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59 Cards in this Set

  • Front
  • Back

Hallucination and delusions are o


Positive symptoms of schizophrenia

Typical anti psychotic drugs


Phenothiazines


Haloperidol

Atypical antisychotics

Clozapine


Rispiridone


Olanzapine


Quetiapine


Sertindole


Phenothiazines(anti psychotics)


Piperidine


Piperazine

Phenothiazine

Antagonist at


D1 and D2 receptor


Muscarinic


Adrenergic


Serotonin (less

Acute dystonia (side of effect of anti psychotics)


antagonist


Use muscarinic antagonistBenztropine or diphenhydramine


Benztropine and diphenhydramine

Peri oral tremor rabbit syndrome

Is a side effect of anti psychotics

Piperazine are more potent anti emetic than others

Side effect of phenothiazines


Include its anti muscarinic,adrenergic and serotonergic effect

Anti psychotics also cause depression of temp regulating area and vasomotor mechanism

Leading to poikilothermic effect

Anti psychotic side effect of being an anti histamine are

Sedation weight gain confusion disturbed concentration

Thioridazine

A piperadine phenothiazines that causes toxic retinopathy

Molidone(anti psychotics )

Least agent that cause weight gain

Leucocutosis is also a side effect of


Antipsychotics

Drug drug interaction with anti psychotics(phenothiazines)

1 inhibit alcohol metabolism


2 potentiate cns depressant


3additive anti cholinergic effect


4 affect the effect of anti hyper tensive drug guanethidine(blocks d reuptake mech)


5 thioridazine have quinidine like effect and can cause nephrotoxicity


Inhibit phenytoin metabolism

Eps side effect are more common

With haloperidol

Haloperidol is a potent D2 antagonist

Fewer ANS effect


Particularly effective for acute amnia


No anticholinergic effect


It causes orthostatic hyootension

Clozapine

Have affinity for d4 receptor


Potent anticholinergic effect


Has no anti anti pakinson effect


Lower affinity for serotonin receptor


Minimal eps

Agranulocytosiz

Side effect of clozapine

Lithium is an anti maniac agent

It takes time for lithium to achieve effective brain level


There is delayed onset of (like 7 days or longer)

Thiazides interfere with lithium excretion

Lithium use can lead to nephrotoxicity (nephrogenic di)


Hydrate properly

Clinical effect of Tca and Mao inhibitor

Takes weeks to manifest

TCA

1st generation imipramine aminotriptyline


2nd generation(heterocyclics) amoxapine maprotiline(resemble the normal tca)


But bupropion and trazodone dont


3rd generation venlafaxine mirtazapine nefazodone (developed on basis of trazodone)


TCA also bock

Alpha receptor histamine and muscarinic receptor

SSRI That is use in depression are

Fluoxetine


Paroxetine


Sertraline


Fluvoxamine


Citalopram

Mao inhibitors

They are either hydrazides: phenelzine


tranylcypromine.


Or non hydrazides:tranylcypromine.Tranylcypromine retain some of it sympathetic characteristics (of the amphitamines


Tranylcypromine retain some of it sympathetic characteristics (of the amphitamines

Chemically

Tca resemble phenothiazine

Tca undergo 1st pass metabolism


Vd is large

Trazodone


And venlafaxine have short half lifes

Fluxetine can be given once weekly (has A very long halflife

Mao inhibitor persist even after the drug is not present

TCA are also use for enuresis

Venlafazine and duloxetine are use for pain


However SSRI are not effective for chronic pain

TCA can cause ejaculatory problem

Some anti depressant causes inhibition of cyp450 enzyme

Digitoxin

Is more lipophilic

Indirect action of digoxin

On SA And AV Node (it slows down conducting tissues generation and propagation of velocity


So it has negative chronotropic effect


Enhancement of vagal activity(parasympathetic tone

Digoxin

Pronlong the av refractory period

In contrast to b4

Digoxin increases the automacity of his purkinje conducting system

Digoxin causes visual disturbances

Yellow (xanthopsia)


Red of green vision


Photophobia


Blurring

Gynecomastia is a side effect of digoxin bcos

It resembles estrogen

CRF causes reduction in volume of distribution and clearance of digoxin

Digibind as a digoxin specific fab fragment use for digoxin overdose

After depolarization activity

Normal ap triggers abnormal ap

Type I na channel blockers

Have little effect on normal tissue it slows conduction primarily in depolarized tissue

Concerning the na channel blockers lidocaine

1 not effective against atrial or av nodal reentrant arrythmia


2 1st line for VT with defect in LV


3 Polymorphic ventricular arrythmia(torsedes de pointes) borderline efficacy


2nd line for ventricular fibrillation and pulseless tachycardia



Lidocaine is known to cause seizure

Lidocaine is not effective orally bcos of 1st pass metabolism

Flecainide has a slow time of recovery from block

Lidocaine has rapid time constant recovery from block

ECG when using lidocaine has no clear changes cos it has little effect on normal tissue

Flecainide cause prolongation of PR and qrs interval but has little effect on qt interval ( little effect on ventricular repolarizatn)

Lidocaine is contraindicated for peri mi ventricular arrythmia

Flecainide can only be used when LV fxn is normal and there is no structural abnormality

Flecainide is used majorly for atrial problems

Atrial fibrillation


Atrial tachycardia contraindicated in ventricular tachycardia

Flecainide is orally active with 90% bioavialbility

Flecainide can increase the level of digoxin when given concurrently

Digoxin has a long half-life and it is highly protein bound

Eliminated via renal route


Oral antacid inhibit d absorption of digoxin


Amiodarone and flecainide increases the level of digoxin


Adenosine act on av nodal re entry(acute)

Methylxanthines (eg theophylline can competitively ) block the effect of digoxin


Dipyridamole can block adenosine degredation

Hypokalemia causes after depolarization and ectopic beat in non pace maker cell


Hyerkalemia slows down conduction velocity

Dofetilide

Prototype of class iii anti arrythmia drug


Others ate sotalol and amiodarone

Di hydropyridine ca channel blocker only block vascular smooth muscle ca channel nifedipine amlodipine

Dialtiazem and verapamil are used for ca channel in the heart

Verapamil have anti hypertensive anti arrhythmic and anti anti anginal property

No MD

There is prolonged PR interval by verapamil

Use for atrial fibrillation and flutter (acute and chronic use ) 1st line

Verapamil undergo extensive 1st pass metabolism

Oral verapamil causes more activity than iv verapamil

Diltiazem and verapamil are rarely use ventricular tachycardia

Diltiazem is also extensively metabolised by 1st pass met.


Diltiazem increases the level of cyclosporine and thus nephtotoxicity

Dofetilide

Inhibit only the rapid component of delayed rectifier of potassium currency


On the ECG there is prolongation of qt interval

Unlike class I agent dofetilide can be use for congestive heart failure

Dofetilide should not be use in pregnant woman and breast feeding woman

Drugs that prevent cationic kidney secretion

Verapamil


Ketoconazole


Cimetidine


Can increase level of digoxij

Amiodarone has d activity as a class I class 2 3 4 anti arrhythmic agent

It blosks na


K



Non competitive inhibitor of b adrenergic receptor


Ca Non competitive inhibitor of b adrenergic receptor Amiodarone causes prolongation of qt interval and PR interval


Ca Non competitive inhibitor of b adrenergic receptor Amiodarone causes prolongation of qt interval and PR interval


Amiodarone causes prolongation of qt interval and PR interval

The most common adverse effect of amiodarone would be pneumonitis leading to pulmonary fibrosis


Can also cause hypotension and hyperthyroidism bcos of it resemblance with iodine

Liver dysfunction can also occur with amiodarone


Amiodarone has a long half-life of 50 days

Amiodarone increases the blood level of warfarin

Dronedarone is less toxic than amiodarone