Tuesday 12 March 2019

Anti anxiety | anti anxiety medications

Anti anxiety
Anti anxiety drugs
Classification of antianxiety drugs
Adverse effects
Anti anxiety medications
Anti anxiety treatment

You will learn in this article above mentioned topics.

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You are learning Pharmacology at onlycology.

ANTI ANXIETY

Anxiety : It is an emotional state, unpleasant in nature, associated with uneasiness, discomfort and concern or fear about some defined or undefined future threat.

Some degree of anxiety is a part of normal life.

Treatment is needed when it is disproportionate to the situation and excessive.



Anti anxiety drugs 

These are an ill-defined group of drugs, these are mostly mild CNS depressants which are aimed to control the symptoms of anxiety.

Drug produce a restful state of mind without interfering with normal mental or physical functions.

The anxiolytic-sedative drugs differ markedly from antipsychotics and more closely resemble sedative-hypnotics.

CLASSIFICATION

1. Benzodiazepines : Diazepam, Chlorodiazepoxide, Oxazepam, Lorazepam, Alprazolam.

2. Azapirones : Buspirone, Gepirone, Ispapirone.

3. Sedative antihistaminic : Hydroxyzine.

4. beta blocker : Propranolol.

ANTI ANXIETY MEDICATIONS

The most commonly used drugs are :

Benzodiazepines - Diazepam, Chlorodiazepoxide, Oxazepam, Lorazepam, Alprazolam.

Some drugs if Benzodiazepines have a slow and prolonged action, relieve anxiety at low doses without producing global CNS depression. 

They have a selective taming effect on aggressive animals and suppress induced aggression.

They also suppress the performance impairing effect of punishment.

They are more selective for limbic system and have proven clinically better in both quality and quantity of improvement in anxiety and stress related symptoms.

They act primarily by facilitating inhibitory GABAergic transmission, but other additional mechanisms of action have been suggested.

Higher doses induce sleep and impair performance.

1. Chlordiazepoxide : 
It was the first BZD to be used clinically.

Oral absorption is slow.

Produces smooth long lasting effect.

Preferred in chronic anxiety states.

Its t1/2 is 5-12 hours but active metabolites are produced which extend the duration of action. It has poor anticonvulsant action.

2. Diazepam : 
Quickly absorbed.

Produces a brief initial phase of strong action followed by prolonged milder effect due to a two phase plasma concentration decay curve (distributive phase t1/2  1 hr, elimination phase t1/2  20-30 hours).

Preferred in acute panic states and anxiety associated with organic disease.

3. Oxazepam :
Slowly absorbed.

Penetration in brain is also slow.

Plasma t1/2 is about 10 hrs.

Duration of action is relatively shorter.

Preferred in the elderly and in those with liver disease.

Mainly used in short lasting anxiety states.

4. Lorazepam :
Has slow oral absorption.

Its rate of entry in brain is slower.

t1/2 (10-20 hrs).

Preferred for shortlived anxiety states, tension syndromes etc.

5. Alprazolam :
Particularly useful in anxiety associated with depression.

Good response has been obtained in panic disorders with severe anxiety and autonomic symptoms.

t1/2 is about 12 hrs.

Cause less drowsiness.

6. Buspirone :
It is  the first azapirone, a new class of antianxiety drugs, distinctly different from BZDs.

Relieves mild to moderate generalized anxiety, but is ineffective in severe cases, in those showing panic reaction and in OCD.

Buspirone is rapidly absorbed.

Undergoes extensive first pass metabolism.

Bioavailability  <5% .

Excretion occurs both in urine and faeces.

t1/2 is 2 - 3.5 hrs.

Adverse effects of Benzodiazepines

Sedation
Lightheadedness
Psychomotor
Cognitive impairment
Vertigo
Confusional state
Increased appetite 
Weight gain
Alterations in sexual function
Rashes

Adverse effects of Buspirone

Dizziness
Nausea
Headache
Light headedness
Excitement 
Rise in BP

ANTI ANXIETY TREATMENT

If anxiety symptoms are frequent and persist in a severe form, they are a cause of distress and markedly impair performance.

It should be treated with drugs only when excessive and disabling in its own right.

Drug should be used in the smallest possible dose. The dose has to be found out for each patient by titration with symptoms of anxiety.

The drug should be withdrawn as soon as it is no longer required. But when large dose have been used for longer periods, withdrawal should be gradual.

The usual practice is to give 1/2 to 2/3 of the daily dose at bed time to ensure good nightly rest; the remaining is divided in 2-3 doses given at day time.

Buspirone is a nonsedating alternative to BZDs for less severe forms of generalized anxiety.
The tricyclic and SSRI anti depressants are now being increasingly used in many forms of severe anxiety.

They produce a delayed but often gratifying response and can be combined with BZDs. The SSRIs are now drugs of choice for social anxiety in which BZDs though effective, carry abuse potential on long term use.

Patient with hypertension, peptic ulcer, ulcerative colitis, irritable bowel, gastroesophageal reflux, thyrotoxicosis, angina pectoris, are often given low dose of BZD in addition to specific therapy, though anxiety may not be prominent manifestation.


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Monday 11 March 2019

Pharmacology Quiz



Question 01) Explanation :
Penicillin inhibits cell wall synthesis in susceptible bacteria, inhibits transpeptidase 》 prevents peptidoglycan synthesis 》 cell wall deficient forms 》 autolysis 》 cell death 》 Bactericidal effect.
Question 02) Explanation : 
Neostigmine is a quaternary ammonium compound, directly stimulates the Nm receptors at NMJ. Thus it improves muscle power in patients with Myasthenia gravis.
Pyridostigmine features are same as Neostigmine. Pyridostigmine is preferred over Neostigmine in Myasthenia gravis because it has longer duration of action.
                                                                                                       
Question 03) Explanation :
Reserpine is chief chemical constituent of Rauwolfia, and its structure contains beta carboline ring, and it is also used as adrenergic blocker.

Question 04) Explanation :                                                                                                                     


Question 06) Explanation :                                                                                                                     
Pyrazinamide is converted to pyrazinoic acid by mycobacterial pyrazinamidase and distrupts cell membrane metabolism and transport function.
Chloramphenicol binds with 50s ribosome and prevents peptide bond formation between the newly attached amino acid and peptide chain.

Question 07 Explanation :
Omeprazole : supresses gastric acid secretion : Gastro esophageal reflux, Peptic ulcer.


Question 08 Explanation :Atropine is an antimuscarinic
Dexamethasone is used to treat allergic disorders, skin conditions, ulcerative colitis, arthritis, lupus, psoriasis, or breathing disorders.Deferoxamine is used in iron poisioning.





Saturday 9 March 2019

Pharmacology mnemonics

                             
             

Wednesday 6 March 2019

Epilepsy treatment | Epilepsy medication | Overview

• Epilepsy overview
• Epilepsy types
• Classification of drugs
• Epilepsy treatment
• Epilepsy medication
• Top 10 antiepileptic drug

EPILEPSY OVERVIEW 

Epilepsy is a Greek word that means convulsions.
Epilepsy is a disorder of brain function characterized by paroxymal cerebral dysrhythmia, manifesting as brief episodes ( seizures) of loss or without characteristic body movements (convulsions), sensory or psychiatric phenomena.



EPILEPSY TYPES

GENERALIZED SEIZURES 

1. Generalized tonic-clonic seizures (GTCS, grand mal epilepsy) : It is characterised by the following sequence of symptoms: Aura-epileptic cry-loss of consciousness-fall to the ground-tonic phase-clonic phase-period of relaxation-post-epileptic automatism with confusional states.

2. Absence seizures  (petit mal epilepsy) : It is characterised by sudden onset of starting, unresponsiveness with momentary loss of consciousness.

3. Myoclonic seizures : It consist of single or multiple sudden, brief, shock-like contractions.

PARTIAL SEIZURES

1. Simple partial seizures (SPS) : The manifestations depend on the region of the cortex involved. There may be convulsions or light flashes without loss of consciousness.

2. Complex partial seizures  (CPS) : It is characterised by aura-amnesia-abnirmal behaviour and automatism.

CLASSIFICATION

1. Barbiturate : Phenobarbitone 
2. Deoxybarbiturate : Primidone
3. Hydantoin : Phenytoin
4. Iminostilbene : Carbamazepine 
5. Succinimide : Ethosuximide
6. Aliphatic Carboxylic acid : Valproic acid
7. Benzodiazepines : Clonazepam, Diazepam
8. Phenyltriazine : Lamotrigine
9. Cyclic GABA analogue : Gabapentin
10. Newer drugs : Vigabatrin, Topiramate, Levetiracetam

EPILEPSY TREATMENT 

Antiepileptic drugs suppress seizures but do not cure the disorder; the disease may fadeout though after years of successful control.

The cause of epilepsy should be searched in the patient; if found and treatable, an attempt to remove it should be made.

General principles of symptomatic treatment with antiepileptic drugs are here :

Choice of drug and dose is according to the seizure type and need of the individual patient.

Initiate treatment early, because each seizure episode increases the propensity to further attacks.

Start with a single drug, preferably at low dose---gradually increase dose till full control of seizure or side effects appear.

If full control is not obtained at maximum tolerated dose of one drug, substitute another drug. 

Use combinations when all reasonable monotherapy fails.

Therapy should be as simple as possible. A seizure diary should be maintained.

All drug withdrawals should be gradual (except in case of toxocity), abrupt stoppage of therapy without introducing another effective drug can precipitate status epilepticus.

Prolonged therapy is needed - may be life long or at least 3 years after the last seizure.

When women on antiepileptic therapy conceive, antiepileptic drugs should not be stopped. Though most antiseizure drugs have been shown to increase the incidence of birth defects, discontinuation of therapy carries a high risk of status epilepticus.

Fits occuring during pregnancy themselves increase birth defects and may cause mental retardation in the offspring.


Also read :
Congestive heart failure treatment and medication

EPILEPSY MEDICATION 

Top 10 antiepileptic drugs used are :
1. Phenobarbitone 
2. Primidone
3. Phenytoin
4. Carbamazepine
5. Valproic acid
6. Gabapentin
7. Topiramate
8. Clonazepam
9. Clobazam
10. Ethosuximide

Phenytoin 

Mechanism of action 
Phenytoin acts by stabilizing the neuronal membrane and prevents the spread of seizure discharges.

The sodium channels exist in three forms: resting, activated and inactivated states.

Phenytoin delays the recovery of Na+ channels from inactivated state, thereby reduces the neuronal excitability.

At high concentrations, phenytoin inhibits Ca2+ influx into the neuron, reduces glutamate levels and increases responses to GABA.

Pharmacokinetics 
Absorbed slowly through GIT,
Widely distributed and highly bound to plasma protiens,
Metabolized in liver.

Adverse effect 

Hypertrophy and Hyperplasia.
Hypersensitivity reactions.
Hirsutism.
Hyperglycaemia.
Megaloblastic anaemia.
Osteomalacia.
Hypocalacaemia.
Foetal Hydantoin syndrome.

Carbamazepine

Mechanism of action 
Like phenytoin, Carbamazepine slows the rate of recovery of Na+ channels from inactivation, thereby reduces the neuronal excitability.

Pharmacokinetics 
Absorbed slowly from GIT,
Binds to plasma protiens,
Well distributed in the body including the CSF and metabolized in the liver.


Repeated use of drug causes enzyme induction and reduces the effectiveness of drug itself.

Adverse effect 

Sedation, drowsiness, ataxia, vertigo, blurred vision, nausea, vomiting, mental confusion.
Rashes
Eosinophilia
Lymphadenopathy
Hepatitis
Bone marrow depression 
Aplastic anaemia 
Agranulocytosis

Valproic acid 

Mechanism of action 
Valproate delays the recovery of Na+ channels from inactivation.
It blocks T-type Ca2+ current in thalamic neurons.
Increases the activity of GABA in brain by...

By increasing synthesis of GABA by stimulating GAD (glutamic acid decarboxylase).
By decreasing degradation of GABA by inhibiting GABA-T (GABA transaminase) enzyme.

Pharmacokinetics

Rapidly and completely absorbed from GIT.
Highly bound to plasma protiens.
Metabolized in liver.
Excreted in urine.

Adverse effect 
Common - Nausea, vomiting, anorexia, abdominal discomfort.
CNS - Sedation, ataxia, tremor.
Rashes, alopecia, curling of hair.
Rare but serious complication is fulminant hepatitis.
Teratogenicity




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