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Questions&Answers in PHARMA

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#1
jody 92

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هنحاول نجمع اسئلة مهمة هنا فى التوبيك دة

وهتكون متجاوبة من دكاترة القسم اللى كلنا بنحترمهم وبنقدرهم




تابعوناااا



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ملحوظة:الاسئلة والاجابات من صفحة قسم الفارما على الفيس


لينك الصفحة

http://www.facebook....21981877863630/

:)


Edited by jody 92, 25 February 2012 - 12:37 PM.

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#2
jody 92

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الاسئلة دى من صفحة قسم الفارما على الفيس
وشكر لدكاترة القسم


**********

Q
Can you explain plz this sentence " propranolol is used in Fallot`s Tetralogy cynotic spells ?

A
this is a sudden onset, progressive event seen in infants with Tetralogy of Fallots. It is associated with progressive


cyanosis, hyperpnea (increased rate and depth of breathing) and disappearance of heart murmur. If not treated in time


it may ultimately lead to DEATH - In a typical case of Tetralogy of Fallot the pressures in the right ventricle and left


ventricle are equal.if the pulmonary stenosis is severe then the right ventricular after load becomes high and hence


the right ventricular pressures become high. If the systemic vascular resistance is low (which is usually the case in TOF


with cyanotic spells) then the shunt flow becomes right to left. This results in progressive cyanosis. Propanolol reduces


dynamic RV outflow obstruction.Slight ↑ in SVR. Blocks hyperpnea response.


ther important measures: Knee chest position and Phenylephrine to increase systemic vascular resistance SVR –

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Q


how prazosin cause fluid retention?
A

Prazocin

The fall in blood pressure is opposed by baroreceptor reflexes causing fluid retention – decrease blood

supply to the kidneys will stimulate the renin angiotensin aldosterone system (RAA) causing more fluid

retention. See figure

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#3
jody 92

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َََََََََQ
what is meaning of prokinetic effect???????

A

increase Upper GIT Motility without evacuation

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Q

why Isoxsuprine produces skeletal muscle V.D.( X) while Isoxsuprine produces smooth muscle V.D. (√).
why Propranolol treats angina by producing coronary VD. (X).
what is Direct α-2 agonist &Indirect α-2 agonist.





A



Isoxsuprine produces relaxation of skeletal muscle. X
Isoxsuprine produces smooth muscle relaxation. √
Isoxsuprine produces VD. √
Isoxsuprine produces relaxation of skeletal muscle. X

Methyl dopa competes with dopa leading to


formation of methyl noradrenaline, acting as a ‘False transmitter’. Methyl NA stimulates alpha 2 receptors


in brain stem, so methyldopa is not a direct stimulant of alpha 2 receptors.



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Q
what's 5-HT receptor and why ergot don't block alpha receptor in blood vessels?

A
‎5-HT is an abbreviation of 5-Hydroxy Tryptamine which is SEROTONIN. Ergot alkaloids are PARTIAL AGONISTS on alpha receptors.
if noradrenaline is given after phentolamine it will not elevate blood pressure and accordingly there will be no reflex bradycardia.


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َQ

In page 77 in the staff book, Phentloamine has Histamine like action
and Phenoxybenzamine has anti-Histaminic action. how is this possible although both drugs are non-selective
alpha blockers?




A


Phentolamine has histamine-like action because it is chemically related to histamine (contains imidazoline ring) and can stimulate histamine receptors, whereas phenoxybenzamine is not chemically related to histamine and it acts by blocking many receptors in addition to alpha receptors, including H1 receptors (antihistaminic action).

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َQ

ايه هى

maximum dose of atropin

اللى ممكن تعالج ال OPC

without atropin toxicity

???

A
initial bolus of 3-5 ampoules of atropin ",6 mg " & doses doupled every 5 minutes untill atropinization happened

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Q

What(CTZ,PVD,tobacco amblyobia )mean????
A
tobacco amblyopia: a rare complication of tobacco smoking leading to optic neuropathy which causes decrease in the field of vision or even blindness. some cases can be treated by stopping smoking, vitamin B12, and hydroxycobalamin.

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Q

alpha blockers blocks the reflex bradycardia induced by nor adrenaline true
A
reflex bradycardia occurs as follows:1-Stimulation of alpha 1 receptors on arterioles leads to vasoconstriction and elevation of blood pressure. 2-Baroreceptors are stimulated by the high blood pressure and send impulses to stimulate the vagal center in the medulla(cardiac inhibitory center= CIC) which increases the vagal tone to the heart.You know that the preganglionic nerve releases acetylcholine which stimulates Nn receptors in the parasympathetic ganglia, then the postganglionic nerve releases acetylcholine which in turn stimulates M2 receptors on the SA node leading to bradycardia. In conclusion: reflex bradycardia is mediated by stimulation of 3 receptors:Alpha1-Nn-M2..and if any of these receptors is blocked the reflex will not occur.


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Q
why Prazosin produces an initial hypertensive effect. X
A
prazocin is an alpha 1 blocker and direct vasodilator, so it produces hypotension not hypertension


Edited by jody 92, 05 December 2011 - 07:47 PM.

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#4
jody 92

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Q



how come>>>> hydrogenation of ergot inc. alpha antagonism ... while dihydroergotamine is VC ?? and


ergotamine already is an alpha agonist VC


A

ergotamine and ergotoxin are considered

as "partial agonists" on alpha receptors, and dihyrogenation of these drugs reduces markedly the agonistic action of ergotamine (i.e. dihydroergotamine is a weaker Vasoconstrictor than ergotamine) and abolishes completely the agonistic action of ergotoxine (i.e dihydroergotoxine is an alpha blocker causing Vasodilatation

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Q




why give serotonine antagonist between attack of migraine &while give sumatriptan(serotongne agonist)


during attak?


A

there is a theory stating that the attack of migraine starts with serotonin release from platelets leading to vasoconstriction (aura phase) followed by vasodilatation and edema of blood vessel wall (headache), that's why serotonin antagonisare given for prophylaxis. On the other hand, in acute attacks we need to constrict the dilated blood vessels -back to normal-and this can be done by triptans (as sumatriptan) which stimulate serotonin receptors.


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#5
jody 92

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coomb's test

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Ryanaud's phenomenon


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Edited by jody 92, 05 December 2011 - 08:04 PM.

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#6
jody 92

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Q

why stimulation of beta1 receptors (through increasing cAMP) induce contraction while stimulation of

beta2 receptors (through "also" increasing cAMP) induce relaxation ?

A
cAMP is only a messanger which increases as a result of B stimulation, in heart CAMP increases free calcium release from sarcoplasmic reticulum which causes increase in contractility , but in the bronchi cAMP has a completely different role as it causes dephosphorylation of MLCK enzyme into inactive form, so no formation of MLC-PO4, so no sliding of actin over myosin which=smooth muscle relaxation
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Q


Depletion of endogenous noradrenaline abolishes the sympathomimetic effects of amphetamine

this is wrong or true? bec in the answers of quiz 5 it is true , and when we answerd it true in the quiz of

thursday el mo3eda said that it is false ???



A
depletion of noradrenaline (e.g. by reserpine) will completely abolish the action of indirect sympathomimetics (as amphetamine and tyramine) because they act by releasing noradrenaline from adrenergic nerves..and will partially antagonize the action of dual-acting sympathomimetics (as ephedrine) becuase they act by both releasing noradrenaline + direct stimulation of adrenergic receptors.

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#7
jody 92

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Q

in angina.......decrease Bl.p lead to reflex 1_tachycardia...2_short diastolic coronary perfusion.....3 add beta


blocker or verapamil ,ana mosh fahma rakam 3 momken any explain!!........


A


beta blockers and verapamil decrease heart rate so one of them is added to nitrate to prevent reflex


tachycardia.


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Q



plllllz DRS


is spironolactone used in heat failure ??


i mean that spironolactone cause hyperkalemia


and that supress cardiac properties


and in Mcq book consider that spironolactone is used in severe heart failure


A

in cases of HF there is excess activity of RAAS leading to secondary hyperaldosteronism, excess


aldosterone leads to: 1-sodium and water retention which increases blood volume and preload, and


edema. 2-cardiac remodeling.Spironolactone-being an aldosterone antagonist -is used in heart failure to:


1-correct hypervolemia and edema. and2- protect the heart against remodeling.


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Q


In AutoCoids which drug is used to close patent ductus arteriosus?!


Alprostadil or indomethacin?


A

yohimbine may increase ABP by blockiing pre-synaptic alpha2 receptors leading to increase in


noradrenaline release, which in turn stimulates post-synaptic alpha1 receptors on blood vessels.


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Q


plezzz drs


*ACEI are contraindicated in patients with unilateral renal artery stenosis with 2 functioning kidneys (T or


F)


hya mktoba FALSE f 2lwr2 why????????????? tb ma 27na kda hn3ml renal failure f one kidney



A

This is not generally a problem with unilateral renal artery stenosis because the unaffected kidney can


usually maintain sufficient filtration after ACE inhibition


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Q


plz Drs ,,

-what is papilledema ?

- how come !!.. After usage of ACE I >>> COP may increase in pt wiz congestive HF ??

- And why loop diuretic _specially_ is used 2 correct edema as a disadvantage of minoxidil ??

Thnx in advance .




A


1-papilledema is edema of the optic disc. 2-ACE Is increase COP in HF because they reduce venous return


(by venodilatation) and afterload (by arteriodilatation) and so the heart can pump more blood from the


congested heart and so COP increases 3-loop diuretics are preferred in this case because we need a


potent diuretic to correct salt and water retention caused by vasodilators as minoxidil.


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Q


Drs ,, hwa ana lw esta5dmt el ACE Inhibitors lma yekon 7d 3ndh renin 3aly ashn y2ll EL pressure bs hwa


kman byzwdm el renin ,,, kda el renin hyzed awe ? dh kda 3ady ?



A


no fear of excess renin because AT I (synthesized from angiotensinogen by the effect of renin) will not


be converted into active AT II because ACE is inhibited by the drug.



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Q


Hey Drs , in heart HF ezay bnedy B1-agonists o B1 blockers ?


A

BB (metoprolol-bisoprolol-carvedilol) are given in very small doses to protect the heart against remodelling


in chronic HF, but B1 agonists (dopamine-dobutamine-prenalterol) are given as positive inotropic drugs


especially in acute HF.


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#8
jody 92

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second term


Q

Doctors please ..in the MCQ ..Aspirin given during labor acts as tocolytic. and it is answered as true ..bs in the book , Aspirin => decrease PG => uterine relaxation=>delays labor ! so how is it given during labor to delay it ? ..thanks in advance :)



A



by dr Amani Nabil



there is a difference between pharmacological action and uses; inspite that aspirin is tocolytic (relax the uterine muscles) but it is not used to delay labour as it has many side effects regarding the mother: bleeding, and fetus: cerebral heamorrhage and may be closure of the ductus arteriosus. Indomethacin is used as tocolytic but with limitations (dose, time and duration of administration).

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Q


INDOMETHACIN is indicated for pharmacologic closure of persistent patentductus arteriosus in

premature infants (TRUE/FALSE) WHY?



A


el egaba tb2a true 3shan el indome. be2alel el PGE2 ely maintains el ductus arteriosus patent(opened),,so the result is its closure :)


N.B

by dr Amani Nabil


:emotion-30:

In the neonate, ductal patency is related to continued production of prostaglandin (PG E). This is

particularly true in the premature infant; therefore, prostaglandin inhibition can affect ductal closure.

NSAIDs inhibit the production of prostaglandins by decreasing the activity of cyclooxygenase. The

result is a functional closure of the patent ductus arteriosus (PDA) in 80% of patients.The 2 NSAIDs

prooved to be effective in patent ductus arteriosus are indomethacin and ibuprofen- but indomethacin

has an onset of action within minutes.


:emotion-30: :emotion-30: :emotion-30:


Edited by jody 92, 25 February 2012 - 12:03 PM.

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#9
jody 92

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Q
1-Cimetidine blocks selectively H2 receptors in the GIT.X
2-PPIs are not advised to be combined with antacids. T
3-Metoclopramide decreases absorption of drugs from the stomach e.g. digoxin. T
4-Synthetic Pg analogue useful in NSAID-induced ulcer.(a.Paracetamol ) or (e. Misoprostol) in match no 1 -a
5- what is Droperidol??



A



by dr.


Ahmed Abdelrahman

‎1-Cimetidine blocks H2 receptors everywhere (Stomach-Heart-Blood vessels)

2-because PPIs are activated in acidic medium and antacids will reduce acidity.

3-Metoclopramide decreases absorption of slowly disintegrated drugs as digoxin becuase metoclopramide is a prokinetic agent that accelerates gastric emptying.

4-Misoprostol-not paracetamo;-is the PG analogue

. 5-Droperidol is a D2 blocker used in treatment of psychosis and as antiemetic.)

:)


Edited by jody 92, 13 March 2012 - 09:23 PM.

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