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MEDICINE Yr2 Sem2 > PHARMACOLOGY > Flashcards

PHARMACOLOGY Flashcards

1
Q

What is first line therapy for anxiety disorders? And how does it work?

A

SSRIs
Unclear MOA
Maybe receptor down regulation, or gradual mood elevation which allows for better coping strategies

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2
Q

What is the onset of action for SSRIs?

A

2-6wks

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3
Q

What are BENZODIAZEPINES? How does it work?

A

Used to be first line for anxiety.
Allosteric modulator of GABA Channel, keep it opened.
Increase influx of Cl-, thus hyper polarise.
Cause down regulator of neuronal excitability

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4
Q

Why are BENZODIAZEPINES no longer first line therapy?

A

Side effect profile
Drowsiness, Dec Alertness, Lack of coordination.
Stronger capacity of tolerance and thus dependence, so abuse is a risk.
Therefor only short term use. (4-6wk blocks)

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5
Q

What is PREGABALIN? How does it work

A

GABA ANALOGUE
Binds to a-2-d subunit of voltage gated calcium channels.
Well tolerated in general anxiety as monotherapy + with anti-depressants

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6
Q

What are some side effects of PREGABALIN?

A

Dizziness, Headache, Diarrhea
(Generally at higher doses)

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7
Q

What is combination therapy (non-pharm) for Anxiety?

A

1- Cognitive behavioural therapy - (Talk therapy)
2- Symptomatic - acute meds (b-blockers)
3- Lifestyle (exercise + diet)

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8
Q

What is basic mechanisms to hyperpolarising a neuron?

A

High Conc K+ inside
High Conc Cl- outside
Thus, opening either channel would lead to greater negative charge within the neuron.
Therefor hyper polarise.

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9
Q

What is M.A.C?

A

Minimum Alveolar anaesthetic Concentration.
Concentration that leads to immobility in 50% of patients.
Tied directly to solubility.

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10
Q

Is there a correlation between solubility and potency of GenAnaes and Induction?

A

YES
Neuron = covered by fatty myelin sheath.
Lipophillic properties = more easily to cross the barrier.
HOWEVER
Higher MAC typically see a slower INDUCTION RATE. (Theory not fully understood)

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11
Q

Is there a correlation between potency and recovery?

A

YES
Lower the potency, the faster the recovery

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12
Q

What is ISOFLURANE, DESFLURaNE, SEVOFLURANE used for, and what is A/E?

A

Maintenence of General Anesthesia

AE - Laryngospasm + Apnoea

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13
Q

What is METHOXYFLURANE used for, and what is A/E?

A

‘Green whistle’
Provide V. strong analgesia at sub-anesthetic doses

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14
Q

What is NITROUS OXIDE used for, and what is A/E?

A

Maintenance fo General Anesthetic

AE - Hypoxia

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15
Q

Why are intravenous induction agents useful.

A

There is a need to supply ventilation once diaphragm is paralysed, especially for emergency intubation.
They have short but rapid duration
Target GABA.

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16
Q

What are PROPOFOL and THIOPENTAL?

A

Positive Allosteric Modulators of GABAa
Intravenous Induction agent

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17
Q

Why is KETAMINE sometimes used?

A

Used in children
Bc show less risk of respiratory depression
Used as induction agent (intravenous)

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18
Q

What are Focal Seizures?

A

Occurs + Stays in 1 area of brain.
Can have AWARE or IMPAIRED.
(Conscious vs Not)

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19
Q

What are Generalised Seizures?

A

Involves multiple regions in brain w/ loss of consciousness.
Can have MOTOR or NON-MOTOR/ABSENT (mistaken for day dreaming)

Motos - alternating muscle stiffness
Non-motor - typically seen in children + zone out w/ no recall

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20
Q

What are the 2 ways in which seizures can be prevented?

A

1- Enhancing GABA neurotransmission

2- Disrupting neuronal membrane excitability –> Block Na2+, Ca2+ channels

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21
Q

Why and How do we enhance GABA neurotransmission?

A

GABA = major inhibitory effect on CNS –> Calm brain down.

1 - GABA Transaminase - breaks down GABA in presynaptic

2- GAT-1 - Re-uptake into presynaptic

3- GABAa - Receptor of post synaptic

22
Q

What is VALPROATE and VIGABATRIN, and how do they work?

A

GABA Transaminase Inhibitors

First line = Generalised Seizures

Inhibit activity of GABA Transaminase –> Decrease breakdown of GABA –> Increase intracellular conc of GABA

23
Q

What is TIAGABINE, and how does it work?

A

GAT - 1 Inhibitor

Stop re-uptake og GABA –> Increase in extracellular GABA

24
Q

What is MIDAZOLAM, and how does it work?

A

GABAa Receptor Modulator
(Benzodiazepine)

Bind allosterically to GABAa receptor –> Enhance GABA action

***Good for Status Epilepticus

25
Q

What is Status Epilecpticus?

A

Continuous seizure activity (30+ min)

Drug treatment needs to start after 5 min of commencement

Can be generalised of focal

26
Q

What is the role of Na+ in neuronal activity?

A

It depolarises the neuron –> make it reach action potential.

Thus by disrupting –> less action potential –> slower neuronal activity

27
Q

What is the role of Ca2+ in neuronal activity?

A

When action potential reaches terminal –> depolarisation of Ca2+ channels –> influx of Ca2+ –> triggers presynaptic vesicles to release NTs

Thus disrupting means less NTs being released –> less neuronal acivity

28
Q

What are Na+ Channel Blockers?

A

Target Inactive state of channels (higher proportion for faster firing neurons)

CARBAMAZAPINE (First line Focal Seizures)
LAMATRIGINE
PHENYTOIN

29
Q

What are Ca2+ Channel Blockers - High Voltage Association?

A

Eg ; GABAPENTIN

HVA = associated w partial seizures

Often as adjunct therapy

30
Q

What are Ca2+ Channel Blockers - T-type?

A

Eg; ETHOSUXIMIDE

T-type = located within thalamic neurons deep in the brain –> provide ‘pacemaker’ current to cortex

Associated w Absence Seizures

31
Q

Is there a Correlation between Anti-epileptic drugs and pregnancy?

A

YES
All AEDS = Teratogenic –> have effect on developing baby.

Child-bearing age FEMALES = MUST be on effective contraception while on AEDs

32
Q

Why does Parkinsons occur?

A

Loss/Degeneration of dopamine producing neurons in the ‘substantia nigra’

33
Q

What are the 4 strategies to pharmacologically manage Parkinsons?

A

1- Increase synaptic concentration of Dopamine.

2- Direct activation of Dopamine Receptors

3- Prevent Dopamine metabolism

4- Modulate efficacy of other NTs

34
Q

How can we increase synaptic levels of Dopamine?

A

LEVODOPA - Dopamine pre-cursor

Turns into Dopamine by Dopa Decarboxylase (Which is in both CNS and Periphery)

35
Q

Why cant we just administer LEVODOPA by itself?

A

Levodopa –> Dopamine by DOPA DECARBOXYLASE

DOPA DECARBOXYLASE exists in periphery –> When Levodopa = administered –> Becomes Dopamine in Periphery not Brain

<1% will enter brain

36
Q

What do we have to administer Levodopa with?

A

DDC inhibitors (WHICH CANT CROSS BBB)

Eg; CARBIDOPA + BENZERAZIDE

Wont allow it to transform into Dopamine unless in brain.

37
Q

What are some unwanted effects with LEVODOPA?

A
  • Dyskinesias = related to dose and duration
  • Nausea + HypOtension = increase in peripheral Dopamine levels
  • Hallucinations = Increase in CNS Dopamine Levels
38
Q

What is PRAMIPEXOLE + ROTIGOTINE used for?

A

Stimulate D2 Receptors –> AGONIST

AE - Similar to Levodope -> Nausea, hypotension, hallucinations

39
Q

What is the function of Monoamine Oxidase, and why are Monoamine oxidase inhibitors used?

A

MAO = Metabolises NTs, especially Dopamine.

Inhibitors –> Increase Dopamine levels

Eg; Selegiline

40
Q

What is the function of COMT, and why are COMT inhibitors used?

A

COMT = Metabolises Catecholamines, especially Dopamine.

Inhibitors –> Increase Dopamine levels

Eg; Entacapone + Tolcapone

41
Q

Why would modulating activity of other NTs be important when trying to manage Parkinsons?

A

Dopamine Neurons = Have inhib effect on Cholinergic neurons.

Thus, decrease in Dopamine Neurons –> Increased Cholinergic activity

Thus must be suppressed. –> Muscarinic Receptor Antagonists

Eg; BENZTROPINE

42
Q

What is Huntingtons Disease?

A

Inherited Autosomal Dominant = Affected have 50% passing to offspring

Death = 10-15 yrs after symptoms

43
Q

What are some Neuro chemical changes involved with Huntingtons?

A

-Abnormal Huntingtin Protein (Htt) Production
- Selective loss of GABA neurons –> Dopamine hyperactivity

44
Q

Treatments for Huntingtons?

A

Aim to suppress Dopamine Signalling OR enhance GABA

  • D2 receptor Antagonist - CHLORPROMAZINE
  • GABAb receptor Agonist - BACLOFEN
  • VMAT (transporting NTs) inhibitor - TETRABENAZINE
45
Q

What are the Neuro Changes that occur in schizophrenia

A
  • Elevated levels of Dopamine in MESOLIMBIC PATHWAY
  • Increased D2 receptor expression
46
Q

What is the goal when trying to manage Schizophrenia?

A

Inhibit action of Dopamine in Mesolimbic pathway.

*** AVOID INHIBITION in NIGROSTRIATAL PATHWAY —> Imitate effects of PARKINSONS

***AVOID TUBEROHYPROPHYSEAL PATHWAY –> INCREASED Prolactin, Gyno, Amenorrhoea

47
Q

Why do anti-psychotic drugs ain to inhibit Dopamine in the MESOLIMBIC PATHWAY?

A

Decrease in MESOLIMBIC Dopamine

  • Emotional Quietening
  • Psychomotor Slowing
  • Decreased agitation
48
Q

What is the difference between TYPICAL and ATYPICAL Anti-psychotics?

A

TYPICAL = Antagonise Dopamine receptors –> Reduce positive symptoms

ATYPICAL = Antagonise Dopamine + Serotonin receptors –> Reduce positive and negative symptoms

49
Q

What is the difference in POSITIVE and NEGATIVE symptoms in Schizophrenia?

A

POSITIVE - Excess of normal behaviours > Hallucinations, Delusions, Agitation

NEGATIVE - Loss in normal behaviours > Emotion blunting, Social withdrawal

50
Q

Examples of TYPICAL Anti-psychotics

A

Haloperidol + Chlorpromazine

51
Q

Examples of ATYPICAL Anti-psychotics?

A

Risperidone + Clozapine + Quetiapine

52
Q

What is depress

A

MEDICINE Yr2 Sem2 (8 decks)

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