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)

PHARMACOLOGY OBJECTIVES FROM YAKUBU H.YAKUBU

1. Mechanism(s) of drug permeation:
   1.   lipid diffusion
   2.   aqueous diffusion
   3.   use of carrier molecules
   4.   endocytosis and exocytosis
   5.   all of the above
2. Bond type that is seen in some drug-receptor interactions and tends to very strong, often nearly irreversible:
   1.   hydrophobic
   2.   electrostatic
   3.   covalent
   4.   A & C
   5.   B & C
3. Drug delivery method LEAST suitable for long term (days to weeks) slow release.
   1.   pellet implant under the skin (subcutaneous)
   2.   time release capsule
   3.   i.m. injection of a drug-oil suspension
   4.   transdermal patch
   5.   none of the above
4. Most drug have molecular weights between:
   1.   10 - 100
   2.   100 and 1000
   3.   7 - about 60000
   4.   above 60000
   5.   none of the above
5. Most important factor influencing drug absorption rate following intramuscular injection:
   1.   needle diameter
   2.   rate of administration
   3.   injection site blood flow
   4.   injection volume
6. Most common mechanism of drug permeation:
   1.   endocytosis
   2.   carrier-mediated transport
   3.   active-transport
   4.   passive diffusion
   5.   none of the above
7. Weak organic acid, pKa 6.5. Percent ionization at pH 7.5
   1.   1%
   2.   10%
   3.   50%
   4.   90%
   5.   99%
8. General term having to do with actions of the body on the drug:
   1.   pharmacodynamics
   2.   pharmacogenetics
   3.   pharmacokinetics
   4.   absorption
   5.   none of the above
9. Drug-transport system described as "energy requiring":
   1.   glomerular filtration
   2.   facilitated diffusion
   3.   active transport
   4.   B & C
   5.   A, B & C
10. Drug with this ionization property most likely to diffuse from intestine (pH 8.4) to blood (pH 7.4)
    1.   weak acid (pKa 7.4)
    2.   weak base (pKa 8.4)
    3.   weak acid (pKa 8.4)
    4.   weak base (pKa 6.4)
    5.   weak acid (pKa 6.4)
11. Term having to do with drug actions on the body:
    1.   pharmacokinetics
    2.   pharmacodynamics
    3.   pharmacogenetics
    4.   placebo
    5.   all of the above
12. Dramatic decrease in systemic availability of a drug following oral administration is most likely due to:
    1.   extreme drug instability at stomach pH
    2.   hepatic "first-pass" effect
    3.   drug metabolized by gut flora
    4.   tablet does not dissolve
    5.   patient non-complance
13. Pharmacological antagonists:
    1.   cause receptor down regulation
    2.   prevent binding of other molecules to the receptor by their binding to the receptor
    3.   atropine (blocks ACh action on the heart
    4.   A & B
    5.   B & C
14. Increasing ionization at pH ABOVE pKa:
    1.   weak acid
    2.   weak base
15. Example(s) of covalent drug-receptor interactions:
    1.   activated phenoxybenzamine-receptor
    2.   anti-cancer DNA alkylating drugs, like cyclophosphamide (Cytoxan)
    3.   norepinephrine
    4.   A & B
    5.   A, B & C
16. Faster drug absorption:
    1.   lung
    2.   stomach
    
    
    1. Stereoselectivity and metabolism:
       1.   enzymes typically exhibit stereoselectivity -- a preference for one or the other enantiomeric form
       2.   duration of action of one enantiomer may be different from the other
       3.   both
       4.   neither
    2. Percentage of all drugs that exist as enantiomeric pairs:
       1.   less than 1%
       2.   5%-15%
       3.   30%
       4.   > 50%
       5.   > 90%
    3. The binding of the activated form of phenoxybenzamine (alpha-receptor antagonist) with the alpha receptor is an example of this type of chemical force/bond:
       1.   electrostatic
       2.   covalent
       3.   hydrophobic interactions
    4. Characteristic(s) of enantiomers:
       1.   chemically identical
       2.   mirror images of each other
       3.   both
       4.   neither
    5. Saturable transport system(s):
       1.   facilitated diffusion
       2.   passive diffusion
       3.   active transport
       4.   A & B
       5.   A & C
    6. Characteristics those aqueous diffusion:
       1.   occurs within large intracellular and extracellular components
       2.   occurs across epithelial membrane tight junctions
       3.   occurs across endothelial blood vessel lining -- often through pores
       4.   A & C
       5.   A, B & C
    7. Examples of enantiomeric differences important in anesthesia:
       1.   cardiotoxicity is probably associated with both enantiomers of bupivacaine
       2.   Ropivacaine is less cardiotoxic compared to bupivacaine because it is metabolized faster
       3.   cisatracurium is an atracurium isomer that doesn't cause histamine release
       4.   both l- and d- morphine occur in nature
    8. Factors that influence the rate of passive movement to molecules down the concentration gradient (Fick's Law)
       1.   concentration difference across the barrier
       2.   area across which diffusion occurs
       3.   drug mobility in the diffusion panel
       4.   thickness -- length of the diffusion pass
       5.   all the above
    9. Description of enantiomers:
       1.   may be readily superimposed
       2.   enantiomers, when presence in equal proportions, are referred to as racemates
       3.   may be characterized by absolute configuration or by direction in which enantiomers rotate polarized light
       4.   A & C
       5.   B & C
    10. Major types of chemical forces/bonds:
        1.   hydrophobic interactions
        2.   electrostatic
        3.   covalent
        4.   A & C
        5.   A,B, & C
        
        
        1. Sympathetic nervous system anatomy and properties:
           1.   gangionic neurotransmitter: acetylcholine
           2.   generalized response upond sympathetic stimulation
           3.   thoraco-lumbar origin for preganglionic cell bodies
           4.   all of the above
        2. Comparing autonomic and somatic nerves:
           1.   somatic nerves, like autonomic nerves contain ganglia.
           2.   Most of the fibers in the vagus nerve ar sensory
           3.   denervated smooth muscle show spontaneous activity
           4.   motor nerves are typically unmyelinated.
        3. Major anatomical site for integration of autonomic information:
           1.   cerebellum
           2.   sensory cortex
           3.   hypothalamus
           4.   spinal cord--dorsal horn
        4. Division of the autonomic nervous system associated with diffuse autonomic responses.
           1.   sympathetic
           2.   parasympathetic
           3.   both
           4.   neither
        5. Activation of the sympathetic nervous system will caus which change in the skeletal muscle versus cutaneous vascular beds.
           1.   vasoconstriction, vasoconstriction
           2.   vasodilatation, vasodilatation
           3.   vasodilatation, vasoconstriction
           4.   vasoconstriction, vasodilation
        6. Adrenergic receptor type(s) mediating pupillary dilation
           1.   beta-2
           2.   alpha-1
           3.   muscarinic
           4.   serotonergic
        7. Cholinergic receptor type that mediates vasodilation following low-dose i.v. acetylcholine administration:
           1.   nicotinic
           2.   muscarinic
           3.   nitric oxide receptor
           4.   substance P receptor
        8. "True" acetylcholinesterase is found in:
           1.   glia
           2.   liver
           3.   erythrocytes
           4.   plasma
        9. Catalyzes rate-limiting step in catecholamine biosynthesis:
           1.   DOPA decarboxylase
           2.   phenylethanolamine N-methyl transferase
           3.   tyrosine hydroxylase
           4.   dopamine-beta-hydroxylase
        10. Inhibited by drugs such as phenelzine or tranylcypromine;
            1.   COMT (catechol-O-methyl transferase)
            2.   MAO (monoamine oxidase)
            3.   choline acetyltransferase
            4.   reuptake-I inhibitor
        11. Concentation increased by epinephrine:
            1.   blood free fatty acids
            2.   blood glucose
            3.   skeletal muscle glycogen
            4.   A & B
        12. Due to receptor specificity, catecholamine LEAST likely to produce bronchiolar smooth muscle relaxation:
            1.   epinephrine
            2.   terbutaline (Brethine)
            3.   phenylephrine
            4.   phentolamine (Regitine)
        13. Alpha adrenergic receptor blocker
            1.   phentolamine (Regitine)
            2.   phenoxybenzamine (Dibenzyline)
            3.   terbutaline (Brethine)
            4.   A & B
        14. Covalent inhibitor of acetylcholinesterse:
            1.   edrophonium (Tensilon)
            2.   diisopropylphosphate (DFP)
            3.   atropine
            4.   muscarine
        15. Alpha-adenergic receptor agonist:
            1.   terbutaline (Brethine)
            2.   atropine
            3.   methoxamine (Vasoxyl)
            4.   isoproterenol (Isuprel)
        16. Parasympathetic direct cardiac effects:
            1.   decrease heart rate; increase contractility
            2.   increase heart rate; decrease contractility
            3.   decrease heart rate; decrease contractility
            4.   increase AV nodal conduction velocity
        17. Choline ester substrate for acetylcholinesterase:
            1.   carbachol
            2.   methacholine (Provocholine)
            3.   both
            4.   neither
        18. Alkaloid agonist acting at muscarinic, cholinergic receptors:
            1.   DFP
            2.   pilocarpine (Pilocar)
            3.   physostigmine (Antilirium)
            4.   ipratropium (Atrovent)
        19. Effective in treating both organophosphate and muscarine intoxication:
            1.   nicotine
            2.   echothiophate (Phospholine)
            3.   atropine
            4.   pilocarpine (Pilocar)
        20. Cholinergic activity on stomach acid secretion
            1.   increased
            2.   decreased
            3.   no changed
            4.   one of the others is right
            
            
            1. Most likely to reduce blood pressure by directly decreasing heart rate:
               1.   phentolamine (Regitine)
               2.   propranolol (Inderal)
               3.   nitroprusside sodium (Nipride)
               4.   phenylephrine (Neo-Synephrine)
            2. From the point of view of Starling's law which antihypertensive would be most likely to reduce contractility.
               1.   methoxamine (Vasoxyl)
               2.   nitroprusside sodium (Nipride)
               3.   propranolol (Inderal)
               4.   metoprolol (Lopressor)
            3. Negative inotropism
               1.   isoproterenol (Isuprel)
               2.   epinephrine
               3.   diltiazem (Cardiazem)
               4.   norepinephrine
            4. Increases pulmonary congestion in congestive heart failure (CHF)
               1.   dopamine (Intropin)
               2.   metoprolol (Lopressor)
               3.   nitroprusside sodium (Nipride)
               4.   digoxin (Lanoxin, Lanoxicaps)
            5. Major neurotransmitter released at end organ effectors of the thoracolumbar division of the autonomic nervous system:
               1.   dopamine (Intropin)
               2.   epinephrine
               3.   norepinephrine
               4.   acetylcholine
            6. Neurotransmitter of preganglionic fibers:
               1.   norepinephrine
               2.   substance P
               3.   epinephrine
               4.   acetylcholine
            7. "Fight or flight" activation of the ANS:
               1.   pupillary constriction
               2.   blood flow shifted from cutaneous beds to skeletal muscle
               3.   blood glucose falls
               4.   bronchiolar constriction
            8. Methoxamine (Vasoxyl)-induced bradycardia would be prevented by:
               1.   phentolamine (Regitine)
               2.   mecamylamine (Inversine)
               3.   atropine
               4.   all of the above
            9. Dopamine beta hydroxylase catalyzes:
               1.   tyrosine to DOPA
               2.   DOPA to dopamine
               3.   dopamine to norepinephrine
               4.   norepinephrine to epinephrine
            10. Primary mechaism for termination of norepinephrine and epinephrine action:
                1.   metabolic transformation catalyzed by MAO
                2.   metabolic transformation catalyzed by COMT
                3.   diffusion away from the synaptic cleft and uptake at extraneuronal sites
                4.   reuptake into nerve terminals
            11. Most potent at beta adrenergic receptors
                1.   epinephrine
                2.   isoproterenol (Isuprel)
                3.   norepinephrine
                4.   dopamine
            12. Interferes with norepinephrine release:
                1.   alpha-methyltyrosine by preventing synthesis of a protein that promotes fusion of the vesicle and the presynaptic membrane
                2.   bretylium (Bretylol) following a transient stimulation of release by displacement
                3.   reserpine
            13. alpha-2 receptor agonist; peripheral sympathomimetic
                1.   yohimbine (Yocon)
                2.   dobutamine (Dobutrex)
                3.   clonidine (Catapres)
                4.   phenylephrine
            14. Primary antihypertensive effect due to nitric oxide mediation of smooth muscle relaxation.
                1.   atropine
                2.   nitroprusside sodium (Nipride)
                3.   mecamylamine (Inversine)
                4.   captopril (Capoten)
            15. Inhibits neurotransmitter enzymic degradation:
                1.   tubocurarine
                2.   phenoxybenzamine (Dibenzyline)
                3.   physostigmine (Antilirium)
                4.   bretylium (Bretylol)
            16. Cardiac effects not like to be directly affected by the presence of an anticholinesterase:
                1.   acetylcholine
                2.   methacholine (Provocholine)
                3.   vagal stimulation
                4.   carbamylcholine (carbachol)
            17. Pilocarpine (Pilocar):
                1.   dry mouth
                2.   pupillary dilation
                3.   increased gastrointestinal tone
                4.   bronchiolar relaxation
17. Elaboration of vesicular content (neurotransmitter) into the synaptic cleft is an example of:
    1.   carrier transport
    2.   passive diffusion
    3.   endocytosis
    4.   exocytosis
    5.   lipid diffusion
18. Most acidic
    1.   urine
    2.   breast milk
    3.   jejunum,ileum contents
    4.   stomach contents
    5.   vaginal secretions
19. Lipid solubility and drugs:
    1.   more of the weak acid drug will be in the lipid-soluble form at alkaline pH.
    2.   more of the weak acid drug will be in the lipid soluble form at acid pH.
    3.   more of the weak base drug will be in the lipid soluble form at alkaline pH
    4.   A & C
    5.   B & C
20. Definition: Therapeutic Index
    1.   ED50/LD50
    2.   potency/selectivity
    3.   EC50/LD50
    4.   TD50/ED50
    5.   ED50
21. Ion-trapping in the kidney:
    1.   Weak acids are usually excreted slower in alkaline urine
    2.   Weak bases are usually excreted faster in acidic urine
    3.   both
    4.   neither
22. Weak base:
    1.   neutral molecule that dissociates into an anion and a proton
    2.   neutral molecule that forms a cation upon combining with a proton
    3.   charged molecule that remains charged independent upon pH
    4.   neutral molecule that remains uncharged independent of pH
    5.   none of the above
23. Driving force for passive flux of molecules down a concentration gradient:
    1.   area/thickness
    2.   difference in concentration
    3.   permeability coefficient
    4.   area x permeability coefficient/thickness
    5.   thickness
24. Most common drug permeation mechanism:
    1.   passive diffusion in aqueous or lipid medium
    2.   active transport
25. Most likely to be transportred into cells by endocytosis:
    1.   propranolol
    2.   iron-complex with its binding protein
    3.   erythromycin-macrolide antibiotic
    4.   phenylalanine
    5.   peptide
26. Permanently charged amine:
    1.   primary amine
    2.   secondary amine
    3.   tertiary amine
    4.   quaternary amine
    
    
    
    1. Cytochrome-P450 INDEPENDENT oxidation
       1.   amine oxidase
       2.   epoxidation
       3.   N-oxidation
       4.   S-oxidation
       5.   deamination
    2. Most drugs are oxidized in the:
       1.   smooth endoplasmic reticulum
       2.   rough endoplasmic reticulum
       3.   smooth and rough about equally
       4.   nucleus
       5.   none of the above
    3. Drug mixed-function oxidase (p450) mainly localized:
       1.   mitochondrial fraction
       2.   cell membranes
       3.   golgi bodies
       4.   microsomal fraction
       5.   nucleolus
    4. Primary site for drug metabolism:
       1.   stomach
       2.   small intestine
       3.   kidney
       4.   muscle
       5.   liver
    5. Drug biotransformation:
       1.   mainly, but not exclusively in the liver
       2.   products are usually less biologically active
       3.   biotransformation products can be toxic
       4.   A & B
       5.   A, B & C
       
       
       1. Weak base:
          1. phenobarbital (Luminal)
          2. acetaminophen (Tylenol, Panadol)
          3. morphine
          4. aspirin
          5. pentobarbital (Nembutal)
       2. Ion trapping:
          1. the fetal pH is higher than maternal pH
          2. in fetal distress alkalosis contributes to local anesthetic accumulation
          3. local anesthetics may tend to accumulate in the fetus
          4. A & C
          5. B & C
       3. Drug transport:
          1. Very hydrophilic drugs may not be well absorbed
          2. Excessively lipid-soluble (hydrophobic) drugs may not be soluble enough to cross a water layer near the cell membrane
          3. both
          4. neither
       4. Lipid diffusion:
          1. uncharged form: lipid-soluble
          2. charged form: lipid-soluble
          3. charged form: lipid insoluble
          4. charged and uncharged forms equally lipid-soluble
       5. Weak base at alkaline pH:
          1. relatively lipid-soluble
          2. probably uncharged
          3. both
          4. neither
       6. Disadvantages of the oral route of drug administration
          1. emesis
          2. gastric acidity may destroy the drug
          3. inconsistent absorption due to food or other effects
          4. usually expensive
       7. Percentage of oral digoxin (Lanoxin, Lanoxicaps) dose likely to reach systemic circulation:
          1. 100%
          2. 90%
          3. 70%
          4. 30%
          5. 10%
       8. Quaternary amine
          1. permanently charged
          2. charge dependent on pH relative to pKa
          3. uncharged
       9. First pass effect:
          1. requires passage of the drugs through the portal venous system
          2. lidocaine (Xylocaine)
          3. may result in minimal drug delivery to the systemic circulation
          4. A & C
          5. A, B & C
       10. A weak acid at acid pH:
           1. likely to be lipid-soluble
           2. probably will be uncharged
           3. both
           4. neither
       11. Primary factor in determining the rate of an orally ingested drug onset: rate and absorption extent by the gastrointestinal tract
           1. true
           2. false
       12. Aqueous diffusion:
           1. within large aqueous components
           2. across endothelial blood vessel lining
           3. across epithelial membrane tight junctions
       13. Transdermal delivery
           1. clonidine (Catapres)
           2. fentanyl (Sublimaze)
           3. scopolamine
           4. nitroglycerin
           5. none of the above
       14. Site(s) of drug metabolism following oral ingestion:
           1. blood
           2. intestinal wall
           3. liver
           4. A & C
           5. A, B & C
       15. Parenteral administration:
           1. less likely to be certain of active drug absorption
           2. acceptable route of administration for the unconscious patient
           3. rated systemic absorption will depend on drugs solubility in interstitial fluid
           4. aqueous channels (vascular endothelium) promote high diffusion rates of drugs, independent of their lipid solubility
       16. Rectal administration:
           1. Absorption of drug into superior hemorrhoidal veins results in the absence of the first-pass effect
           2. Low rectal administration may allow drugs to enter the systemic circulation without passing to the liver
           3. both
           4. neither
       17. Transport system requiring energy, e.g. ATP hydrolysis
           1. facilitated diffusion
           2. active transport
           3. both
           4. neither
       18. Weak acid:
           1. morphine
           2. chlordiazepoxide (Librium)
           3. phenobarbital (Luminal)
           4. cocaine
           5. ephedrine
       19. Release of neurotransmitter by synaptic terminal:
           1. endocytosis
           2. exocytosis
           3. both
           4. neither
       20. Important factor(s) in determining flux (molecular transport per unit time)
           1. concentration gradient
           2. area across which diffusion occurs
           3. lengthly of diffusion path
           4. A & C
           5. B & C
       21. Renal pharmacology/pharmacokinetics:
           1. Most drugs are not filtered by the glomerulus
           2. lipid-soluble drugs are typically reabsorbed by passive diffusion after glomerular filtration
           3. weak acids tend to be excreted faster in alkaline pH
           4. weak bases tend to be excreted faster in alkaline pH
       22. Optimal factors contributing to reliable transdermal drug absorption:
           1. drug promotes histamine release
           2. molecular weight < 1000
           3. daily drug requirement < 10 mg
           4. pH range < 4
       23. The lower the pH relative to the pKa the greater fraction of protonated drug is found
           1. true
           2. false
       24. More likely to require transport system to cross biological membranes:
           1. glucose
           2. ethanol
           3. both equally likely
           4. both equally unlikely to require transport systems
       25. Magnitude of first-pass hepatic effect
           1. depends on hepatic blood flow (Q)
           2. depends on clearance
           3. both
           4. neither

ROAD CARNNAGE IN GHANA ALARMING WITH NO MANAGEMENT SYSTEM

Road accidents always bring pain to victims and their families. Currently in the news is the accident which has claimed more than 35 lives on the Tamale-Bolgatanga truck road over the weekend. When such accidents occur, one is compelled to ask whether the fight against carnage on the roads is being lost. Road accidents in Ghana continue to claim more lives than HIV and AIDS, malaria and other deadly diseases combined. This situation has given the country the tag of being one of the accident prone zones in the sub region. Regrettably though, majority of these fatal accidents can be prevented especially those caused through human errors. In the Central Region alone, 134 people have died from road accidents between January and October this year according to the MTTU. This is only an average of what happens in the country. Unfortunately, as a nation, it appears all efforts to reduce the carnage on our roads are not yielding the desired results. It is true that certain accidents are inevitable and of course that is why we call it accidents. It is also true that most of the accidents are self inflicted. The situation is so serious that today on our roads it is not enough as a driver to be extra careful. This is because another reckless driver can get people involved in an accident. It is a fact that most of the young people who drive are simply under the influence of drugs and alcohol and therefore have no business being behind the wheel. If the work of the doctor is tagged as an essential service, because he deals with lives, then the work of the driver should equally be regarded as essential because their actions also impact on human lives.

A couple of years ago, the GPRTU banned the sale of alcohol at lorry stations, yet the practice goes on with impunity. The net effects are accidents. This makes some people wonder if Ghana is actually committed to ending the needless accidents on the roads, after the formation of committees of enquiries and heated debates in the media on how to reduce such horrific accidents. The MTTU early this year started arresting drivers who use their phones while driving. Those who saw the exercise as cosmetic are being proved right as both commercial and private drivers continue to chat on phones whilst driving. For fear of being tagged ‘too known’, as we call it in Ghana, many passengers prefer to be quiet when the driver is over speeding, doing wrongful overtaking, talking on the phone or stopping to pick a passenger at the wrong place.

Tackling accidents on the road is multi-sector. The DVLA, Police, Road Safety Commission, government and passengers should not relent in their collaborative effort to effectively tackle the needless deaths through road accidents. The hard truth is that some of the vehicles that ply the countries roads right from the nation's capital to the remotest parts are death traps to say the least. Can the DVLA feign ignorance as to how such vehicles pass the test for road worthiness? The barking has only yielded brutal and costly accidents. The time to bite is now. Christmas is just about two weeks away, where we will witness many commercial drivers over speeding, all in an effort to make more money. It is their cocoa season and the wiser ones will want to reap supernormal profits at all costs and by all means. It is not enough to put numerous adverts, painting the picture that over speeding kills as well as construct more speed humps. The road safety rules need to be religiously enforced.

The decision by the Ghana police Service to deploy five thousand personnel on the roads is welcome news. The police must however bear in mind that it will be an indictment on their image if they look on for the wrongs to go on. Major transport companies should ensure that they use at least two drivers to ply long distance roads. Above all passengers should endeavour to speak with one voice when the driver is misbehaving, after all what is wrong is wrong even if everybody says it is right. Accidents are no respecter of ones status and this must be drawn in the consciousness of everybody. Whilst we pray for the souls of those who have perished through road accidents, Let us pray that the Holy Spirit will lead every vehicle on the road bearing in mind the scriptural admonition that by strength shall no man succeed. Indeed we need the intervention of God as we prepare for the yuletide and the New Year. Long live Ghana, long live all drivers.