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Neurology > Principles of neuropharmacology > Flashcards

Principles of neuropharmacology Flashcards

1
Q

How is a brain capillary different to a general capillary?

A
  • pericytes
  • more mitochondria (for active transport)
  • astrocytes
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2
Q

Which drugs enter the brain?

A

the more lipophilic the drug, the better the penetration (e.g. diazepam is very lipophlic)

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3
Q

Outline glucose and L-DOPA uptake into the brain

A

Much more reaches the brain than would be expected with their level of lipophilicty due to active transport

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4
Q

Outline phenobarbital (PB) and phenytoin uptake into the brain

A
  • quite lipophilic but not as much penetration to brain as would be expected
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5
Q

What is PGP?

A
  • p-glycoprotein
  • an efflux pump that pumps foreign material out of cells
  • expressed in BBB
  • overexpressed in epileptic focus therefore decreased anti-epileptic drug action
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6
Q

Define AED

A

anti-epileptic drug

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7
Q

Why are collies sensitive to ivermectin?

A

They lack the PGP molecule to pump ivermectin out of brain cells –> seizure activity when administered this.

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8
Q

Are the neural impulses in all seizures hypersynchronous?

A

Yes - it means all neurons are firing at the same time

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9
Q

When to treat seizures?

A
  • status epilepticus or animals with cluster seizures
  • severe postictal signs
  • when severity or frequency increases
    ? one seizure every 6 weeks?
    ? 2 or more isolated seizures within 6 months?
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10
Q

How many seizure dogs respond to AED?

A

2/3

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11
Q

How do AEDs affect epilepsy?

A

suppress seizures, don’t actually tx the epilepsy

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12
Q

Why encourage an owner to chart seizure frequency?

A

to give them something to do by de-emtoionalising the situation. You can give diazepam to owners to put in rectally (this is done in humans too)

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13
Q

Considerations for starting seizure tx

A
  • monotherapy
  • seizure frequency may influence choice of AED
  • monitor plasma levels
  • owner compliance
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14
Q

What is the best aim of seizure tx?

A

to increase inhibition in the brain (as there are no advantages to blocking excitation route)

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15
Q

Tx - refractory epilepsy

A

Ketamine (NMDA antagonist)

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16
Q

Mode of action - barbiturate

A

increases the duration of chloride ion channel opening at the GABA-A-R. This increases the efficacy of GABA.

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17
Q

Mode of action - benzodizepines

A

Increase the frequency of chloride ion channel opening at the GABA-A-R. This increases the potency of GABA. Diazepam may nt work with long seizures because GABA may already be depleted.

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18
Q

Tx for a seizure of 2 hours duration

A

give diazepam and phenobarbitone at the same time

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19
Q

Tx for a seizure of

A

Give 2 doses diazepam and then give phenobarbitone. (barbiturates need no/less GABA to act than benzodiazepines)

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20
Q

PB- half life

A

24- 40 hours

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21
Q

PB - time to steady state

A

10-14 days

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22
Q

Side effects - PB

A

sedation, PD, polyphagia, hepatotoxicity
- TT4 and fT4 reduction, no effect on ACTH stimulation test
- hepatotoxicity
- routine biochem +/- bile acid stim. q6-12 months
- may reduce elimination half-life with chronic life
RARE, BUT SEVERE (idiocyncratic reactions):
- behavioural alterations
- immune-mediated neutropaenia, thrombocytopaenia, anaemia
- superficial necrolytic dermatitis (SND)
- idiosyncratic hepatotoxic reactions
*ACTION: stop immediately, load with alternative AED (KBr)
- withdrawal seizures due to drug dependence

23
Q

Metabolism - PB

A

liver

24
Q

Administration - PB

A
  • loading dose if indicated.
  • adjust dose if seizure frequency is equal or increased after 30 days
  • increment of 5 m, icrog/ml
25
Q

How does PB affect metabolic clearance in liver?

A

increases metabolic clearance in liver so lower 1/2 life of itself and other drugs. also increases ALT and other enzymes due to generalised increased liver activity

26
Q

Calculate oral daily dose for mg PB

A

= (desired concentration/ actual concentration) * total mg PB per day

27
Q

KBr - half-life as an AED

A

15-20 days

28
Q

KBr - time to steady state

A

100-200 days

29
Q

Side effects - KBr AED

A

sedation, weakness, PU, PD, GIT irritation (V and D), (pancreatitis)

30
Q

Outline bromide toxicity

A

RARE

  • severe ataxia, sedation, somnolence, skin reactions
  • dogs with renal insufficiency
  • ACTION: I.V. saline to enhance renal excretion
31
Q

Why do you get a pseudohyperchloraemia with KBr?

A

biochem test can’t distinguish Cl- from Br- so counted as one and the same.

32
Q

What is imepitoin? How does it compare with diazepam?

A
  • a partial benzodiazepine agonist
  • it is 1000x less potent than diazepam (both benzodiazepines) but patient is less dependent on imepitoin so no withdrawal seizures if tx stopped unlike diazepam.
33
Q

Use -imepetoin

A
  • first like tx for dogs with newly diagnsoed idiopathic epilepsy
  • relatively good side effect profile so can be considered is ‘less severe’ epilepsy cases sooner
  • dogs with severe side effects on PB or other anti-convulsants
  • alternative for dogs with unsatisfying seizure control on PB or other anti-convulsant drugs
  • NOT for dogs with acute seizures (cluster seizures / status epilepticus) OR in cats
34
Q

Half- life PB

A

2 hours

35
Q

Time to steady state - PB

A

1-2 days

36
Q

side effects - PB

A

sedation, polphagia, hyperactivity

37
Q

Reasons for AED tx failure

A
  • incorrect diagnosis (-> perform MRI)
  • incorrect choice AED
  • incorrect dosage
  • low AED levels
  • newly developed disease (liver, kidney, pancreas)
  • change in BWt
  • patient tolerance to drug
  • monotherapy is insufficient
  • refractory seizures
  • poor compliance
38
Q

Actions in case of tx failure

A
  • monitor drug levels - adjust dose
  • if still failure - adjust more
  • if still failure - add anticonvulsant
  • if still failure - monitor drug levels - adjust dose
  • if still failure - consider new drug
  • keep in touch with a neurologist
39
Q

Signs of refractory epilepsy / non-responder

A
  • seizure frequency reduction of less than 50%

- 20-30% poorly responsive with combination of PB and KBr

40
Q

First choice AED in cats

A

Phenobarbital

41
Q

PB - side effects - cats

A

polyphagia, BM suppression, cutaneous hypersenstivity

42
Q

2nd choice AED in cats

A

diazepam

43
Q

Side effects - diazepam in cats

A
  • (acute) hepatotoxicosis (important to evaluate liver enzymes 5- 7 days after initiation). Can progress to fulminant hepatic necrosis.
44
Q

Outlien KBr in cats as an AED

A

contraindicated as –> bronchial asthma

45
Q

Name 2 other AEDs in cats

A
  • levetiracetam

- gabapentin

46
Q

What type of damage does status epilepticus cause?

A
  • primary

- secondary / complications (may be more important)

47
Q

Problems experienced with seizure of 30 minutes duration

A
  • arterial hypertension
  • increased cerebral BF
  • hypoxaemia
  • hypercarbaemia
  • hyperglycaemia
  • lactic acidosis
48
Q

Problems experienced with seizure > 30 minutes duration

A
  • continuous mm contraction
  • hyperthermia (–> brain damage)
  • acidosis (–> mm failure)
  • myolysis (myoglobinuria, hyperkalaemia, cause renal failure)
  • hypoglycaemia (energy deposition)
  • hypotension
  • cardiac arrhythmias
49
Q

What does the initial AED tx (e.g. diazepam, PB) do?

A
  • decreases HR
  • increases RR
  • decreases BP
  • the animal is then hypoxic and hypotensive so never forget to also treat with these 3 things: oxygen, cool down, fluids)
50
Q

What causes multiple organ failure

A
  • energy depletion
  • circulatory collapse
  • organ hypoperfusion
51
Q

3 tx goals for seizure

A
  • stop the seizures
  • protect the brain
  • think about the future
52
Q

What should you monitor with seizures?

A
  • HR
  • BP
  • O2
  • electrolytes/ fluid balance
  • body temperature
53
Q

How can you minimise seizure complications?

A
  • MINIMIMISE BRAIN INJURY:
  • tx hypotension (volume expansion, fluid balance)
  • tx hypoxaemia (O2 supplementation)
  • MINIMISE HYPERTHERMIA (critical to reducing damage)
  • MINIMISE RENAL IMPAIRMENT
54
Q

Ddx - underlying disease –> seizures

A
  • HYPOGLYCAEMIA/ ELECTROLYTE IMBALANCE: correct
  • POSSIBLE TOXICITY? diuresis, decontaminate
  • SUSPECT INTRACRANIAL CAUSE: advanced imaging, CSF analysis
  • REFERRAL?

Neurology (26 decks)

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