Pharma sheet 31 - Karam Elias

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Pharma sheet 31 - Karam Elias

Post by Shadi Jarrar on 23/12/2010, 12:24 am

بسم الله الرحمن الرحيم

_____________________________________ ?ct5otw67bhxbj4g


*Mostly ... 2 types:
1) Quite patients... NO response ... Loss of interest in life  called “–ve person”
* -ve person: always think that life is bad and all life has no meaning.
*Happens mostly with women more than men ...ex. ¼ populations in west must experience depression in his life (especially ladies)..... While Men 10-12 % ... why? Because women are always under the menstrual cycle, steroids and they are more sensitive.
NOTE regarding steroids: they have a big relation with mood changes.

2) The DR. didn’t mention it but I think it is the aggressive type...

*Mostly... Genetics have nothing to do with depression also methods of parents don’t cause depression.
* Post-partum cause depression with women (usually 1-2 days or 1 week) then depression will decrease (normal depression)....But sometimes depression persist for longer time especially if the women had twins ! Why? The dr. doesn’t know....but maybe because of the responsibility & babies depend on her...
*Depression is currently the FOURTH most significant cause of suffering and disability worldwide.
* Probably the financial problems will increase in 2020 so there will be more depression around the it will be the most debilitating human’s condition by 2020....

Brain has many neurotransmitters:
There are serotonin, norepinephrine, and dopamine.
*And the most imp in depression is serotonin... why? Because it is important in regulating the mood.
* Good mood  high serotonin level.
*14 receptor of serotonin in the brain and each has its own particular complicated function.....But the end result is  serotonin regulate mood .
* If the level of serotonin is LOW the patient will be depressed (bad mood).
*SO... most drugs we will talk about will increase the level of serotonin.
The level of dopamine which is related to movement like in Parkinson disease (we replaced the dopamine in all drugs that we talked about.

*Dopamine is related to 2 ideas:
1) Parkinson disease
2) Schizophrenia  if the patient has pleasure, emotions, rewards, motivation, attention ...All these will put the patient in a psychotic diseases (related to dopamine & Parkinson)
SO... in 1 & 2 we try to target the dopamine

 In contrast in serotonin ... if the patient has depression, the level of serotonin will be less this will result in 2 types:
1) The patient is a sleep.
2) Or the patient is very aggressive (ex. suddenly the patient may hit you!!!!)

NOTE: norepinephrine has relation with depression but more toward synapses...& heart rate and stress and alertness.

**Symptoms of depression:
1) Cognitive...
*thoughts of hopelessness
*poor confidence
*-ve thoughts.

2) Emotional
*Feeling sad
* Unable to feel pleasure ... because of loss of interest (no emotion)

3) Psychomotor / physical.
*sleep changes (level of sleep differs between patients ...most of them can’t sleep, 70% of them decrease & 30 % increase)
*Appetite changes (30% increase... 70% decrease)
* Decrease libido (related to serotonin
* Decrease energy  weak , not interested & very –ve person.

*Antidepressants are divided into 4 types:
1. SSRI  serotonin specific reuptake inhibiters
2. TCA Tricycle antidepressant
3. A typical antidepressant
4. MAOI  monoamine oxidase inhibitors (we talked about it when with Parkinson disease).

First : SSRI
• Mostly used.
• Drug of choice in mild to moderate depression (most common manifestation to depression)
NOTE: in severe depression we may use the second type.

• SSRI inhibit the procedure of the reuptake of the serotonin from the synapse the level of serotonin in synapse of the CNS.....SO the deficiency that occurs in the patient we give him motivation (we change the mood of the patient).
REMEMBER ...we regulate the mood by increasing the serotonin level.

• SSRI is the drug of choice.
• Fluoxetine  most famous drug.
• Antidepressant drugs are very important because they have drug-drug interaction with dentistry.
• These antidepressants inhibit cytochrome p-450.
• They interact with :
1) NSAID  not because they inhibit cytochrome p-450 BUT because they may deplete platelet serotonin required for aggregation.... But why this is important?
REMEMBER... Patients take NSAIDs which have main side effect which is GI bleeding (ex.aspirin) so in All NSAIDs may increase bleeding from GI with SSRI.
*if the patient takes fluoxetine and you will describe him NSAIDs...this will increase GI bleeding (this doesn’t mean that you shouldn’t prescribe NSAIDs for him, it means that you have to monitor them)
* You should keep NSAIDs away from the patient that has ulcer & takes fluoxetine.

2) SSRI interacts with codeine & its derivatives.
*It is hard to give him codeine because fluoxetine inhibit conversion of
prodrug to active morphine.
*Codeine must be converted to morphine to be codeine is a
prodrug which is the drug that is activated within the body.
*You give the patient a not active drug and inside the body it will
Convert to an active one EX. is levodopa.
1. Levodopa...inactive drug & we prevent the breaking down of it by
Given the carbidopa and enters the brain, then decarboxylation
happen to levodopa and it is converted to dopamine.
2.Codeine has the same idea.
Codeine is converted to morphine to give the wanted activity.
SO...keep codeine away from the patient who takes SSRI, you
should give morphine instead of codeine because if you give him
codeine ,there will be NO activation because SSRI inhibit conversion
of codeine to morphine.

3) SSRI inhibit oxidation of benzodiazepines but not all benzodiazepines
Undergo oxidation

• If you must give the patient benzodiazepines ...give him
- Lorazepam
- Temazepam
So ... these drugs can be given to patients with SSRI if you want to do dental sedation.

4) Meperidine and tramadol (which is like meperidine synthatic
& narcotic)
• Combination may precipitate an acute serotonin syndrome (increase serotonin)
• Interaction between themif we give merperidine & fluoxetine (serotonin level will be so high) – called serotonin syndrome: A- diarrhea B- insomnia (many manifestation)
• SO... keep the patient away from meperidine.
*NOTE: The table on slide # 3 is very important..... because drugs are related to dentistry.

* Meperidine produce toxicity (hyperthermia) and we can’t give it with MAOI
*you can’t give MAOI with narcotics (opoids)and we must decrease the dose to the half

If the patient doesn’t respond to the SSRI ( fluoxetine) the second choice is to give him an old drug TCAs

- Old drug.
- most used  amitriprtyline.
-The problem is that they don’t have selectivity so they affect many levels...most imp. Is the neuronal reuptake of norepinephrine and serotonin is inhibited, with a resultant increase in activity of the patient.
NOTE: remember SSRI (serotonin selective reuptake inhibitor).
-No selectivity for these drugs so they go and bind to any receptor present, they go to:
1. Muscarinic receptors and produce anticholinergic.
2. Alpha-adrenoreceptors blockingproduce hypotension.
3. 5-HT blocking.
4. Histamine receptors block (means sleep).
~ Every thing is blocked.
-Because of alpha-adrenoreceptor blocking produce hypotension (orthostatic hypotension) because alpha1-blocking  vasodilatation polling of blood in the legs orthostatic hypotension.

*Side effects:
1) Drug induces sedation because of blocking (H1) histamine.
2) Orthostatic hypotension block alpha 1
3)Cardiac effect  related to muscarnic receptor...patient with bradicardia atropine.
4)Anticholinergic constipation ,blurred vision ,urinary retention and dry mouth.
Opposite to (SLUD) that we took before.
1 ,2 ,3 ,4  happens because of the non-selectivity.

*Dentist should be a wake when the patient takes TCAs, why?? Because they have interaction with vasoconstrictors.
*Dentists must take precautions when administering local anesthetic containing adrenergic vasoconstrictors to patients receiving TCAs.
*Local anesthetics containing vasopressers can be used but caution must be exercised; recheck vital signs (most imp are heart rate &blood pressure) following each cartridge or two.
NOTE: Don’t give more than 0.05 mg of epinephrine.
Don’t give more than 3 cartridges or more than 2% lidocaine.

*Remember... There is sedation here because you give antidepressant and this type affects H1 & produce histamine blocking, produce depression when you gave hypnotics (additive or synergistic effect).

*Sedative-hypnotics, barbiturates & narcotics may have their depressant effects potentiated by tricyclcis, and severe respiratory depression may ensue.

**Respiratory depression:
1. Barbiturates
2. Narcotics.
3. Note that benzodiazepines don’t cause it alone, but if they are given with TCAs (antihistamine &depression) may produce respiratory depression.

*if you give narcotic like morphine with TCA you have to reduce the dose.
*The dr. doesn’t prefer to give benzodiazepine with TCA because the patient is depressed.
*Acetaminophen has ability to increase TCA levels in some patients, how?? They don’t know.
*NOTE: if the lady has hypertension & she is pregnant …we start by giving her magnesium sulfate. (Don’t give her drugs at first).

THIRD: A typical type
*Drug name Duloxetine.
* No interaction.
*The patient who takes duloxetine is depressed.
*Serotonin And norepinephrine reuptake inhibitor (like TCA)
*Advantage (over TCA)  no H1 nor alpha1 and they are selective (toward serotonin & norepinephrine) but it is not that imp like SSRI.

• Phenelzine  most drugs used.
• Interaction (we should give 1\2 with narcotics)!!
• Interactionmeperidine -hyperthermia
(We took it last time)

 Why the patient takes fluoxetine, amitriptyline??
A) If the patient was aggressive (this is a characteristic), means if the patient was depressed, anxious and agitative  the drug of choice is “Amitiptyline (TCA) “WHY??
Because amitriptyline (TCA) 1)Decrease drive.
2)Decrease energy.
We give anticholinergic & antihistamine so we let the patient more comfortable but it has anxioytic activity.
3)Alpha1 – blocking.
4) Parasympathetic activity.
SO…* characteristic of depression of a patient  that he is aggressive so we give him TCA
*MAOI (moclobemidia) , fluoxetine….advantages:
1. increase drive
2. Increase energy.

B) If the patient is -depressed
-Lack of drive & energy. (Second type of depression)
We increase the drive & energy and remove the other effects

NOTE….. A+B Go to the last slid & sees the pic =)

Last topic in CNS is

*Not common 1% ..Agitated patient
*Disorganized symptoms:
1) Confused
2)Thinking ,speech and behavior that doesn’t make sense.

* -ve symptoms:
1. Patient lack of expression.
2. No emotion sense (loss of interest).

*+ve symptoms:
Dilatation and hallucination ….because the patient has lost touch with reality in certain imp ways.

**Most symptoms (+ve ,-ve, & disorganized ) happen together.
** Patients stop taking their medication because they do very bad side effects
**they should take the medication for life.
**Patients with schizophrenia who stop taking the prescribed medication are at high risk of relapse into acute psychotic episodes.

There are 2 types of drugs:
1)Respirdon  give the patient motivation.
Trade name ….disperdal (NEW drug)
2) Chlorpromazine (old generation)
**I’m not sure of there name…. = (

• Selectivity of these drugs is weak (new+ old).
• New drugs are better in reliving the –ve symtoms
• Old drugsdecrease hallucination and decrease non-sense acts.
• Side effects:
 Dry mouth.
 Dizziness.
 Blurred vision.
 Constipation.
……… interaction with anticholinergic activity

* Tablet dyskinisia is a side effect on long term usage.
Extrapridmal side effect.
Miniaturization in the tongue (can’t move his tongue properly) (even in new agents ).

NEW agents:
1) Less likely to cause tablet dyskinisia.
2) Tremor
3) Muscle spasms
4) Targious dyskinisia (irreversible)!!!
*if something like this happen (1-4) days we change the drug for the patient.

• One of the depressant.
• Risks are more than benefits.
• Benzodiazepines, barbiturates & even narcotics with alcohol there would be potentiating for the activity.
• CNS problems.
• Hangover (side effect of barbiturates).


Bone by: Karam Yasir Elias
Date of lect.:13.12.2010

Last edited by Shadi Jarrar on 23/12/2010, 1:17 am; edited 2 times in total
Shadi Jarrar
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عدد المساهمات : 997
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تاريخ التسجيل : 2009-08-28
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الموقع : Amman-Jordan

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Re: Pharma sheet 31 - Karam Elias

Post by Dyala Al-Armouti on 23/12/2010, 12:43 am

Dyala Al-Armouti

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تاريخ التسجيل : 2009-09-06
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