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Pharmacology > CNS & GI block 4 > Flashcards

CNS & GI block 4 Flashcards

1
Q

What are neuronal signals in the brain control?

A

Breathing, movements, thoughts and emotions.

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2
Q

Illnesses associated with dysfunction of the brain.

A

Schizophrenia, depression, anxiety and Parkinsonism associated with chemical transmitter imbalances/changes in the brain.

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3
Q

brain neurotransmitters

A
  • noradrenaline (norepinephrine)
  • dopamine
  • acetylcholine
  • 5-hydroxytryptamine (5-HT, serotonin)
  • gamma-amino butyric acid GABA
  • glutamate (an excitatory amino acid)
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4
Q

Noradrenaline (NA) brain function and illnesses

A 
-Arousal, sleep, mood,
appetite, hormone release,
body temp
-Depression, insomnia,
eating disorders,
narcolepsy, ADD
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5
Q

Dopamine (D) brain function and illnesses

A 
-Skeletal muscle
movement, behaviour,
emesis, hormone release
-Parkinson’s disease,
schizophrenia,
aberrant behaviour,
psychoses; vomiting
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6
Q

Serotonin
5-hydroxytryptamine
(5-HT)
brain function and illnesses

A 
-As for NA plus behaviour,
pain transmission, emesis
-Depression, ADD,
headaches, eating
disorders, insomnia;
vomiting
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7
Q

Acetylcholine brain function and illnesses

A 
-Cognition, skeletal
muscle movement,
memory, consciousness
-Parkinson’s disease,
dementia
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8
Q

Gamma-amino butyric

acid (GABA) brain function and illnesses

A 
-Motor control, memory,
consciousness
-Anxiety, insomnia,
aberrant behaviour,
epilepsy
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9
Q

Glutamate brain function and illnesses

A

-Memory, learning
-Alzheimer’s, stroke,
Huntington’s,
epilepsy, ?depression

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10
Q

How does neurotransmitter work?

A

A signal travels to the axon terminal, neurotransmitter is released from the storage vesicles into the synapse. neurotransmitter must cross the synapse and bind to its specific receptor in order to transfer message from a neuron to effector tissue.

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11
Q

Where is neurotransmitter stored?

A

storage vesicles

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12
Q

What happens to remaining neurotransmitter in the synaptic space?

A

it is either degraded by enzymes found in the area or it re enters the neuron and stored in the storage vesicles to be use again.

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13
Q

Parkinson’s disease chemical Imbalance/alterations

in neurotransmitter in levels

A

Low dopamine and high

acetylcholine activity

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14
Q

Anxiety/Insomnia chemical Imbalance/alterations

in neurotransmitter in levels

A

High glutamate, low GABA and low

serotonin activity

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15
Q

Psychoses; Schizophrenia chemical Imbalance/alterations

in neurotransmitter in levels

A

High dopamine activity

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16
Q

Epilepsy chemical Imbalance/alterations

in neurotransmitter in levels

A

High glutamate and low GABA

activity

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17
Q

Mode of action of antidepressant drugs

A

Increase/boost levels and/or activity of the excitatory
neurotransmitters - serotonin, noradrenaline
- has different adverse effect
- responses may differ between individuals.

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18
Q

Antidepressant groups

A

SSRIs- Selective serotonin reuptake inhibitors
TCAs- tricyclic antidepressant.
MAOIs- Monoamine oxidase inhibitors
RIMAs- Reversible Monoamine Oxidase Inhibitor Antidepressants

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19
Q

Newer antidepressant

A

SNRIs- Serotonin and noradrenaline reuptake inhibitor
TCAs- Tetracyclic antidepressants
NRIs- Noradrenaline re-uptake inhibitors
NaSSA- Noradrenergic and specific serotonergic antidepressant

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20
Q

Drug examples of SSRIs

A
  • fluoxetine
  • citalopram
  • sertraline
  • paroxetine
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21
Q

Drug examples of TCAs

A

-amitriptyline
-nortriptyline
-doxepin
-dosulepin
(dothiepin)

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22
Q

Drug examples of RIMAs

A

-moclobemide

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23
Q

Drug examples of MAOIs

A
  • tranylcypromine

- phenelzine

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24
Q

What are some adverse effects of TCAs?

A

anticholinergic; antiadrenergic (postural
hypotension) antihistaminic (sedative);
weight gain; cardiac arrhythmias

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25
Q

What are some adverse effects of MAOIs?

A

anticholinergic; risk of hypo-
(antiadrenergic) and hypertensive
responses (hypertensive crisis); sedation

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26
Q

What are some adverse effects of RIMAs?

A

lower risk of adrenergic; nausea;

insomnia; dizziness

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27
Q

What are some adverse effects of SSRIs?

A

nausea; insomnia; sexual dysfunction

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28
Q

What are some adverse effects of SNRIs?

A

Similar to SSRIs – GI symptoms, sexual
dysfunction, headache, anxiety
But also hypertension, tachycardia (due to
inhibition of noradrenaline reuptake)

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29
Q

Drug interactions to watch out for TCAs

A

Other antidepressants; antimuscarinics;
hypnotics; anxiolytics; anaesthetics;
antihypertensives; caution with
anticonvulsants

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30
Q

Drug interactions to watch out for MAOIs

A

Sympathomimetics (e.g. phenylephrine,
dopamine, adrenaline, etc); other
antidepressants, antihistamines; hypnotics;
anxiolytics

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31
Q

Drug interactions to watch out for SSRIs

A

Other antidepressants; anticonvulsants;
antipsychotics; other drugs that increase
serotonin (e.g. St John’s Wort, tramadol, etc)

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32
Q

What happens when there’s too much neurotransmission?

A
  • neurons overexcited
  • increased neurotransmitters or receptors
  • increased neurotransmitter activity
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33
Q

What happens when there’s too little neurotransmission?

A
  • neurons not being excited
  • decreased neurotransmitters or receptors
  • decreased neurotransmitter activity
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34
Q

Two ways that drugs can help diseases where chemical imbalances occur are:

A
  • Drugs can be designed to enhance the activity of a neurotransmitter by
    acting on different areas of the neurotransmission pathway
    -Drugs can be designed to block the neurotransmitter’s action or
    response.
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35
Q

CNS cause variety of side effects

A

adverse effects are dependent on where the receptors for the neurotransmitter are located. the drug will act on the area of the brain that is required for therapeutically.

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36
Q

Antipsychotic drugs also called

A

• major tranquillisers
• neuroleptics
it modify abnormal psychotic
behaviour

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37
Q

What is the first generation of antipsychotics medication?

A

Typical antipsychotics

  • Phenothiazines-chlorpromazine, pericyazine, fluphenazine
  • Butyrophenones- haloperidol
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38
Q

What is the second generation of antipsychotics medication?

A

Atypical antipsychotic

  • clozapine (oral liq, tablet)
  • olanzapine (inj, tablet, tablet, depot inj)
  • quetiapine (tablet)
  • risperidone
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39
Q

What are some adverse effects of antipsychotic medications?

A
  • Extrapyramidal effects
  • Postural hypotension
  • Anticholinergic
  • Sedation
  • Weight gain
  • Endocrine effects - e.g. hyperprolactinaemia
  • Neuroleptic Malignant Syndrome (NMS)
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40
Q

What are some adverse effects of extrapyramidal

A

-Akathisia - restlessness, fidgety
-Dystonia – muscle spasms, wry neck,
torticollis
-Oculogyric crisis - upward rolling of
eye balls
-Parkinsonism - fine tremors, bradykinesia,
drooling, shuffling gait
-Tardive dyskinesia - irreversible, occurs
with long term use, stereotyped
involuntary movements

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41
Q

Time frame of adverse effects

A 
-Initial adverse effects (hours, days)..
Sedation, postural hypotension, anticholinergic,
acute dystonic reactions
-Initial weeks - months…
Akathisia, Parkinsonism, weight gain, endocrine
effects
-After longer term treatment
Tardive dyskinesia – irreversible
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42
Q

Atypical antipsychotics - adverse effects

A
  • Weight gain, dyslipidaemia
  • T2DM
  • Acute severe hypertension
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43
Q

Key concerns with ALL antipsychotics

A
  • managing adverse effects
  • compliance
  • limited response
  • recurrence of symptoms
  • monitor of BG,risk factors
  • neuroleptic malignant syndrome
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44
Q

what is mood stabilisers

A

medications used for people who cycle between mood swings. eg depression and bipolar

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45
Q

Mood stabiliser drugs include

A 
lithium carbonate,
carbamazepine and
sodium valproate and
lamotrigine
Lithium is the best-reduce noradrenaline
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46
Q

What is lithium?

A
  • Controls both manic and depressive state

- Takes about a week to reach therapeutic levels

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47
Q

Contraindications of lithium

A

pregnancy, lactation, cardiac and renal
insufficiency
-Narrow therapeutic index drug. Need for very strict monitoring

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48
Q

How is lithium distributed?

A

Lithium distributes itself in both intracellular and
extracellular spaces like sodium and impedes normal
functioning.

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49
Q

How is lithium treated in the body?

A

Lithium is treated like sodium as they have similar chemical structure

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50
Q

Symptoms of lithium toxicity

A

-Initially – slight nervousness, abdominal pain, anorexia,
vomiting, diarrhoea
-Potentially fatal outcome- cardiovascular, renal, failure

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51
Q

What are involve in treatment for depression?

A

Pharmacological and psychosocial interventions. for severe depression, electroconvulsive therapy may need to be used as well.

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52
Q

What is psychosis?

A

a disordered thinking and disturbed emotional tome. it is a symptom not a disease

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53
Q

What is neurosis?

A

a thinking patterns which are normal but disturbed emotional tone

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54
Q

Antipsychotic drugs for schizophrenia positive type symptoms includes?

A

acute illness, with delusions, hallucinations, incongruous behaviour. This type of manifestation is responsive to antipsychotics.

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55
Q

Antipsychotic drugs for schizophrenia negative type symptoms includes?

A

chronic illness, i.e. apathy, lack of motivation, social withdrawal, and is usually less responsive to antipsychotics.

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56
Q

commonly used anxiolytics and hypnotics drugs for treatment of anxiety and sleep disorders.

A
  • triazolam
  • midazolam
  • diazepam
  • clonazepam
  • zopiclone
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57
Q

barbiturates

A

caused problems of dependency, tolerance, drug interactions and were potentially fatal in overdose.

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58
Q

barbiturates is replaced by benzodiazepines

A

has fewer problems with drug
interactions, were not fatal in overdose and were not considered to cause
physical dependency.

59
Q

Benzodiazepines

A

act on receptors in the CNS to potentiate the inhibitory

action of gamma-aminobutyric acid (GABA).

60
Q

Therapeutic uses of Benzodiazepines

A
  • Anxiety and panic disorders – anxiolytics. e.g. diazepam, lorazepam
  • Sleeping disorders – hypnotics, sedative e.g. triazolam, diazepam
  • Muscle spasms and seizure disorders – muscle relaxants; anticonvulsants
    e. g. diazepam
  • Preoperative medication, conscious sedation. eg midazolam
61
Q

What is a sedative?

A

a substance that diminishes the activity of an organ or tissue, in our contextCNS

62
Q

What is hypnotic?

A

(sleeping pills) medications that induce sleep

63
Q

What is anxiolytics?

A

medications that prevent or

treat anxiety.

64
Q

Zopiclone

A

short-acting hypnotic which is structurally different to the benzodiazepines.
It is a preferred option to the
benzodiazepines, as it shortens the time to get to sleep, decreases the number of nocturnal awakenings

65
Q

Antihistamines

A

such as promethazine have sedation

as a SE and so are sold as sleep aids

66
Q

Melatonin

A

a hormone produced by the pineal gland

67
Q

list of drugs in the treatment of

Parkinson’s disease and drug induced Parkinsonism

A

-levodopa (L-Dopa) – Note: not available in NZ on its own
-Sinemet (L-Dopa & carbidopa) and Madopar (L-Dopa &
benserazide)
-pramipexole-dopamine-receptor agonists
-ropinirole-dopamine-receptor agonists
-selegiline – monoamine-oxidase (MAO)-B inhibitor
-entacapone - catechol-O-methyltransferase (COMT) inhibitors
-benzatropine – antimuscarinic

68
Q

In both Parkinson’s disease and drug-induced Parkinsonism there is a decreased in what?

A

dopamine activity in a certain area of the brain called the
substantia nigra. imbalance between two neurotransmitters occurs. The imbalance is low dopamine activity and high
acetylcholine activity.

69
Q

what happens when you have Parkinson’s disease?

A

the number of cells producing dopamine declines

lowering the level of dopamine activity. cause is unknown.

70
Q

what happens when you have drug-induced Parkinsonism ?

A

there is a blockage of the dopamine receptor sites in the substantia nigra (e.g. by some antipsychotic drugs) resulting in lowered dopamine activity

71
Q

Parkinson’s disease drug treatment

A

restoration of the
dopamine/acetylcholine imbalance i.e. increasing the dopamine activity and
decreasing the acetylcholine activity.

72
Q

drug-induced Parkinsonism drug treatment.

A

the acetylcholine imbalance is addressed, and the treatment aims to decrease
acetylcholine activity.

73
Q

how does Levodopa (L-Dopa) works?

A

precursor of dopamine and can pass through the blood–brain barrier. Once in the brain, levodopa is converted to dopamine so raising the
level for use.

74
Q

pramipexole and ropinirole drugs

A

are used in the treatment of both Parkinson’s disease and drug induced Parkinsonism.

75
Q

drugs that are used to decrease the acetylcholine activity.

A

benzatropine, procyclidine.

76
Q

list of commonly used anticonvulsants. drugs used in the treatment and control of
epileptic seizures

A
  • phenytoin
  • lamotrigine
  • carbamazepine
  • clonazepam
  • sodium valproate
  • gabapentin
  • diazepam
77
Q

what is Epilepsy?

A

a seizure disorder that can result from a biochemical imbalance (e.g. electrolytes) or a structural abnormality (e.g. tumour, injury) A seizure associated with epilepsy results from abnormal electrical discharges from thecerebral neurons and is characterised by a loss or disturbance of
consciousness and usually by a convulsion.

78
Q

what is a partial (focal) seizure?

A

a cluster of neurons and present with unilateral symptoms

79
Q

what is a generalised seizure?

A

involves both

hemispheres of the brain.

80
Q

Drugs used to treat epileptic seizures are called

A

anticonvulsants or

antiepileptics

81
Q

what are Anticonvulsants drugs?

A

are CNS depressants and suppress abnormal electric impulses from the seizure focus to other cortical areas.

82
Q

dose related adverse effects of anticonvulsants?

A

sedation, tiredness, dizziness, confusion, slurred

speech, ataxia, tremor, decreased co-ordination, dry mouth and GI upsets

83
Q

what is Status epilepticus?

A
  • Continuous series of seizures without reawakening, may get permanent brain damage
  • Can result from abruptly discontinuing an anticonvulsant
84
Q

drugs used for Status epilepticus?

A

diazepam, clonazepam

85
Q

Principles of antiepileptic therapy

A

to control seizures without the person having intolerable adverse effects

86
Q

why is it important to use Monotherapy for anti epileptic therapy?

A
  1. Lower risk of drug-drug interactions
  2. Lower risk of adverse effects
  3. Easier monitoring
  4. Improved compliance
  5. Lower risk of teratogenicity
87
Q

Mode of action of phenytoin and carbamazepine.

A

Affecting the movement of sodium ions across the membrane.

88
Q

Mode of action of ethosuximide.

A

Stabilising the nerve membranes directly.

89
Q

Sodium valproate

A
  • first line choice for all generalized epilepsies,

- possibly should be avoided in women of child-bearing age/

90
Q

Carbamazepine

A
  • first line choice for partial epilepsies

- can also be used in the treatment of generalized or mixed epilepsies

91
Q

Lamotrigine

A
  • alternative first line choice for partial epilepsy
  • also useful for most forms of epilepsy
  • alternative choice if sodium valproate is not suitable
92
Q

Phenytoin

A

-has a narrow therapeutic index drug
-highly protein
bound so phenytoin will compete with other drugs

93
Q

what is Gabapentin?

A

indicated for the treatment of partial seizures with or without secondarily generalised tonic-clonic seizures in adults and children age three years and above who have not achieved adequate control with standard anti-epileptic medicines

94
Q

what is Diazepam used for as anticonvulsant?

A

treating status epilepticus and clonazepam may be used to treat refractory (non respondent) absence or myoclonic seizures.

95
Q

list of commonly used drugs in the field of GENERAL anaesthesia

A
  • propofol
  • hiopental sodium
  • isoflurane
  • sevoflurane
  • nitrous oxide
96
Q

list of commonly used drugs in the field of LOCAL anaesthesia

A
  • lidocaine
  • bupivacaine
  • tetracaine
97
Q

what is term anaesthesia is defined as?

A

loss of feeling or sensation in all or part of the body. Anaesthesia will reduce or abolish the person’s sensation of pain which enables surgery to be performed.

98
Q

what does General anaesthetics do?

A

depress the central nervous system, ease pain and cause loss of consciousness and these drugs are used for major surgery.

99
Q

what does local anaesthetics do?

A

block pain at the site where the drug is administered, and this allows consciousness to be maintained eg.dental, minor surgery.

100
Q

Difference between analgesics VS anaesthetics.

A

-Analgesics are used to control pain
-anaesthetics are used to prevent pain for a limited period of time, during
surgery.

101
Q

Examples of drugs given prior and during general anaesthesia

A

-Premedication e.g benzodiazepine (e.g. midazolam),acid lowering drug (e.g. hyoscine, glycopyrronium)
- Opioid analgesic (e.g. fentanyl)
- Propofol or a short acting barbiturate e.g. sodium
thiopental IV for induction
-An inhaled gas e.g. isoflurane, desflurane
-. A muscle relaxant if needed e.g. rocuronium,suxamethonium

102
Q

General anaesthesia mode of action?

A
  • alter movement of ions in and out of nerve cells and interfering with conduction of nerve impulse and
  • enhance GABA activity and cause hyperpolarisation of CNS
103
Q

General anaesthesia proceeds through four stages, what are they?

A
  1. Analgesia or Induction
  2. Excitement or Delirium
  3. Surgical
  4. Medullary Paralysis
104
Q

Analgesia or Induction

A

Auditory and visual hallucinations may occur.

Speech difficult and sensations of smell and pain are lost.

105
Q

Excitement or Delirium

A

Client more or less unconscious. Confusion,

excitement or delirium may occur.

106
Q

Surgical

A

Surgery performed in phase 2 and upper phase 3.
Important that there is muscle relaxation. As anaesthesia deepens, respirations become more shallow and respiratory rate is increased.

107
Q

Medullary

Paralysis

A

Toxic stage of anaesthesia. Respirations are lost and

circulatory collapse occurs.

108
Q

The effect of the general anaesthetic is generally confined where?

A

Central nervous system

109
Q

Adverse effects of general anaesthetics

A
  • CV – drop in blood pressure
  • CNS – respiratory depression
  • Liver – “Halothane Hepatitis”
  • Uterus – relaxes uterine muscles
  • Malignant hyperthermia – rare
  • CTZ - nausea/vomiting
110
Q

Local anaesthetics

esters and amides

A
  • Block pain at site where drug administered
  • Allows consciousness to be maintained
  • Administration route: topical, intradermal, subcutaneous, epidural, intrathecal, intravenous
111
Q

Local Anaesthetics Mode of Action

A
  • block pain transmission between the PNS (nociceptors) and CNS
  • block movement of sodium ions through channels in plasma membrane
112
Q

Amides (has an extra I in front of caine)

A

-Lidocaine (lignocaine): effective for producing analgesia. A wide range of formulations available. Rapid onset and moderate duration of action [1-3 hr]
-Bupivacaine: if given during childbirth it does not cross placental barrier. Onset of action slow [approximately 15-20 minutes after injection] and
long duration of action [3-10 hr]

113
Q

Esters

A

Tetracaine (amethocaine): used in topical preparations e.g. gel to be applied before
cannulations or drops for ocular anaethesisa

114
Q

Epidurals

A
  • Nerve block used during childbirth, major surgery.

- Blocks pain during labour with minimal interference to muscle function/contraction

115
Q

Potential problems with local

anaesthetics

A

1)Local anaesthetics can also affect sodium channels in other parts of the body e.g. heart. This can lead to an abnormal heart beat.
2)Epidural anaesthetic could introduce foreign substances
into the CSF.
3) Overdosage of local anaesthetic could lead to dose dependent CNS side effects
4)The ester containing local anaesthetics can cause
allergic reactions

116
Q

Monitoring and care associated with general

and local anaesthetics

A

1)Make sure vital signs and consciousness are monitored
before, during and after general anaesthetic use.
2)Evaluate local anaesthetised areas for sensation and movement.

117
Q

Inhalation anaesthetics

A

can be gases or volatile liquids administered as a gas. absorbed through the lungs into plasma

118
Q

Intravenous anaesthetics

A

-Propofol is the most widely used intravenous anaesthetic. It can be used for the induction or maintenance of general anaesthesia. It has a rapid onset of action and loss of unconsciousness can occur within 10 seconds.
-Thiopental sodium is another IV anaesthetic that
can be used for induction of anaesthesia

119
Q

Side effects of Intravenous anaesthetics

A

These drugs are potent respiratory depressants, but in the setting of controlled ventilation this is usually not a problem.

120
Q

list of drugs used as anaesthetics/analgesics in childbirth

A 
-50% nitrous oxide &
50% oxygen
-pethidine
-fentanyl
-bupivicaine
121
Q

what are the sources of pain in labour ?

A

myometrial ischaemia, cervical dilatation, vaginal/perineal distension and pelvic girdle pressure

122
Q

Potential Adverse Reactions or Complications of analgesics in childbirth

A
  • Hypotension
  • Ineffective labour/reduced effectiveness of voluntary effort
  • Post dural puncture headache
  • Urine retention
123
Q

list of antiemetic drugs that are commonly used. drugs used to control nausea and vomiting

A
  • prochlorperazine
  • promethazine
  • metoclopramide
  • hyoscine
  • ondansetron
124
Q

what triggers nausea and vomiting and how our body responds to these triggers.

A

The central controls of vomiting are two areas in the brain called the vomiting centre and the chemoreceptor trigger zone (CTZ.)

125
Q

how antiemetics work

A

blocking the receptors, stopping the neurotransmitters from binding to the receptors and hence stopping the
vomiting or CTZ from being stimulated

126
Q

five categories of

antiemetic drugs:

A
  • antihistamines [H1-receptor antagonists]
  • antimuscarinics [Muscarinic receptor antagonists]
  • dopamine antagonists [D2-receptor antagonists]
  • phenothiazines
  • serotonin blockers [5-HT3 receptor antagonists]
127
Q

antihistamines such as promethazine and cyclizine

A

bind to the H1- receptor in the vomiting and vestibular centres, block histamine from binding and hence inhibit or reduce vomiting

128
Q

dopamine antagonists such as metoclopramide and domperidone

A

treat vomiting caused by delayed gastric emptying, infection-induced, cytotoxic-induced, and drug-induced vomiting.

129
Q

anticholinergics such as hyoscine

A

are used for motion sickness (action peaks 1-2 hrs after ingestion), as a gastro-intestinal antispasmodic and as premedication. The adverse effects include dilated pupils, tachycardia,
drowsiness, and dry mouth.

130
Q

serotonin blockers such as ondansetron, granisetron and tropisteron

A

drugs of choice for treating nausea and vomiting induced by chemotherapeutic drugs, i.e. anticancer drugs and post-operative nausea and
vomiting

131
Q

Main functions of the GI tract which are important from a pharmacological
viewpoint are

A
  1. gastric secretion
  2. the motility of the bowel and expulsion of the faeces
  3. vomiting (emesis)
  4. formation and excretion of bile.
132
Q

list of drugs that are commonly used Antiulcer Drugs and Antacids

A
  • H2-receptor antagonists – cimetidine, ranitidine
  • proton-pump inhibitors – omeprazole
  • antacids [weak bases] – aluminium hydroxide, magnesium hydroxide
  • misoprostol – prostaglandin analogue
  • antibiotics necessary for eradicating H. pylori
133
Q

Mucous and bicarbonate combine to form what?

A

form a protective layer over the mucosa.

134
Q

Once the parietal cell has been stimulated to produce hydrochloric acid, the acid will
be released or secreted from the parietal cell via?

A

Proton pump

135
Q

Gastrin, acetylcholine and histamine can all stimulate

A

the parietal cell (by binding to their specific receptors on the parietal cell) to produce hydrochloric
acid

136
Q

gastrin (a hormone)

A

acts on the gastrin receptor to stimulate production and release of HCl.

137
Q

acetylcholine (a neurotransmitter)

A

s released from nerve cells and acts on muscarinic receptors to stimulate production and release of HCl

138
Q

histamine (a local hormone)

A

is released from mast cells and acts on H2-receptors to stimulate production and release of HCl.

139
Q

Prostaglandins have a duel role in the stomach.

A

Prostaglandins will inhibit
gastric acid production and promote formation of the protective mucosal
layer.

140
Q

The ulcer healing drugs that work by

A

decreasing gastric acid secretion are the

proton pump inhibitors, H2-receptor antagonists, and the anticholinergics.

141
Q

drugs that are used to neutralise gastric acid secretions are termed
antacids

A

Antacids work by neutralising the acid in the
stomach. Antacids are effective at relieving symptoms caused by excessive secretion and are used for treatment of peptic ulcers and dyspepsia.

142
Q

Diarrhoea

A

First line of treatment (emergency) for

diarrhoea is rehydration and electrolyte replacement therapy

143
Q

Antimotility drugs

A 
Opium-related drugs
Dose of narcotics less than that needed for
central analgesia
-loperamide – tablet, capsule
-codeine – tablet
-diphenoxylate* – tablet

Pharmacology (7 decks)

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