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PAR2031 - Pharmacology > Week 9 > Flashcards

Week 9 Flashcards

1
Q

What is an affective disorder

A

Characterised by disturbances in mood, associated with alterations in behaviour, energy, apetite and sleep.

Extremes range from mania to depressive states

eg. Bipolar, Depression, Anxiety

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2
Q

What are the major diagnostic criteria for depression?

A
  • pervasive depressed mood and/or marked loss of interest in pleasure

along with 4 of the following:

  • Marked change in weight
  • Insomnia or hypersomnia
  • fatigue/loss of energy
  • Feeling worthlessness
  • Excessive/inappropriate guilt
  • indecisiveness or diminished concentration
  • feelings of hopelessness
  • thoughts of death, suicidal ideation
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3
Q

What is the monoamine theory of depression?

A

depression resulted from a decrease in activity of noradrenaline, serotonin in the CNS

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4
Q

What is an issue with the monoamine theory?

A

full antidepressant affect takes 6-8 weeks (some improvement seen in 1-3 weeks) but the drugs have an immediate effect on NA and serotonin

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5
Q

What are some of the treatments for depression?

A
  • Psychotherapy (for mild to moderate depression)
  • Cognitive behavioural therapy (eg hypnosis)
  • improvement in socialisation, exercise and diet
  • Electroconvulsive therapy
  • Antidepressant medication
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6
Q

What is the goal of antidepressant pharmacology?

A
  • provide relief from psychological and physiological symptoms
  • enhance functional capacity
  • reduce likelihood of self-harm or suicide
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7
Q

What % of adult patients respond to antidepressiant treatment (drugs)

A

half

30% with placebo.

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8
Q

Are antidepressant drugs equal in efficacy?

A

yes

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9
Q

What factors may influence the choice of antidepressants?

A
  • the amount of sedation
  • adjunctive drugs
  • toxicity
  • weight gain
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10
Q

What are some adverse effects of antidepressants?

A
  • Serotonin toxicity can occur with just a single dose, resulting in hyperstimulation
  • Most antidepressant drugs decrease threshold potential for seizures.
  • in children has risk of increasing suicidal thoughts and behaviour - can work in adults too
  • may provoke manic episode when used in people with bipolar
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11
Q

how do tricyclic antidepressants (TCA’s) work?

A

acts as an amine

  • amine re-uptake pump
  • stops neurotransmitters from being returned above synaptic cleft. Hang around in cleft longer. noradrenaline and serotonin
  • keeps all neurotransmitters as it’s generalised. acts on all amine pumps
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12
Q

How are tricyclic antidepressants dangerous?

A

Most dangerous in overdose

  • sedative
  • autonomic side effects
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13
Q

what are autonomic side effects of Tricyclic antidepressants?

A
  • include blocking of mAChR’s, histamine but more importantly SODIUM channel blocking.

Which has significant cardiovascular impact

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14
Q

What are the 3 signs of toxicity?

A
  • Less than adequate perfusion
  • QRS >0.12 (>0.16 indicates severe toxicity)
  • QT prolongation (>1/2 R-R interval)
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15
Q

What are Selective Serotonin Reuptake Inhibitors (SSRIs)

A
  • Works at the Amine reuptake pump but targets serotonin
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16
Q

What are some benefits of SSRIs?

A

Have a wide margin of safety and a different spectrum of side effects

Have fewer autonomic NS as lower effect of Noradrenaline

17
Q

What are some disorder SSRI’s are prescribed for?

A
  • Anxiety
  • Panic
  • OCD
  • Bulimia nervosa
  • premenstural dysphoric disorder
18
Q

What are Monoamine Oxidase Inhibitors?

A
  • Monoamine oxidase is an enzyme that breaks down neurotransmitters
  • meaning more are left and less broken down
  • works on both noradrenaline and serotonin
19
Q

Why are Monoamine Oxidase Inhibitors used less often?

A
  • dangerous interactions with some food and drugs

- hypertensive crisis common

20
Q

What are some mood stabilisers?

A

Lithium - drug of choice

Mode of action unknown but it inhibits dopamine release

21
Q

What is the therapeutic range for lithium?

A

is extremely low

0.5-1.2mmol

22
Q

Where is emesis coordinated in the brain?

A

Vomiting centre in the medulla (medulla in brainstem)

23
Q

Explain the Chemoreceptor trigger zone and its relationship to the vomiting centre

A

Chemoreceptor sits outside blood brain barrier, monitoring circulating toxins - triggers the vomiting centre

called chemoreceptor trigger zone

24
Q

What nerve does the vomiting centre project to?

A

Vagus nerve… parasympathetic effects… and motor neurons supplying the abdominal muscles and coordinating emesis

25
Q

What is reverse peristalsis?

A

transfers contents from upper intestine to the stomach.

26
Q

What neurotransmitter is rich in the chemoreceptor trigger zone

A
  • dopamine and serotonin
27
Q

What neurotransmitter does the vomiting centre contain?

A

mACh receptors

28
Q

What is anticipatory emesis?

A

Emesis bought on by smell, taste, thought

29
Q

How does vestibular disease impact emesis?

A

any pathological process that alters balance can cause dizziness, nausea and vomitting.

30
Q

What are contraindications for stemetil (prochlorperazine)?

A
  1. Circulatory collapse (cool, pale, clammy skin, tachycardia, hypotension)
  2. CNS depression
  3. Previous hypersensitivity
  4. Children
  5. Pregnancy
31
Q

what is the best way to deal with hyperemesis in preggo’s?

A
  • treat dehydration and relieve symptoms
32
Q

what receptors do antiemetics effect?

A

receptors in CNS

33
Q

Where does stemitil work on and what type of receptors?

A

Chemoreceptor trigger zone on dopamine receptors (D2)

34
Q

Where does ondansetron work on and what type of receptors?

A

Chemoreceptor trigger zone on 5-HT3 (serotonin)

and

Pharynx and GIT (on serotonin)

35
Q

What happens when ondansetron is combined with apomorphines?

A
  • can induce hypotension and LOC

- Can cause long QT syndrome

36
Q

What is ondansetron preferred for?

A
  • patients younger than 21

- prophylaxis in spinally immobilised patients

37
Q

Which antiemetic is contraindicated for children?

EXAM QUESTION

A

Stemetil

and metoclopramide

38
Q

How is stemitil administered?

A

12.5mg IM

39
Q

What are the 3 extrapyrimidal reactions caused by prochlorperazine (stemetil)?

A
  • Dystonias (spasms, trismus etc)
  • Akathsia - Feeling pf motor restlessness
  • Parkinsonism - tremor, rigidity
  • Tardive dyskinesia - involuntary movements of face, mouth, neck etc

PAR2031 - Pharmacology (13 decks)

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