so)

51
Q

Give examples of Dopamine Receptor Agonists

A
  • Non Ergot (Ropinirole Pramipexole)
  • Patch (Rotigotine)
  • Subcutaneous (Apomorphine)
  • De Novo therapy
  • Add on therapy
  • Apomorphine -> only for patients with severe motor fluctuations
52
Q

Dopamine Receptor Agonists
Advantages

A
  • Direct acting (do not require dopaminergic neurones to work)
  • Less dyskinesias/ motor complications
  • Possible neuroprotection
53
Q

Disadvantages of dopamine receptor agonists

A
  • Less efficacy than L-DOPA
  • Impulse control disorders
  • More psychiatric s/e (e.g. hallucinations) -> Dose limiting
  • Expensive
54
Q

Impulse Control Disorders

A
  • Pathological Gambling
  • Hypersexuality
  • Compulsive Shopping
  • Desire to increase dosage
  • Punding (Collecting & sorting impulse)

​

55
Q

Dopamine Receptor Agonists -side effects​

A
  • Sedation
  • Hallucinations
  • Confusion
  • Nausea
  • Hypotension
56
Q

Monoamine oxidase B Inhibitors

  1. What is the function of Monoamine oxidase B, location, effect of monomine oxidase B inhibitors?
  2. Examples of Monoamine oxidase B inhibitors, can they be used alone? Function?
A
  1. • Metabolises dopamine
  • Predominates in dopamine containing regions in brain
  • MAOB inhibitors enhance dopamine
  1. • Selegiline • Rasagaline
  • Can be used alone
  • Prolong action of L-DOPA • Smooths out motor response • May be neuroprotective
57
Q

Catechol-O-methyl Transferase (COMT) Inhibitors

  1. Give examples of Catechol-O-methyl Transferase (COMT) Inhibitors
  2. Can it be given alone?
  3. Function
A
  1. • Entacapone – doesn’t cross BBB

(• Tolcapone – crosses BBB but main effect peripheral » Monitor liver function)

  1. No therapeutic effect alone
    » Can use combination tablets COMT inhibitor and L-DOPA & peripheral dopa decarboxylase inhibitor - Stalevo
  2. Reduce peripheral breakdown of L-DOPA to 3-O-methyldopa » 3-O-methyldopa competes with L-DOPA active transport into CNS

Have L-DOPA ‘sparing’ effect

• Prolongs motor response to L-DOPA » Reduces symptoms of ‘wearing off’

58
Q

Anticholinergics

  1. Function
  2. Give examples
  3. Is it important in treatment
A
  1. • Acetyl Choline may have antagonistic effects to dopamine
  2. • Trihexyphenidydyl • Orphenadrine • Procyclidine
  3. • Minor role in treatment of PD
59
Q

Anticholinergics

  1. Advantages
  2. Disadvantages
A
  1. • Treat tremor

• Not acting via dopamine systems

  1. • No effect on bradykinesia

• Side effects -> • Confusion • Drowsiness • Usual anticholinergic s/e

60
Q

Amantadine

  1. Mechanism action?
  2. Advantages and disadvantages
A
  1. uncertain – possibly
  • enhanced dopamine release
  • Anticholinergic NMDA inhibition
  • Poorly effective
  • Few side effects
  • Little effect on tremor
61
Q

Surgery

  • Carried out stereotactically
  • Of value in highly selected cases (• Dopamine responsive • Significant side effects with L-DOPA • No psychiatric illness)
  • Controlled trials
  • Lesion (• Thalamus for tremor • Globus Pallidus Interna for dyskinesias)
  • Deep brain stimulation (• Subthalamic nucleus)
A
62
Q

• Know how myasthenia gravis may present LO

  1. Signs and symptoms
A
  1. Eye - ptosis due to weakness of levator palpebrae superioris & double vision diplopia

Eating - dysphagia

trouble talking, trouble walking

Fluctuating, fatiguable, weakness skeletal muscle

– Extraocular muscles – commonest presentation

– Bulbar involvement – dysphagia, dysphonia, dysarthria

– Limb weakness – proximal symmetric

– Respiratory muscle involvement

63
Q

Pathophysiology

A

an autoimmune disease which results from antibodies that block or destroy nicotinic acetylcholine receptors at the junction between the nerve and muscle

64
Q

Drug affecting neuromuscular transmission exacerbate Myasthenia Gravis

A
  • Aminoglycosides
  • Beta-blockers, CCBs, quinidine, procainamide
  • Chloroquine, penicillamine
  • Succinylcholine
  • Magnesium
  • ACE inhibitors
65
Q

Complications of Myasthenia Gravis

A

• Acute exacerbation

– Myasthenic crisis

(Respiratory muscle involvement
Drool
Face is drooping
Breathy quality to speech as air I escaping
Cannot lif soft palate)

• Overtreatment

– Cholinergic crisis

(Same clinical picture to myasthenic crisis)

66
Q

Therapeutic management

A

• Acetylcholinesterase inhibitors

(• Corticosteroids -> Decrease immune response

  • Steroid sparing -> Azathioprine
  • IV immunoglobulin Acute decline or crisis – 60% will respond after 7-10 days
  • Plasmapheresis – Removes AChR antibodies and short-term improvement
67
Q
  • Recognise the range of treatments for myasthenia gravis LO
  • Understand the mechanism of action of acetylcholinesterase inhibitors LO

Therapeutic management

  1. Function of Acetylcholinesterase inhibitors
  2. Give two examples which one is more important, administration?
A
  1. – Enhance neuromuscular transmission
    – Skeletal and smooth muscle
    – Excess dose can cause depolarising block – cholinergic crisis
    – Muscarinic side effects
  2. Pyridostigmine - oral -> Very effective
    Patients at risk of cholinergic crisis

Neostigmine – oral and IV preparations (ITU)
• Quicker action, duration up to 4 hours
• Significant antimuscarinic side effect

68
Q

Pyridostigmine

  1. Function?
  2. Onset, peak, duration
  3. Antimuscarinic side effects:
A
  1. • Prevents breakdown of ACh in NMJ

• ACh more likely to engage with remaining receptors

  1. Onset 30min; peak 60-120min; duration 3-6hr

• Dose interval and timing crucial

Has to be given regularly
3x daily
severe 6 x over 24hrs but unusual

  1. miosis and the SSLUDGE syndrome:

» Salivation,

» Sweating,

» Lacrimation

» Urinary incontinence

» Diarrhea,

» GI upset and hypermotility

» Emesis

(Need to be give 30-40 mins before meals. As at risk of aspiration.)

69
Q
A

Clinical Pharmacology, Therapeutics & Principles of Prescribing (19 decks)

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