1. Trang chủ
  2. » Y Tế - Sức Khỏe

AN ATLAS OF DEPRESSION - PART 10 pot

7 197 0

Đang tải... (xem toàn văn)

THÔNG TIN TÀI LIỆU

Thông tin cơ bản

Định dạng
Số trang 7
Dung lượng 807,58 KB

Các công cụ chuyển đổi và chỉnh sửa cho tài liệu này

Nội dung

Blocks presynaptic a2 -adreno-ceptors Trazodone is a weak inhibitor of 5-HT reuptake 5-HT terminal Blocks postsynaptic 5-HT2 receptors Figure 9.31 The mode of action of trazodone.Trazodo

Trang 1

NE terminal

Norepinephrine (NE) receptor

(b 1 , b 2 , a 1 etc.)

Serotonin receptor (5-HT 1A , 5-HT 2 etc.)

Blocks presynaptic

a2 -adreno-ceptors

Trazodone

is a weak inhibitor

of 5-HT reuptake

5-HT terminal

Blocks postsynaptic 5-HT2 receptors

Figure 9.31 The mode of action of trazodone.Trazodone is a weak inhibitor of serotonin reuptake and can increase norepinephrine

release as a result of its antagonistic action on presynaptic a2-adrenoceptors It also blocks postsynaptic 5-HT2receptors

N

N

Cl

Cl

N

O N(CH2)3N

(CH2)3NHMe

H

COOH

CH2CH

NHC(CH3)3

NH2 N

COCHCH3

Figure 9.30 Molecular structures of trazodone, maprotiline, L-tryptophan and bupropion

Trang 2

Drowsiness

Anxiety

(in high doses)

Nausea

Orthostatic

hypotension

Priapism

Figure 9.32 Side-effects of trazodone

NE terminal

Norepinephrine (NE) receptor

(b 1 , b 2 , a 1 etc.)

Serotonin receptor (5-HT 1A , 5-HT 2 etc.)

Maprotiline acts at uptake site

Maprotiline acts at uptake site

5-HT terminal

Figure 9.33 The mode of action of maprotiline Maprotiline is a modified tricyclic antidepresssant (TCA) that has similar efficacy to

the TCAs

Trang 3

NE terminal

Norepinephrine (NE) receptor (b 1 , a 1 etc.)

or a 1 -receptor on serotonergic cell body

or a 2 - heteroceptor on serotonergic

nerve terminal

Serotonin receptor

5-HT terminal

Mianserin

blocks a2

-autoreceptor

Desensitization of 5-HT1B/5-HT1D receptors

Increased activity

of 5-HT1A receptors

5-HT2 and 5-HT3 receptors blocked

a2-heteroceptor

on serotonergic nerve terminal stimulates increased release of serotonin

Figure 9.36 The mode of action of mianserin Mianserin, like mirtazapine, enhances noradrenergic and serotonergic function by

block-ing the inhibitory a2-adrenoceptors on noradrenergic terminals and the a2-heteroceptors on serotonergic terminals However, mir-tazapine is more effective than mianserin in enhancing serotonergic function, as it increases the firing rate of serotonergic neurons Mianserin is less potent in blocking postsynaptic serotonin receptors

* But to a lesser extent than

older TCAs

Rashes Possible weight gain

Blurred vision*

Glaucoma*

Cardiotoxicity

Tachycardia*

Orthostatic hypotension*

Urinary retention*

Constipation

Dry mouth*

Confusion*

Sedation*

Dizziness*

Reduced sexual function*

N

N

CH3

Figure 9.34 The side-effects of maprotiline

Figure 9.35 Molecular structure of mianserin

Trang 4

Drowsiness Dizziness Sedation Weight gain

Lowering of white blood

cell count (rare)

Agranulocytosis (rare)

Orthostatic hypotension

Hepatitis (very rare)

Arthritis (very rare)

Dyspepsia Nausea

Figure 9.37 The side-effects of mianserin

Sedation Headache

Nausea

Myoclonus Eosinophilia–myalgia syndrome *

Figure 9.38 The side-effects of L-tryptophan *, Eosinophilia– myalgia syndrome was linked to contamination of some trypto-phan-containing products during the manufacturing process, therefore close monitoring is required

Insomnia Headache

Seizures

Nausea Vomiting

Dry mouth

Taste disorders

Fever Rashes

Figure 9.39 The side-effects of bupropion

Trang 5

Drugs used for

treatment of

generalized

anxiety disorder

Benzodiazepines

Partial 5-HT receptor agonist (buspirone) Some tricyclic antidepressants Paroxetine Trazodone Venlafaxine Trifluoperazine

Proven efficacy from randomized

control trials

Causes troublesome sedation and long-term risk of dependance – best used when anxiety symptoms are particularly distressing or disabli

Antipsychotic sometimes used – effect

in reducing anxiety, but associated w

a number of long-term side-effects

Discuss need for long-term treatment Establish degree of affective morbidity

Aim for lithium level of 0.5–1.0 mmol/l

Use a starting dose of approximately 600 mg

in otherwise healthy young adults

Weigh the patient Perform pregnancytest in women of

child-bearing potent

Perform blood tests for renal and thyroid function

Determine lithium level after 5–7 days

Figure 9.41 Lithium treatment plan Lithium should only be used in bipolar prophylaxis

when it is reasonable to anticipate treatment lasting more than 2 years Shorter periods of

treatment are associated with an increased risk of rebound mania on stopping lithium

Figure 9.40 Drug treatment of generalized anxiety disorder

Trang 6

1.0

0.4

0

Confusion Slurred speech, ataxia Coarse tremor, vomiting, diarrhea Death

Side-effects

Polyuria Tremor of hands Metallic taste Reversible nephrogenic diabetes insipidus Weight gain Hypothyroidism

Toxic doses

Therapeutic doses

Toxic effects

Figure 9.42 The side-effects of lithium and its spectrum of

action Graph reproduced with permission from Stevens L, Rodn

I Psychiatry: an Illustrated Colour Text Edinburgh: Churchill

Livingstone, 2001:25

N

CONH2

Figure 9.43 Example of an anticonvulsant drug (carbamazepine).

Carbemazepine has the tricyclic structure of many older antide-pressants and conventional antipsychotic drugs

Side-effects

Weight gain

Teratogenic effects

on fetuses

Impaired attention

Impaired memory

Thirst

Leukocytosis

Polyuria

Impaired renal

tubular function

Skin problems

Tremor

Toxic effects

Drowsiness Disorientation Dysarthria Convulsion Coma Pulmonary complications Cardiac complications Nausea and vomiting Tremor

Hypothyroidism

Non-toxic goiter

Headache Drowsiness

Nausea and vomiting Hepatic problems

Skin rashes

Blood dyscrasias Teratogenic effects

Figure 9.44 The general side-effects of anticonvulsants However, drugs differ in their relative propensity to cause par-ticular adverse effects Always refer to the prescribers informa-tion

Trang 7

Sudden or unexpected death Miscarriage,

death of baby, child or sibling

Multiple prior bereavements

A history of mental illness (e.g depression

or anxiety)

Death of cohabiting part-ner, same-sex partner, etc (may result in disen-franchized grief) Ambivalence of

dependent relationships with the person who has been lost

Death occurred

as a result of a disease with a potential stigma (e.g AIDS)

Death resulted from accident in which bereaved was involved/responsible

Death occurred due to murder or where legal proceedings involved

Death following which a postmortem and/or inquest

is required

Risk factors associated with poor outcome

in bereavement

Figure 11.2 Risk factors associated with bereavement

Figure 10.1 Light therapy for treatment of depression Photograph

courtesy of SAD Lightbox Co Ltd., High Wycombe, UK

Figure 10.2 Transcranial magnetic stimulation is stil an

experi-mental approach to the treatment of depression It appears to show efficacy in acute treatment and may have value in continu-ation treatment

Figure 11.1 The techniques of cognitive–behavior therapy

Keeping a daily record of activities and negative thoughts

Monitoring negative thoughts associated with worsening mood

Challenging negative thoughts

Using imagination to ‘replay’ events

Questioning the assumptions that lead to negative thoughts

Planning rewarding activities throughout the day

Praising oneself for achievements

Dividing complex tasks into achievable components

Anticipating performance in challenging situations

Ngày đăng: 12/08/2014, 00:22

🧩 Sản phẩm bạn có thể quan tâm