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Pharmacology > PHAR301 > Flashcards

PHAR301 Flashcards

1
Q

phenytoin

A

-works on partial and generalized tonic-clonic seizures.
-Act by blocking Na channels
-Its metabolism has saturation kinetics (can only get rid for a fized a mount of phenytoin in a given time, therefore it is very hard to find the right dose. The DR is very steep)
Also phenytoin is n competition with aspirin (can have overdose of phenytoin)
-It can induce gingival hyperplasia and hirsutism

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2
Q

carbamazepine

A
  • works on partial and generalized tonic-clonic seizures. Works by blocking Na+ channels
  • can have drug-drug interactions with contraceptive pills
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3
Q

valproate (vigabatrin)

A
  • works all partial, absence and generalized tonic-clonic seizures.
  • Acts by blocking Na+ channels and increases GABA transmission by inhibiting GABA-T
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4
Q

ethosuxamide

A
  • Works only on generalized absence seizures
  • Blocks (inhibits) T-type Ca channels found on thalamocortical neurons which is part of the pacemaker activity of these cells in therapeutic doses
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5
Q

phenobarbital

A

-Works on partial and generalized tonic-clonic seizures
-Increases GABAa (stimulate the receptor function) and decreases (NMDAreceptors) glutamine transmission
-Side-effects: hepatic microsomal enzymes, possibility of overdosesedative, teratogen.
(NMDA receptor blockers produce ataxia)

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6
Q

benzodiazepine (e.g diazepam)

A
  • Drugs of choice for status epilepticus. The drug is given as a an emergency.
  • they work on all partial, generalized tonic-clonic and absence seizures
  • Increase GABA transmission (contrarily to phenorbarbital on its own who can open GABA channels, BZ needs an agonist to work.
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7
Q

Sinemet

A
  • L-Dopa + Carbidopa

- gives the most complications (dyskinesia), but the most effective drug. It becomes less and less useful

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8
Q

selegiline (deprenyl)

A
  • Treament for parkinsons
  • Inhibits MAO B (which converts MPTP into MPP+)
  • Could be neuroprotective by blocking the conversion of MPTP into neurotoxic MPP+ and inhibiting conversion ofDA into free radicals.
  • Can last 1 year before using L-Dopa
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9
Q

DAT blocker e.g Nomifensine

A

-prevents MPP+ from entering the DA neurons

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10
Q

DA agonist e.g bromocriptine

A

-Drug for parkinsons
-should work in complete absence of DA
-Fewer oxyradicals because of less DA release
-Longer half-life thn L-DOPA
work better in animals than in humans. It is less effective than L-DOPA. useful in early PD (can last 5 years before using L-DOPA). Useful adjunct use with L-Dopa

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11
Q

terfenadine

A

-has long-lasting blocking effect
with increasing dose, its effect goes down because of the fact that it is a competitive antagonist, slow dissociation (when it binds to the receptor, it basically stays there) and that it occupies almost all spare receptors

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12
Q

hydrochlothiazide

A
  • Antihypertensive drug
  • Diuretic (thiazide family)
  • Preferred first drug.
  • for mild to moderate HT.
  • Work on distal convoluted tubules. (Block Na+/Cl- symporter, augment Ca++ absorption)
  • Orally active.
  • Toxic when there is K+ depletion (hypokalemia) which is not good for patients who experience arrhythmia.
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13
Q

Furosemide

A
  • Antihypertensive drug and congestive heart failure (increase CO)
  • Loop diuretic family
  • They work very quickly.
  • For moderate to severe HT.
  • Act on thick ascending tubules (loop). Work by blocking Na/K/2Cl symporter and by increasing Ca excretion.
  • Adminisitration can be oral and intravenous.
  • Toxic when there is K+ depletion/hypokalemia.
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14
Q

Clonidine

A
  • Antihypertensive drug
  • Centrally acting agent (sympathoplegic)
  • a2 agonist
  • Works presynaptically in order to reduce NE in the brain* —-For mild/moderate HT.
  • Sympathoplegic mechanism unknown.
  • Toxicity is minimal, but sudden cessation causes high HT.
  • Can inhibit insulin secretion
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15
Q

Ganglion Blockers

A
  • antihypertensive drug
  • nicotinic cholinoceptor antagonist
  • for severe HT (it has a rapid onset).
  • It works by blocking the nAChR in the autonomic ganglia. —Its toxicity is intolerable (constipation,..) and therefore it is used rarely. (not very clinically important because they affect the ganglia which affect the sympathetic muscles directed by the ganglia)
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16
Q

Reserpine, guanetidine

A
  • Antihypertensive drug
  • Postsympathetic ganglion neuron blocker
  • It is rarely used.
  • Reserpine works by blocking the reuptake of NA into the vesicles, whereas Guanetidine works by preventing neurotransmitter release.
  • Its toxicity is that they are intolerable. (not clinically important because it has a broad effect, even on the CNS)
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17
Q

Prazosin

A
  • Anti-hypertensive drug
  • Adrenoreceptor blocker: a1 receptor antagonist
  • Important monotherapy if used for mild/moderate HT (a and ß blockers). And ß blockers are used in polypharmacy for moderate/severe HT. Toxicity is mild for a1 blockers (monotherapy).
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18
Q

Propanolol

A
  • Anti-hypertensive drug and myocardial ischemia and antiarrhythmia (Slow AV conduction and prolong PR interval)
  • Adrenoreceptor blocker: ß1 receptor antagonist
  • Important monotherapy if used for mild/moderate HT (a and ß blockers).
  • Used for effort angina and acute coronary syndrome. ———Works by reducing blood pressure and cardiac work.
  • Side effects include orthostatic hypotension, tachycardia and headache.
  • And ß blockers are used in polypharmacy for moderate/severe HT.
  • toxicity is moderate for ß1 blockers (polypharmacy)
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19
Q

Nitroprusside

A
  • Anti-hypertensive drug
  • Vasodilator category of drugs
  • release of NO causes vasodilatation of arterioles. It is a Nitrovasodilator.
  • Can be used for hypertensive emergency.
  • Works by activating soluble guanylate cyclase (converts GTP –>cGMP) which reduces Ca voltage channels activity leading to relaxation of vascular smooth muscle.
  • Toxicity leads to excessive hypotension and tachycardia.
  • Part of Polypharmacy for Severe Hypertension
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20
Q

Diazoxide

A
  • Anti-hypertensive drug
  • Vasodilator
  • Opening of K+ channels and hyperpolarization.
  • Vasodilatation is caused by Opening of K+ channels (agonist) and hyperpolarization of blood vessel, taking away the potential where v-gated Ca channels open up, reducing BP.
  • Can be used for hypertensive emergency.
  • Toxicity can lead to mild tachycardia.
  • Part of Polypharmacy for Severe Hypertension
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21
Q

Verapamil

A

-Anti-hypertensive drug and myocardial ischemia
-Vasodilator
-blocking L-type Ca channels (voltage- and frequency- dependent block). Works by peripheral vasodilation and reduction of cardiac work.
Used for effort angina and variant angina (prophylactic).
-It is used as a monotherapy for mild/moderate HT.
-Each drug has a distinct binding site. Therefore they can have an additive effect if combined. All three binding sites are located on the same subunit.
-Toxicity due to excessive vasodilation and cardiodepression. toxicity can include orthostatic hypotension, AV block and edema.
-Part of Polypharmacy for Severe Hypertension

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22
Q

Diltiazem

A

-Anti-hypertensive drug and myocardial ischemia
-Vasodilator
-blocking L-type Ca channels (voltage- and frequency- dependent block). Works by peripheral vasodilation and reduction of cardiac work.
Used for effort angina and variant angina (prophylactic).
-It is used as a monotherapy for mild/moderate HT.
-Each drug has a distinct binding site. Therefore they can have an additive effect if combined. All three binding sites are located on the same subunit.
-Toxicity due to excessive vasodilation and cardiodepression. toxicity can include orthostatic hypotension, AV block and edema.
-Part of Polypharmacy for Severe Hypertension

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23
Q

Nifedipine

A
  • Anti-hypertensive drug and for myocardial ischemia
  • Vasodilator
  • blocking L-type Ca channels (voltage- and frequency- dependent block). Works by peripheral vasodilation and reduction of cardiac work.
  • Used for effort angina and variant angina (prophylactic).
  • It is used as a monotherapy for mild/moderate HT.
  • Each drug has a distinct binding site. Therefore they can have an additive effect if combined. All three binding sites are located on the same subunit.
  • Toxicity due to excessive vasodilation and cardiodepression. toxicity can include orthostatic hypotension, AV block and edema.
  • Part of Polypharmacy for Severe Hypertension
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24
Q

Captopril

A
  • Anti-hypertensive drug and congestive heart failure (First line agents (with diuretics) in Heart Failure)
  • ACE inhibitors
  • Also prevent breaking down of bradykinin –> vasodilatation
  • Toxicity leads to cough and severe renal damage in the fetus. It also prevents the break down of bradykinin which is involved in vasodilatation in addition to blockin conversion of agiotensin 1 into angiotensin 2 (active molecule).
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25
Q

Losartan

A
  • Anti-hypertensive drug and congestive heart failure (First line agents (with diuretics) in Heart Failure)
  • Angiotensin Receptor Inhibitor (AT1-type)
  • It is a substitute when not tolerant to ACE inhibitors. Competitive block of AT1 receptor.
  • Toxicity leads to milder cough and renal damage in fetus than for ACE inhibitors. Contraindicated in pregnancy.
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26
Q

Nitroglycerin

A

-Myocardial ischemia symptomatic drug and congestive heart failure (Acute decompensation in heart failure (reduce afterload by increasing ejection fraction and preload by reducing myocardial O2 requirement)).
Works by reducing venous return, cardiac size and diastolic myocardial oxygen consumption —> relaxation of smooth muscle.
-Used for effort angina, variant angina and acute coronary syndrome.
-Side effects include orthostatic hypotension (fainting when getting up because the drug interferes with the sympathetic nervous system), tachycardia (reflex) and headache.

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27
Q

lovastatin

A

-Myocardial ischemia prophylactic drug
-Statins family (lipid lowering drug)
-Inhibition of cholesterol synthesis
Inhibit HMG-CoA reductase.
-Side effects can include damage of skeletal muscle or liver and interference with myelination of infants (do not give when pregnant). Statins are given in a more ambiguous ways.

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28
Q

Cholestyramine

A
  • Myocardial ischemia prophylactic drug
  • Resins family (lipid lowering drug)
  • Prevention of cholesterol reabsorption
  • They are non-absorbable macromolecules (big sponge that soaks out all of the lipids) that bind cholesterol preventing reabsorption from the gut.
  • Side-effects include unpleasant gritty taste, GI tract discomfort and interference of vitamin or drug absorption (because lipids are needed to absorb some vitamins and drugs).
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29
Q

Niacin

A
  • -Myocardial ischemia prophylactic drug
  • Lipid lowering drug
  • reduction of VLDL secretion
  • Decrease in secretion of VLDL particles from liver (mechanism not well understood).
  • Side effects include occasional flush with itching and rarely some glucose intolerance.
  • It is not the first drug used, first we try statins.
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30
Q

Gemfibrozil

A
  • Myocardial ischemia prophylactic drug
  • Fibrates family (lipid lowering drug)
  • Increase the synthesis of Lipoprotein lipase
  • Activate peroxisome proliferation receptor-a which increases lipoprotein lipase synthesis (that break down low density lipoprotein and take them out of the circulation). -Side-effects can include nausea, skin rash and occasional increase risk of gallstones
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31
Q

Warfarin

A
  • Myocardial ischemia prophylactic drug
  • Anti-coagulant drug (Inhibition of blood coagulation)
  • Warfarin blocks reactivation of vit. K epoxide and binds to coagulation factors II, VII, IX and X
  • Used for prevention and treatment of venous clotting (especially deep vein thrombosis).
  • Side-effects are that warfarin is teratogenic and both drugs can prolong bleeding. (warfarin effect is monitored with prothrombin test time)
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32
Q

Heparin

A
  • Myocardial ischemia prophylactic drug
  • Anticoagulant drug (Inhibition of blood coagulation)
  • Heparin binds coagulation factor Xa and antithrombin III. –
  • Heparin available in high molecular weight (HMW) (less predictable, must be monitored but more effective) and low molecular weight (LMW) form (more predictable, less effect on ATIII)
  • -Used for prevention and treatment of venous clotting (especially deep vein thrombosis).
  • Side effect is that the drug can prolong bleeding
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33
Q

Streptokinase

A
  • Myocardial ischemia prophylactic drug
  • Fibrinolytic drug (plasmin activation)
  • Streptokinase (cost effective) converts plasminogen to fibrin
  • Used for pulmonary embolism and myocardial infarction. —Streptokinase can cause an allergic response and both can lead to bleeding.
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34
Q

Tissue Plasminogen Activator (TPA)

A
  • -Myocardial ischemia prophylactic drug
  • Fibrinolytic drug (endogenous)
  • tPA (expensive) activates plasminogen bound to fibrin.
  • Used for pulmonary embolism and myocardial infarction. —Can lead to bleeding.
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35
Q

Aspirin

A
  • Myocardial ischemia prophylactic drug
  • Cyclooxygenase inhibitor (irreversible)
  • works by inhibiting platelet cyclooxygenase blocking the syntheesis of TXA2.
  • Used for transient ischemic attacks and myocardial infarction.
  • Side-effect for aspirin comprise GI ulceration and bleeding
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36
Q

Ibuprofen

A
  • Myocardial ischemia prophylactic drug
  • Cyclooxygenase inhibitor (competitve)
  • works by inhibiting platelet cyclooxygenase blocking the synthesis of TXA2.
  • Used for transient ischemic attacks and myocardial infarction.
  • Side-effect can be bleeding.
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37
Q

Ticlopidine

A

–Myocardial ischemia prophylactic drug
-Adenosine receptor blocker
Used as alternative if allergic to aspirin. Inhibit platelet response to secreted ADP at the adenosine receptors. Side effects can include bleeding and skin rashes.

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38
Q

Digoxin

A
  • Drug for Heart Failure
  • Positive Ionotropic drug (cardiac glycosides family)
  • Works by blocking the Na-K ATPase and has cardiac parasympathetic effects (slow AV conduction, useful atrial fib).
  • Used primarily for heart failure and atrial fibrilation.
  • Its therapeutic value and toxic value have to be carefully monitored.
  • Side-effects (very toxic) include cardiac arrhytmias, GI upset, neuroendocrine effects (do not give to patient unless really needed).
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39
Q

Metoprolol

A
  • Congestive heart failure
  • ß-blocker
  • prolong life in chronic heart failure
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40
Q

Dobutamine

A
  • Congestive heart failure
  • ß1-selective (ß-agonist) for severe heart failure.
  • helps increasing contractility of the heart (increase cardiac force, reduces afterload result of increasing cardiac output)
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41
Q

Theophylline

A
  • Congestive heart failure
  • Phosphodiesterase inhibitor family
  • Acute decompensation in HF. It increases cAMP level (has effect on adenylate cyclase) in cardiac and vascular tissue) (Na-K atpase effect?)
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42
Q

Class I

A
  • Anti-arrhythmic drugs
  • Na Channel-blockers like Quinidine
  • IA: slow intraventricular conduction (increase QRS) and increase ventricular AP (increase QT)
  • IB: selective for abnormal tissue
  • IC: slow intraventricular conduction only
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43
Q

Class II

A
  • Anti-arrhythmic drugs
  • ß-blockers like propanolol
  • Slow AV conduction and prolong PR interval
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44
Q

Class III

A
  • Anti-arrhythmic drugs
  • I(Kr) channel blockers like Sotalol
  • Prolong ventricular AP therefore prolong PR interval
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45
Q

Class IV

A
  • Anti-arrhythmic drugs
  • L-type channel blocker like Veparimil.
  • Slow AV conduction and prolong PR interval
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46
Q

Class V

A
  • Anti-arrhythmic drugs

- Miscellaneous (including adenosine, K and Mg ions)

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47
Q

Nebulizers or inhaler solutions

A
  • Drugs for asthma
  • Selective ß2-agonist (increase ATP–>cAMP which leads to bronchodilatation)
    • major problem with regular use: exarcerbated bronchial hyperresponsiveness owing to: tachyphylaxis-involving less ß2 adrenergic receptors to compensate for overactvation
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48
Q

atropine and non-absorbable quaternary ammonium congeners iptratropium bromide

A
  • Drugs for asthma
  • Anticholinergic agents
  • Block activities of Ach, which activates M3 receptors on smooth muscle cells leading to inhibition of AC through Gi and activation of K+ channels through ßy subunits of Gi GPCR.
  • Bronchodilation less intense than ß2 agonist but in combination with them gives greater and more prolonged bronchodilation
  • It is of particular benefit for patients with coexistent heart disease
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49
Q

Methylxanthines

A
  • Drugs for asthma
  • They inhibit phosphodiestarase thus increase cAMP, membrane hyperpolarization, uncoupling of Ca i with contractility, antagonism of adenosine receptors which are G protein coupled (most important effect)
  • They have positive and adverse effects: positive (less drowsiness and fatigue, more flow of thoughts, less delicate muscular coordination), negative (more CNS stimulation, more nervousness and anxiety, restlessness, insomnia, tremors, focal and general convulsions, more nausea and vomiting through medullary respiratory center*, can give tachycardia and arrhytmia), are diuretics
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50
Q

Glucocorticoids

A
  • Drugs for asthma
  • GR dimers through DNa binding lead to transactivation of anti-inflammaotry proteins + has metabolic and endocrine side-effects. GR monomers through DNA binding lead to transrepression of inflammatory proteins and inhibition of TFs involved in inflammation.
  • Systemic glucocorticoids are used for acute exacerbations and chronic severe asthma
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51
Q

Montelukast

A
  • Drugs for asthma
  • Leukotriene inhibitor
  • Taken orally once daily, approved for little children.
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52
Q

Mast cells stabilizing agents (e.g chromolyns)

A
  • Drugs for asthma
  • Inhibit pulmonary mast cell degranulation, release of histamine and leukotriene is markedly reduced, can reverse functional changes induced in leukocytes in response to an allergen, inhibiting the activating effects of chemoattractant peptides on neutrophiles, eosinophiles and mococytes, devoid of bronchodilating capability
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53
Q

Phenylpropanolamine (PPA)

A
  • Drug for colds and allergies

- oral + topical decongestant. Indirect agonist of postsynaptic adrenergic receptors. Increase NA

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54
Q

Phenylephrine

A
  • Drug for colds and allergies
  • oral+topical decongestant. Direct agonit of postsynaptic a1 receptors. Activate Ca dependent kinase through PLC then IP3 (causes vasoconstriction)
  • Can be broken down by MAO
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55
Q

Pseudoephedrine (Sudafed)

A
  • Drug for colds and allergies

- oral degongestant. Indirect agonist of postsynaptic adrenergic receptors. Increases NA

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56
Q

-Diphenydramide

A
  • Drug for colds and allergies

- 1st generation anti-histaminic

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57
Q

Terfernadine

A
  • Drug for colds and allergies

- 2d generation anti-histamine

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58
Q

magnesium oxide, magnesium hydroxide

A
  • GI ulcer drug
  • Antiacid neutralizes pH, effective management of peptic ulcers
  • sodium bicarbonate has systemic side effects
  • General side-effects: frequent dosing required and disagreable taste
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59
Q

Cimetidine

A
  • -GI ulcer drug

- H2 receptor blocker

60
Q

propantheline

A
  • GI ulcer drug

- M1 or M3 blockage

61
Q

omeprazole

A
  • GI ulcer drug
  • Irreversibly inactivates H/K pump in parietal cells
  • Side effects: gastric mucosa hyperplasia
62
Q

Ranitidine

A
  • GI ulcer drug
  • H2 receptor blocker
  • Longer duration of action than cimetidine, does not have p450 interaction, less antiadrogenic effects.
63
Q

Sucralfate

A
  • -GI ulcer drug

- Protect the mucosa (complexes with protein at the ulcer site to form a protective layer and binds to pepsin)

64
Q

Metoclopramide

A
  • GI drug: for gastroparesis and reflux esophagitis
  • Prokinetic drug
  • D2 Antagonist (increase lower sphincter tone and force of gastric contraction, gastric emptying and coordination of gastroduodenal contraction)
  • 5HT4 agonist (same effect as D2 antagonist)
  • suppress emesis
  • Parkinson like side effects and gynecomastia, breast tenderness due to increase of prolactin
65
Q

cisapride

A
  • GI drug: for gastroparesis and reflux esophagitis
  • Prokinetic drug
  • 5HT4 agonist and 5HT3 antagonist (antiemetic effect due to inhibition of CTZ by inhibiting 5HT3 receptors)
66
Q

Castor oil

A
  • GI drug, secretory laxative
  • It’s a prostaglandin: lead to more fluid accumulation in the bowel and more fluid flow and persistalsis, inhibition of water reabsorption in lower intestine.
  • -Disadvantages: lead to habituation, damage to the myenteric plexus, colonic atony, excessive loss of water and electrolyte and Ca
67
Q

Mineral oil

A
  • Gi drug, laxative
  • emollient
  • lubricate lower bowel in condition of irritation, non absorbable
  • side effects: elicitation of foreign body reactions, malabsoroption of fat-soluble vitamins, lipid pneumonitis
68
Q

bran, psyllium, methylcellulose

A
  • GI laxative
  • Bulk forming agents
  • increase bulk and water content in GI, therefore decreasing intestinal transit time –> more flow through the bowel
  • Disadvantages: lead to habituation, damage to the myenteric plexus, colonic atony, excessive loss of water and electrolyte and Ca
69
Q

Saline laxatives (e.g magnesium hydroxide, sodium phosphate, sodium sulfate, magnesia milk)

A
  • GI laxative
  • drawing water into the intestine by osmotic process
  • -Disadvantages: lead to habituation, damage to the myenteric plexus, colonic atony, excessive loss of water and electrolyte and Ca
70
Q

loperamide, diphenoxylate

A
  • GI antidiarrheal drug
  • decreases secretion and increases absorption
  • increase segmental contraction and decrease propulsive contraction
71
Q

Penicilin G

A
  • Antibiotic
  • Act on the bacterial cell wall
  • Inhibit the cross-linking of peptidoglycan chain (inhibits transpeptidase)
  • Classic penicilin
  • Works mostly on Gram + bacteria
72
Q

Ampicillin

A
  • Antibiotic, smaller than penicillin
  • Act on the bacterial cell wall
  • Inhibit the cross-linking of peptidoglycan chain (inhibits transpeptidase)
  • Can go easier through the membrane of gram - bacteria due to its small size.
  • Can be taken orally
73
Q

Methicillin

A
  • Antibiotic
  • Act on the bacterial cell wall
  • Inhibit the cross-linking of peptidoglycan chain (inhibits transpeptidase)
  • Antistaphiloccocal penicillin: Resistant to ß-lactamse but inactive against PBP -/- penicillin resistant bacteria.
  • Cannot be taken orally
74
Q

Cephalosporin

A
  • Antibiotics

- Act on bacterial cell wall

75
Q

Naficillin, Clavulanic acid

A
  • Antibiotic
  • Act on the bacterial cell wall
  • Inhibit the cross-linking of peptidoglycan chain (inhibits transpeptidase)
  • Antistaphiloccocal penicillin: Resistant to ß-lactamse but inactive against PBP -/- penicillin resistant bacteria.
76
Q

Vancomycin

A
  • Antibiotic
  • Last resort agent against PBP mutated bacteria
  • Active against methicllin resistant gram + bacteria.
  • Has to be administered IV.
  • Primarliy used against gram + bacteria.
  • Synergistic action with aminoglycosides against S. Aureus. Combination with aminoglycosides is bactericidal against enteroccocus.
77
Q

Sulfonamides

A
  • Antibiotics
  • Rarely used as a single agent,
  • Used for treatment of urinary tract infections, topical ophthalmic solution or ointment.
  • Topically applied on burn wound.
  • Side-effects: Cross-allergenic with thiazides, hypoglycemic agents and others. Precipitates in urine. Hemolytic or aplastic anemia, granulocytopenia, thrombocytopenia, hemolytic reactions in G6PD deficient patients.
78
Q

Trimethoprim

A
  • Antibiotic
  • DHFR inhibitor.
  • Used as a single agent in urinary tract infections, most community acquired organisms susceptible.
79
Q

co-trimoxazole

A

-Antibiotic

= Trimethoprim + Sulfamethoxazole

80
Q

Amphotericin

A
  • Antifungal
  • Targets a ergosterol in yeast.
  • Infusion related toxicity and slower toxicity (renal damage, abnormal liver functions, CNS seizures). Drug of choice for life-threatening mycotic infections, used for induction therapy followed by azoles. Topical administration
81
Q

Clotrimazole

A
  • Antifungal
  • Azoles
  • Inhibitors of 14a-demethylase.
  • Broad spectrum anti-fungal agent, resistance emerging, fluconazole has high oral bioavailability and low hepatic enzymes interactions, prophylaxis in AIDS and transplantation, drug of choice for cryptococcal meningitis.
82
Q

Flucytosine

A
  • Antifungal
  • Thimidylate synthetase inhibitor.
  • Block cytosine deaminase enzyme.
  • Bone marrow toxicity and derangement of liver function.
  • Has a narrow therapeutic window. Used in combination with amphotericin B or itraconazole
83
Q

Acyclovir

A
  • Antiviral
  • analogs of guanine.
  • Causes chain termination.
  • Treatment of genital HSV infections, is ineffective in eliminating latent infections.
  • Topical treatment is beneficial in primary genital HSV infection and in mucocutaneous HSV infection in immunocompromised hosts.
84
Q

Ganciclovir

A
  • Antiviral
  • Analog of guanine. Less specific than acyclovir.
  • Causes chain termination.
  • low oral bioavailability.
  • Used for CMV retinitis in immunosuppressed patients . Prevention of CMV disease in transplant recipients.
  • Adverse effect include profound bone marrow suppression, particularly neutropenia, bone marrow toxicity is potentiated with AZT, resistance may develop through a mutation in either the viral UL97 gene of the viral DNA polymerase.
85
Q

Ribavirin

A
  • Antiviral
  • It’s a purine nucleoside analog that inhibits de novo synthesis of GTP (inhibits inosinate dehydrogenase).
  • It is administered as a small particle aerosol, treat respiratory syncytial virus (RSV) infection in infants, less-extensively to treat parainfluenza virus infections in children (last resort).
  • Adverse effects include reversible hematopoietic toxicity (not observed with aerosolized ribavirin), is mutagenic, teratogenic and embryotoxic.
86
Q

Amantidine

A
  • Antiviral
  • inhibits M2 protein of influenza A.
  • Prevents viral uncoating.
  • Used for prophylaxis in a documented influenza A epidemic.
  • CNS effects (anti-Parkinson) and side-effects.
87
Q

Oseltavimir (Tamiflu)

A
  • Antiviral
  • Neuranimidase inhibitor.
  • Zanamivir has low oral bioavailability and Oseltamivir has high oral bioavailability.
  • Therapeutic effects result in 3 days reduction in duration of disease in those with febrile illness treated within 30h of symptom onset, reduced complication, prophylaxis reduces the risk of influenza febrile disease by 90%, clinical benefits in both infleunza A and B (Very effective).
  • Zanamivir not recommended for treatment of patients with underlying airway diseases.
  • Side-effect: Allergic like symptoms and potential source for bacterial infections.
88
Q

Lamivudine 3TC

A
  • Anti-viral
  • Reverse transcriptase inhibitors (nucleoside RT inhibitors) –Adverse effect include rapid selection for M148 resistant mutants.
  • A combination of 3TC with AZT is highly effective, however, strains resistant to both 3TC and AZT developed. Can cause mild GI discomfort, headache and insomnia.
89
Q

Non-nucleoside reverse transcriptase inhibitors (NNRTIs)

A
  • Anti-viral
  • Poor penetration into the CSF and good penetration into the seminal fluid.
  • Efavirenz and Defaviridine cause CNS adverse effects (wooziness, profound dizziness, abnormal dreams and headache).
  • Nevirapine and efavirenz decrease protease inhibitor conc. through induction of hepatic metabolism.
90
Q

Zidovudine (AZT)

A
  • Anti-viral
  • Is an analog of thymidine.
  • Resistance caused in common mutation of RT enzyme which limits the clinical use of AZT.
  • Frequent adverse effect, myelosuppression causes anemia or neutropenia, GI intolerance, headache and insomnia.
91
Q

Protease inhibitors

A

-Anti-viral
-The drug sits next to the peptide to block the scissors (blocks the ability of the protease to cleave)
Poor penetration into CSF, good penetration into the seminal fluid.
-Work very well but get resistance very soon.
-Adverse effects include GI disturbance, hypercholesterolemia, hyperglycemia, hypertriglyceridemia, nephrolithiasis (kidney stones)

92
Q

Sumatriptan

A
  • Drug for migraine
  • 5HT2 agonist
  • mainstay for moderate to severe migraine. Triptans are more effective, with fewer side-effects (works on non-headache symptoms too like light/sound sensitivity and nausea but does not inhibit aura).
  • -it stimulate 5HD1 receptor which are inhibitory of the neuron so it will lead to inhibited impulse sent to the brain
  • It also stimulate 5HT1-B which vasodilate the blood vessel.
  • sumatriptan is more effective than the ergotamine+caffeine mixture at relieving migraine.*
  • Triptans adverse effect: constricts coronary arteries so would not be given to people who suffer from cardiovascular disease. Side-effects for triptan are chest « tightness » and myocardial ischemia
93
Q

NSAIDS

A
  • Drugs for migraine

- often taken with an anti-emetic

94
Q

Ergotamine, dihydroergotamine

A
  • Drugs for migraine
  • pharmacologically rich but less selective than triptans
  • Side effects for ergotamine and DHE are peripheral vasoconstriction and mental disturbances.
95
Q

Clorpromazine (CPZ)

A
  • The first typical antipsychotic
  • CLZ has similar affinity for D1 and D2 receptors, blocking two for the same extend.
  • The three symptoms of antipsychotic drugs are that they produce acute EPS, a prolactin surge and tardive dyskinsia after a few years of taking the drug
  • It shuts down DA cell firing in both the NS and MS by blocking DA autoreceptors.
96
Q

Haloperidol (Haldol)

A
  • A typical antipsychotic
  • Haloperidol is more selective for D2 receptors, more blocking them than the other.
  • The three symptoms of antipsychotic drugs are that they produce acute EPS, a prolactin surge and tardive dyskinsia after a few years of taking the drug
  • -It shuts down DA cell firing in both the NS and MS by blocking DA autoreceptors.
97
Q

Clozapine

A

-An atypical antipsychotic
-Works in more patients than classic antipsychotics
-No EPS or prolactin surge
-No tardive dyskinesia
BUT Severe, infrequent adverse effect on blood cells (agranulocytosis), Weight gain (diabetes?), Risk of seizures
-not a first-line drug
-block less D2 receptors (less EPS side-effects) but block much more 5HT2 than classical antipsychotic.
–Clozapine stands out from the other drugs because it can alleviate negative symptoms, can improve treatment resistant patient, but the problem is that there is a 1-4% risk that it will cause fatal cardiovascular problem (leads to agranulocytosis).
-Atypicals produce little or no tardive dyskenesia
-They selectively inhibit the mesolimbic pathway
-It only turns down DA cell firing in the mesolimbic system. by blocking DA autoreceptors.

98
Q

Phencyclidine (PCP)

A
  • antipsychotic
  • can temporarily mimic schizophrenia, has hallucinogenic effects. We can see both positive and negative symptoms of schizophrenia.
99
Q

reserpine

A
  • Antidepressant
  • blocks the vesicular monoamine pump which is not selective for DA vs. NA. vs. 5HT (less 5HT and NA release), blocks all of them equally well
100
Q

Iproniazid

A
  • Antidepressant
  • MAO inhibitor
  • increase NA and serotonin levels by inhibiting MAO. —-Side-effects include Postural hypertension, dry mouth and « cheese » reaction
101
Q

Imipramine (Tofranil)

A
  • Tricyclic Antidepressant
    -blocks the NA and serotonin transporter.
    -Adverse effects :postural hypotension (cause is uncertain), dry mouth etc (muscarinic ACh receptor block), “cheese reaction », MAO in gut normally breaks down tyramine. MAOI —> excess tyramine —> blood pressure
    TCAs - adverse effects. TCAs initially cause sedation, confusion, and incoordination
    TCAs can antagonize certain receptor types:
    sedation (histamine H1), dry mouth etc (muscarinic ACh)
    TCAs interact with certain drugs, e.g. aspirin (plasma binding proteins), steroid drugs reduce TCA breakdown (compete for P450), STRONGLY potentiate ethanol’s effects)
    -very potent synergy between alcohol and TCAs—> dangerous)
    TCA overdose: convulsions, then coma, cardiac arrhythmias
102
Q

Fluoxetine (Prozac)

A
  • Antidepressant
  • SSRI
  • block serotonin transporter more that NAT. -Safer side-effects but dangerous when combined with an MAOI.
  • SSRIs produce sexual dysfunction, loss of libido, erectile function. There is also an SSRI syndrome.
103
Q

Diazepam (Valium)

A
  • Antianxiety drugs
  • binds to a2-GABA receptors, increased the frequency of GABA induced channel opening. –Metabolized into active metabolites like nordiazepam, which has a half-life of 30-200hrs. - -Addictive, rebound anxiety, sedative, potentiate ethanol, hypnotic, anticonvulsant, muscle relaxant.
104
Q

Busipirone

A
  • Antianxiety drug
  • a partial 5-HT1A receptor agonist
  • For generalized anxiety, less side-effects than diazepam
105
Q

Propanolol

A
  • Antianxiety drug
  • ß-blocker
  • Unwanted effects include bronchoconstriction, cardiac failure, blocking signs of hypoglycemia, physical fatigue, bad dreams.
  • Widely used, not proven to work longterm, second-line.
106
Q

Isofluorane

A
  • Inhalational anesthetic
  • commonly used. -Isofluorane exerts stereoselective effects on K+ currents but not on lipid bilayers.
  • Inhibits the ouput of thalamocortical neurons
107
Q

Ketamine

A
  • Intravenous anesthetics
  • the (+) isomer is more potent.
  • It selectively inhibit NMDA receptors
108
Q

Phenobarbital

A
  • Intravenous anesthetic
  • the (-) isomer is more potent.
  • Phenobarbital stereoselectively potentiate GABA
109
Q

Lidocaine, procaine

A
  • Local anesthetics
  • block v-gated Na channels, stabilizing the inactivated state.
  • They must enter the membrane and be cationic in order to bind the target. Selective for Ad and c fibers.
  • Adverse effects in the CNS (restlessness, tremors, convulsion) and cardiovascular system (reduced force of contraction and vasodilatation lead to decreased BP). They have 3 domains (lipophilic domain, intermediate ester or amide link and basic amine side-chain) and are weak bases.
110
Q

Nitrogen mustard

A
  • Anticancer drug
  • Alkylation of DNA at the N-7 position of guanine: Miscoding, depurination, strand breaks, cross links. -bi-functional (two chlroethyl groups).
111
Q

Cisplastin

A
  • Anticancer drug
  • Alkylating agent
  • causes DNA damage by causing cross linking.
112
Q

Cyclophosphamide

A

Anticancer drug, immunosuppression

  • cytotoxic drug
  • Alkylating agent: alkylates DNA, induces DNA cross-link and inhibit cell proliferation.
  • can lead to nausea and vomiting, nephrotoxicity and ototoxicity.
  • Phosphoramide mustard is the active compound that cause DNA damage, and acrolein is toxic (another metabolite).
113
Q

Methotrexate

A
  • Anticancer drug, immunosuppression
  • Looks like folic acid
  • inhibits dihydrofolate reductase, starves cells of thymidine.
114
Q

5-fluorouracyl

A
  • Anticancer drug

- pyrimidine analog

115
Q

Cytarabine (AraC)

A
  • Anticancer drug

- Incorporation inhibits DNA chain elongation —> chain termination, and inhibits DNA polymerase

116
Q

Vincristine, Vinblastine

A
  • Anticancer drugs
  • Vinca Alkaloids
  • target microtubules. - - -vicncristine—> neurotoxicity,
  • vinblastine —> myelosuppression.
  • Vinca alkaloids prevent microtubules assembly.
117
Q

Paclitaxel, Abraxane

A
  • Anticancer drugs
  • Taxanes
  • abrataxane is paclitaxel in albumin-coated nanoparticles
  • Taxanes prevent microtubule disassembly and promote microtubule assembly
118
Q

Etoposide

A
  • Anticancer drug
  • Topoisomerase inhibitors
  • DNA strand break, block cell cycle at S-G2. Anti-tumour antibiotic
119
Q

Doxorubicin

A
  • Anticancer drug
  • Antitumour antibiotic
  • Inhibits topoisomerase 2, intercalates DNA (blocking DNA and RNA synthesis), alters cell membrane fluidity and ion transport, generates free radical. ——-Bone marrow and cardiac toxicity.
120
Q

Bleomycin

A
  • Anticancer drug
  • anti-tumour antibiotics. —–Causes DNA single and double-strand breaks, forms free radicals, inhibits DNA synthesis —> cells accumulate in G2.
121
Q

Prednisone

A
  • Anticancer drug, immunosuppression
  • Hormonal approach. –Glucocorticoid receptor agonist: decrease transcription of inflammatory genes and increase transcription of anti-inflammatory genes —> decrease in immune cell signalling and proliferation. —-Anti-lymphocytic effects
122
Q

Tamoxifen

A
  • Anticancer drug
  • Hormonal approach.
  • A competitive partial agonist/antagonist at the estrogen receptor. Suppresses IGF-1, and upregulates TGF-ß.
123
Q

Anastrazol

A
  • Anticancer drug
  • Hormonal approach.
  • An aromatase inhibitor, blocking the synthesis of estrogen from androgens.
124
Q

Flutamide

A
  • Anticancer drug
  • Hormonal approach.
  • Inhibit androgen action at the receptor level (blocking the receptor).
125
Q

Finasteride

A
  • Anticancer drug
  • Hormonal approach.
  • Blocks the synthesis of DHT
126
Q

Leuroprolide

A
  • Anticancer drug
  • Hormonal approach. —————–Gonadotropin releasing hormone agonist. Suppresses gonadotropin, induce hypogonadism.
127
Q

L-asparaginase

A
  • Anticancer drug
  • Hormonal approach.
  • Depletes L-asparagine in acute lymphoblastic leukemia tumour cells, blocking protein synthesis.
128
Q

Imatinib (Gleevec)

A
  • Anticancer drug
  • Target a cancer specific enzyme for chronic myelogenous leukemia. It’s a tyrosine kinase inhibitor (competitive binding with substrate)
129
Q

Trastuzumab

A
  • Anticancer drug

- a monoclonal antibody inhibits activation of human epidermal growth factor receptor, hER2

130
Q

Bevasizumab

A
  • Anticancer drug

- It’s a monoclonal antibody. targets VEGF-A. Blocks angiogenesis

131
Q

All-trans retinoic acid

A
  • Anticancer drug

- Promote terminal differentiation of leukemic promyelocytes (tumour cells to normal cells)

132
Q

Olaparib

A
  • Anticancer drug

- Poly ADP ribose polymerase (PARP) inhibitors

133
Q

Sipeuleucel

A
  • Anticancer drug

- programs a patient’s own immune system to seek out cancer spreading in the body

134
Q

mi-RNAs + anticancer drugs

A
  • Anticancer drug

- promotes apoptosis

135
Q

Interferon alpha

A
  • Anticancer drug

- Immunodulation. Decreased cell proliferation, enhance immune activities

136
Q

Azathioprine

A
  • Immunosupression
  • cytotoxic drug
  • metabolized to 6-mercapthopurine; inhibits purine synthesis, blocks DNA and RNA synthesis.
137
Q

mycophenolate mofetil

A
  • Immunosuppression
  • cytotoxic drug
  • inhibits inosine monophosphate dehydrogenase, blocks de novo purine synthesis, inhibits T and B cell proliferation and function.
138
Q

calcineurin inhibitors

A
  • immunosuppression
  • T cell targets
  • block cytokine IL-2 production
139
Q

cyclosporine, tacrolimus

A
  • immunosuppression
  • T cell targets
  • specifically blocking IL-2 synthesis in T-cells. The T cells fail to respond to the calcineurin stimulus
140
Q

Sirolimus (Rapamycin) + FKBP

A
  • immunosuppression
  • T cell targets
  • Drug-eluting coronary stents. Inhibitors of mTOR blocks cell cycle progression at G1 to S phase transition.
141
Q

-Polyclonal antibodies

A
  • Immunosuppression

- Rapid depletion of peripheral lymphocytes, prevents initial graft rejection.

142
Q

Muromonab (OKT3)

A
  • Immunosuppression
  • Antibody drug
  • Anti-CD3. Binds T-cell CD3; induces T-cell receptor internalization, kills cytotoxic human T-cell, used to reverse acute allograft rejection
143
Q

Daclizumab

A
  • Immunosuppression
  • Antibody drug
  • It’s an IL-2 receptor antagonist. Targets antigen-activated T cells by binding to the alpha chain of IL-2R (CD25).
  • Used with calcineurin inhibitors to prevent acute organ rejection.
144
Q

Infliximab

A
  • Immunosuppression
  • Antibody drug
  • anti-TNF alpha. Anti TNF biologicals are used for Crohn’s disease and rheumatoid arthritis.
145
Q

Bisphosphonate

A
  • Drug for aging and menaopause.
  • Inhibit osteoclast function.
  • Increased risk in femur fracture and in a rare thigh bone fracture.
146
Q

Raloxifene

A
  • Drugs for aging and menopause.
  • Selective estrogen receptor modulators (SERMs).
  • Agonist for bone and lipid, antagonist for breast and endometrium. Represent “ideal” SERM.
147
Q

Hormone replacement therapy (HRT)

A
  • Drug for aging and menopause
  • Decrease in hot flashes and moodiness, prevents bone mass loss, helps with vaginal dryness and itching, increase HDL, decrease LDL
  • Older women with established risk of artherosclerosis given standard oral HRT have increased risk of CDV.
  • Relative risk of venous thromboembolism is greater during the first year of ERT/HRT. -20% less risk of colon cancer for post-menopausal women taking HRT.
  • There is a slightly increased risk of breast cancer for women using HRT.

Pharmacology (2 decks)

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