PHARMACOLOGY OBJECTIVES-----SOKPESH's Antedote

1. Which of the following is not a side effect of the cholinoreceptor blocker (Atropine)?
A. Increased pulse
B. Urinary retention
C. Constipation
D. Mydriasis
2. Which of the following is not a side effect of the Ace Inhibitor (Captopril)?
A. Rash
B. Angioedema
C. Cough
D. Congestion
3. Which of the following is not a side effect of the Vasodilator (Nifedipine)?                
A. Nausea
B. Flush appearance
C. Vertigo
D. Sexual dysfunction
4. Which of the following is not a side effect of the Sympathoplegics (Clonidine)?
A. Hypertension
B. Asthma
C. Dry oral cavity
D. Lethargic behavior
5. Which of the following is not a side effect of the Dieuretics (Loop dieuretics)?
A. Alkalosis
B. Nausea
C. Hypotension
D. Potassium deficits
6. Which of the following is not an effect of the drug (Isoflurane)?
A. Elevated lipid levels
B. Nausea
C. Increased blood flow to the brain.
D. Decreased respiratory function
7. Which of the following is not an effect of the drug (Midazolam)?
A. Amnesia
B. Decreased respiratory function
C. Anesthetic
D. Dizziness
8. Which of the following is not an effect of the drug (Clozapine)?
A. Agranulocytosis
B. Antipsychotic
C. Used for Schizophrenia
D. Increased appetite
9. Which of the following is not treated with (Epinephrine)?
A. Renal disease
B. Asthma
C. Hypotension
D. Glaucoma
10. Which of the following is not treated with (Ephedrine)?
A. COPD
B. Hypotension
C. Congestion
D. Incontinence
11. Which of the following are not treated with Barbiturates?
A. Seizures
B. Hypotension
C. Insomnia
D. Anxiety
12. Which of the following are not treated with opoid analgesics like (dextromethorphan and methadone)?
A. Pulmonary Edema
B. Cough suppression
C. Sedation
D. Pain
13. Which of the following are not treated with Hydrochlorothiazide?
A. CHF
B. HTN
C. Nephritis
D. Hypercalciuria
14. Which of the following are not treated with Nifedipine?
A. Angina
B. Arrhythmias
C. Htn
D. Fluid retention
15. Which of the following are not treated with Methotrexate?
A. Sarcomas
B. Leukemias
C. Ectopic pregnancy
D. Rheumatic fever
16. Which of the following are not treated with Prednisone?
A. Cushing's disease
B. Testicular cancer
C. Lympthomas
D. Chronic leukemias
17. Which of the following are not treated with Dexamethasone?
A. Inflammation
B. Asthma
C. Addison's disease
D. Wilson's disease
18. Which of the following are not treated with Lansoprazole?
A. Zollinger-Ellison syndrome
B. Gastritis
C. Hypertension
D. Reflux
19. Which of the following is the antidote for the toxin Heparin?
A. Protamine
B. Methylene blue
C. N-acetylcysteine
D. Glucagon
20. Which of the following is the antidote for the toxin Copper?
A. Glucagon
B. Aminocaproic acid
C. Atropine
D. Penicillamine

Mark yourself
1. B
2. D
3. D
4. B
5. B
6. A
7. D
8. D
9. A
10. A
11. B
12. C
13. C
14. D
15. D
16. B
17. D
18. C
19. A
20. D 

Objective test Antiarrhythmics

1. 
   Not a class I antiarrhythmic Drug:                                    
   1.   quinidine gluconate (Quinaglute, Quinalan)
   2.   lidocaine (Xylocaine)
   3.   encainide (Enkaid)
   4.   verapamil (Isoptin, Calan)
2. Not classified as a Type I antiarrhythmic
   1.   lidocaine (Xylocaine)
   2.   quinidine gluconate (Quinaglute, Quinalan)
   3.   adenosine (Adenocard)
   4.   encainide (Enkaid)
3. Correct match(es) between antiarrhythmic drugs and side effects:
   1.   quinidine gluconate (Quinaglute, Quinalan): diarrhea, cinchonism
   2.   tocainide (Tonocard): CNS-related side effects including drowsiness, paresthesias
   3.   procainamide (Procan SR, Pronestyl-SR): Like tocainide,CNS-related side effects including, drowsiness, paraesthesias, and hypotension
   4.   A & B
4. Corneal microdeposits, blurred vision, and photophobia:
   1.   adenosine (Adenocard)
   2.   encainide (Enkaid)
   3.   amiodarone (Cordarone)
   4.   diltiazem (Cardiazem)
5. Class III anti-arrhythmic drug which also blocks potassium channels:
   1.   quinidine gluconate (Quinaglute, Quinalan)
   2.   sotalol (Betapace)
   3.   bretylium (Bretylol)
   4.   propafenone (Rythmol)
6. A patient is diagnosed with atrial fibrillation and exhibits a ventricular following rate of 150 beats / min. Quinidine gluconate (Quinaglute, Quinalan) was administered and although atrial fibrillation was converted to atrial flutter, the ventricular rate increased to 190 beats / min. What is the most likely explanation for the effect on heart rate?
   1.   Quinidine activated beta-1 cardiac receptors which cause the increase in heart rate.
   2.   Quinidine converted the atrial fibrillation to atrial flutter which resulted in an increase in heart rate.
   3.   Quinidine produced an anti-vagal effect and converted atrial fibrillation to atrial flutter. Both effects caused the heart rate to increase.
   4.   Quinidine has an anti-vagal effect which facilitated transmission through the A-V node.
7. Agent(s) may be effective in terminating paroxysmal supraventricular tachycardia (PSVT)?
   1.   adenosine (Adenocard)
   2.   methoxamine (Vasoxyl)
   3.   propranolol (Inderal)
   4.   all of the above
8. Useful in treating third-degree (complete) heart block:
   1.   atropine
   2.   isoproterenol (Isuprel)
   3.   edrophonium (Tensilon)
   4.   A & B
9. A 70 year old female patient is being treated for ventricular arrhythmias following a myocardial infarction. Runs of ventricular tachyarrythmias, episodes of ventricular fibrillation requiring cardioversion, and pulmonary congestion have been noted. Myocardial ejection fraction is very poor at 25%. Which drugs might be appropriate in this case to suppress these malignant arrhythmias?
   1.   i.v. bretylium (Bretylol)
   2.   i.v. lidocaine (Xylocaine)
   3.   i.v. propranolol (Inderal)
   4.   A & B
10. Torsades de Pointes, a polymorphic ventricular arrhythmia, is associated with prolongation of Q-T intervals. Which antiarrhythmic agent is most likely to cause this arrhythmia?
    1.   lidocaine (Xylocaine)
    2.   quinidine gluconate (Quinaglute, Quinalan)
    3.   digoxin (Lanoxin, Lanoxicaps)
    4.   propranolol (Inderal)
11. Best indicator of digoxin (Lanoxin, Lanoxicaps) efficacy in treating atrial fibrillation:
    1.   shortened P-R interval
    2.   decreased ventricular rate
    3.   weight loss
    4.   accelerated ventricular repolarization
12. cardiac effects resemble those of quinidine gluconate (Quinaglute, Quinalan):
    1.   digoxin (Lanoxin, Lanoxicaps)
    2.   procainamide (Procan SR, Pronestyl-SR)
    3.   lidocaine (Xylocaine)
    4.   adenosine (Adenocard)
13. Intravenous lidocaine (Xylocaine):
    1.   supraventricular tachycardia
    2.   angina
    3.   congestive heart failure
    4.   ventricular arrhythmias
14. Most ominous sign of digoxin (Lanoxin, Lanoxicaps) intoxication:
    1.   nausea and vomiting
    2.   irregular P waves
    3.   ventricular tachycardia with alterations in the QRS complex
    4.   atrial fibrillation
15. Increases automaticity:
    1.   mechanical stretch
    2.   isoproterenol
    3.   hypokalemia
    4.   all of the above
16. A patient is admitted for treatment of myocardial infarction. During a prolonged recovery period, the patient experienced episodes of vetnricular tachycardia. Following discharge from hospital, the patient was instructed to take a drug to prevent recurrence of ventricular tachycardia. After a few days, the patient complained of dizziness and then lost consciousness. Upon admission to the hospital, the patient was found to be somewhat hypokalemic. A diagnosis of Torsades de Pointes was made. A test to determine the blood level of the antiarrhythmic reveal the drug was present in a slightly subtherapeutic level. What was the drug?
    1.   sotalol (Betapace)
    2.   procainamide (Procan SR, Pronestyl-SR)
    3.   quinidine gluconate (Quinaglute, Quinalan) than
    4.   lidocaine (Xylocaine)
17. Procainamide (Procan SR, Pronestyl-SR) side effects:
    1.   nausea
    2.   hypotension
    3.   drug-induced lupus
    4.   all of the above
18. A patient is being treated with digoxin (Lanoxin, Lanoxicaps) for congestive heart failure. To enhance inotropic effects, the dosage was increased. Soon afterwards, the patient complained of dizziness, fatigue, and disturbances in color vision. An ECG was taken. ECG finding(s) consistent with digitalis intoxication include:
    1.   ectopic A-V junctional beats
    2.   sinus bradycardia
    3.   third degree heart block
    4.   all of the above
19. A patient is being treated with digoxin for congestive heart failure. To enhance inotropic effects, the dosage was increased. Soon afterwards, the patient complained of dizziness, fatigue, and disturbances in color vision. An ECG was taken. What ECG finding(s) would be consistent with digitalis intoxication?A patient is being treated with digoxin for congestive heart failure. To enhance inotropic effects, the dosage was increased. Soon afterwards, the patient complained of dizziness, fatigue, and disturbances in color vision. An ECG was taken and exhibit arrhythmias consistent with digitialis intoxication.
    What antiarrhythmic drugs might be used to treat worsening ventricular arrhythmias with hemodynamic compromise?
    1.   amiodarone (Cordarone)
    2.   lidocaine (Xylocaine)
    3.   adenosine (Adenocard)
    4.   propranolol (Inderal)
20. Phase of ventricular muscle action potential is associated with an inward,depolarizing Ca2+ current and an outward, repolarizing K+ current.
    1.   Phase 0
    2.   Phase 1
    3.   Phase 2
    4.   Phase 3
21. Automaticity:
    1.   Phase 0
    2.   Phase 2
    3.   Phase 4
    4.   none of the above

THE PRIDE OF MY PEOPLE YESTERDAY

It was nearly dawn when the silence of the village was shattered by a ululation which welcomes the late chief's long-awaited son.Before long people trooped to the palace by day break one could count the number of dancers that had come to share joy of the chief.As sun rose promising the heat of the day.An Army vehicle arrived vomiting soldiers everywhere this marred the day's joy.An officer asked a young man standing by Naporoo a head teacher in Zugu primary school who cheated so many people including a policeman he promised securing visas to European countries but had failed.He however did not return to them the five hundred dollar fee he collected from each of them in no time Naporoo was arrested but the chief stood between them and said no..(THE POWER OF CHIEFS IN THE FIGHTING DAYS)
The chief said they could not arrest anyone including Napooro without first consulting him and hence the happiness of the day pave the way for a mixed feelings.To appease the chief for a misconduct the commander veered to the market haven bought some collar and added an amount they apologized to the chief.The blessings of the chiefdom was bestowed and calm was reinstated in the village.My dear youth gone where the days when no one could there the pride of the land.Today chiefs could be arrested,killed and prosecuted all because of our lack of verisimilitude.This was a nabob fish cake and who has taken the fish cake, first-rate it was.........and now the cat has taken the fish cake....The kingdom needs peace !
The kingdom is sold today for one chillings.The potentials of the kingdom is rusted.Hatred is traded from brother to the other and from onr sista to the other.I dream peace to this kingdom before demise.God shall birth and rain peace in this kingdom!

2ND TRIMME PHARMACOLOGY!

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Diuretics
Thiazides Hydrochlorothiazide (HydroDIURIL) Chlorthalidone (Hygroton) Chlorothiazide (Diuril) Indapamide (Lozol) Metolazone (Zaroxolyn)	Potassium Sparing Amiloride (Midamor) Spironolactone (Aldactone) Triamterene (Dyrenium)	Loop Diuretics Furosemide (Lasix), Bumetanide (Bumex), Ethacrynic acid (Edecrin) Torsemide (Demadex)

• Chlorothiazide (Diuril)
• The thiazides act in the distal tubule to decrease sodium reabsorption (inhibits Na/Cl transporter).
• As a result of decreased sodium and chloride reabsorption, a hyperosmolar diuresis ensues.
• Delivery of more sodium to the distal tubule results in potassium loss by an exchange mechanism.
• Thiazides also promote calcium reabsorption, in contrast to loop diuretics.
• The initial decrease in blood volume followed by a longer-termed reduction in vascular resistance appear to account for the hypotensive effects of the thiazides.
•  Adverse Effects
• Potassium depletion is a potentially serious side-effect that may require potassium supplementation and/or concurrent use of potassium-sparing diuretics.
•  Hyperuricemia may occur precipitating gout. 
• The increase in systemic uric acid is due to a decrease in the effectiveness of the organic acid secretory system.
•  Diabetic patient may have difficulty in maintaining proper blood sugar levels.

 

•   Furosemide (Lasix), Bumetanide (Bumex),Ethacrynic acid (Edecrin)
• Furosemide (Lasix), bumetanide (Bumex), and ethacrynic acid (Edecrin) are "high-ceiling" loop diuretics acting primarily at the ascending limb of the loop of Henle.
• The effectiveness of these agents is related to their site of action because reabsorption of about 30 - 40% of the filtered sodium and chloride load occurs at the ascending loop.
• Distal sites are not able to compensate completely for this magnitude of reduction of NaCl reabsorption.
• Loop diuretics increase urinary Ca²⁺ in contrast to the action of thiazides.
• Loop diuretics also increase renal blood flow by decreasing renal vascular resistance.
• These drugs are rarely used in the management of hypertension because of their short duration of action and the availability of better drugs. 
• Adverse Effects
• Ototoxicity
• Furosemide (Lasix) and ethacrynic acid (Edecrin) block renal excretion of uric acid by competition with renal secretory and biliary secretory systems.Therefore these agents can precipitate gout.
• Potassium depletion.

Furosemide

 

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Sympatholytics
Centrally Active Clonidine (Catapres) Methyldopa (Aldomet) Guanabenz (Wytensin) Guanfacine (Tenex)	Adrenergic Neuron Blocker Guanadrel (Hylorel) Guanethidine (Ismelin) Reserpine	Adrenoceptor Antagonists  Labetalol (Trandate, Normodyne) (alpha & beta) Prazosin (Minipress) (alpha), Terazosin (Hytrin) (alpha)

• Clonidine (Catapres) (Sympatholytic)
• Antihypertensive:
• Clonidine (Catapres) acts in the brain, inhibiting adrenergic outflow from the brainstem. Inhibition of sympathetic outflow results in a decrease in blood pressure.
• Mechanism of action: centrally acting selective a₂ adrenergic agonist.
• Especially effective in
• management of severe hypertension or
• in renin-dependent hypertension
• Transdermal clonidine (Catapres) patch: useful for surgical patients unable to take oral formulation
• Clonidine (Catapres) reduces cardiac output (by reducing both stroke volume and heart rate) and peripheral resistance.
• Reduction in stoke volume occurs due to increased venous pooling (decreased preload).
• Clonidine (Catapres) does not interfere with cardiovascular responses to exercise.
• Renal blood flow and function is maintained during clonidine treatment.
• Clonidine (Catapres) has minimal or no effect on plasma lipids.
• Other Clinical Uses
• Analgesia--
• Preservative-free clonidine administered into epidural/subarachnoid space (150-450 micrograms)-- dose-dependent analgesia
• No respiratory depression, nausea, vomiting, delayed gastric emptying or pruritus -- effects associated with opioids
• Probable Mechanism: activation postsynaptic a₂ receptors in the spinal cord substantia gelatinosa
•  Clonidine (Catapres) & morphine: no cross-tolerance when used concurrently in neuraxial analgesia
• Side effects of neuraxial clonidine (Catapres)
•   hypotension, sedation, dry mouth
• Preanesthetic Medication:
• Oral clonidine (Catapres) (preanesthetic medication):
• Enhances intrathecal morphine + tetracaine (pontocaine) for postoperative analgesia (no increase in morphine-related side effects)
• Preanesthetic clonidine (Catapres) also:
• Reduces reflex tachycardia that may be caused by direct laryngoscopy for tracheal intubation
• Reduces intraoperative blood-pressure heart rate lability
• Reduces plasma catecholamines levels
• Significantly decreases anesthetic requirements for inhaled (MAC) and injected agents.
• Adverse Effects
• Dry Mouth (xerostomia)
• bradycardia (in patients with SA nodal abnormality)
• Withdrawal syndrome upon abrupt discontinuation (increased blood pressure, headache, tachycardia, apprehension, tremors

Clonidine

Gyan To Miss Nations Cup?

Asamoah Gyan, the most high-profile UAE Pro League signing over the summer, may be out of action for a lengthy period for a suspected hamstring injury after last night's 4-0 win over Emirates in the Pro League.

The Ghana international who is on a one-year loan from Sunderland, the English Premier League club, pulled up after chasing a through ball early in the game on Friday.

He returned with a heavy strapping around his thigh but was forced to leave on the half hour.

"I don't know the extent of Gyan's injury until I get the medical report but the number of injuries we have had really worries me," said Cosmin Olaroiu, Al Ain's Romanian coach, at the post-match conference.

"I can only wish Gyan's injury is not a serious one. We already have a few players out with injuries and if the damage on Gyan's leg is a serious one it certainly would be a severe blow for us.

"I have not put a lot of pressure on my players already knowing that we have a lot injured players but sometimes they cannot be avoided and sometimes just unfortunate.

"Only time will tell the extent of Gyan's injury," he added.

Gyan opened the scoring from a sixth-minute penalty to take his tally to 10 goals and extended his lead to three from his closest challenger in the Pro League scoring chart to three more than Ricardo Oliveira, Al Jazira's Brazilian forward and the league's most expensive signing at Dh62 million.

If it is a hamstring injury, Gyan, may be out of action for more than a month and would miss the next two league games against Al Shabab on January 4 and Ajman on January 15, and the President's Cup quarter-final with Baniyas on January 9.

He will also likely be out of the Ghana national team in the African Cup of Nations from January 21 to February 12 co-hosted by Gabon and Equatorial Guinea.

Essien returns to action in January

Michael Essien may make his long-awaited return from injury before the end of January, Chelsea coach Andre Villas Boas said on Friday. The Ghana midfielder has been out of action since July when he ruptured the anterior ligament and cartilage in his right knee during training.

He will miss the upcoming African Cup of Nations in Equatorial Guinea and Gabon but is likely to hand Chelsea a major boost next month.

“I think mid-January. He will be introduced to first-team activity in mid-January and contention properly I think we are looking at three weeks for him to gain form and start competing to the level that the others are,” Portuguese boss Villas Boas was quoted as saying by Kick Off.

“It could take less time if we are positive about it and maybe in two weeks he can reach that level of form to come back for the team.”

PHARMACOLOGY OBJECTS:Autonomic Nervous System: Question Set

1. Drugs activating this receptor are used in treating asthma:
   1.   beta1 adrenergic
   2.   muscarinic cholinergic
   3.   beta2 adrenergic
   4.   nicotinic cholinergic
2. Epinephrine effects on the heart
   1.   increased rate
   2.   decreased contractility
   3.   coronary vasodilation
   4.   A & C
3. Receptor activation mainly responsible for positive inotropism:
   1.   alpha1
   2.   beta1
   3.   dopamine D1
   4.   muscarinic cholinergic
4. Epinephrine effects on respiration:
   1.   stimulation
   2.   inhibition
5. Activates alpha receptors
   1.   isoproterenol (Isuprel)
   2.   propranolol (Inderal)
   3.   phenylephrine (Neo-Synephrine)
   4.   terbutaline (Brethine)
6. Blocks cardiac isoproterenol effects
   1.   terbutaline (Brethine)
   2.   esmolol (Brevibloc)
   3.   atropine
   4.   mecamylamine (Inversine)
7. Alpha agonist: vasoconstriction and elevates blood pressure:
   1.   metoprolol (Lopressor)
   2.   methoxamine (Vasoxyl)
   3.   terbutaline (Brethine)
   4.   ipratropium (Atrovent)
8. Nerve terminal reuptake inhibitor
   1.   methoxamine (Vasoxyl)
   2.   cocaine
   3.   reserpine
   4.   timolol (Blocadren)
9. Alpha adrenoceptor COVALENT blocker:
   1.   propranolol (Inderal)
   2.   phenoxybenzamine (Dibenzyline)
   3.   phentolamine (Regitine)
   4.   pilocarpine (Pilocar)
10. Orthostatic (postural) hypotension
    1.   beta receptor activation
    2.   alpha receptor activation
    3.   alpha receptor blocker
    4.   dopamine receptor blockade
11. Norepinephrine pressor response blocked by:
    1.   mecamylamine (Inversine)
    2.   prazosin (Minipress)
    3.   atropine
    4.   propranolol (Inderal)
12. Bronchodilation
    1.   ipratropium (Atrovent)
    2.   timolol (Blocadren)
    3.   albuterol (Ventolin,Proventil)
    4.   A & C
13. Positive chronotropic effects of epinephrine:
    1.   increased SA nodal potassium current
    2.   beta1 receptor activation
    3.   mediated by G protein
    4.   B & C
14. Maximal ß-adrenergic receptor desensitization depends on:
    1.   receptor occupancy by agonists
    2.   an arrestin protein
    3.   receptor phosphorylation
    4.   A, B & C
15. Phase of the cardiac action potential that principally determine heart rate
    1.   phase 0
    2.   phase 4
    3.   phase 2
    4.   phase 3
16. Most likely to increase myocardial afterload
    1.   angiotensin converting enzyme inhibitor (decreases angiotensin II concentration)
    2.   propranolol (Inderal)
    3.   phenylephrine (Neo-Synephrine)
    4.   low-dose epinephrine
17. Pressor effects of epinephrine are blocked by this drug ("epinephrine reversal")
    1.   propranolol (Inderal)
    2.   phentolamine (Regitine)
    3.   phenylephrine (Neo-Synephrine)
    4.   metoprolol (Lopressor)
18. Decreases blood pressure
    1.   propranolol (Inderal)
    2.   mecamylamine (Inversine)
    3.   phentolamine (Regitine)
    4.   all of the above
19. Specific alpha2 receptor agonist
    1.   phenoxybenzamine (Dibenzyline)
    2.   propranolol (Inderal)
    3.   guanfacine (Tenex)
    4.   methoxamine (Vasoxyl)
20. Centrally-acting antihypertensive drug
    1.   nitroprusside sodium (Nipride)
    2.   clonidine (Catapres)
    3.   methoxamine (Vasoxyl)
    4.   captopril (Capoten)