Pharmacology Rapid Revision slides notes

Pharmacology

1. Pharmacology Rapid Revision Dr. Priyanka Sachdev

2. Pharmacology Pharmacokinetics Pharmacodynamics Antimicrobial drugs Renal system Respiratory sustem CVS ANS CNS GIT Endocrine Autocoides Blood Anticancer drugs

3. Pharmacology Pharmacokinetics Pharmacodynamics Antimicrobial drugs Renal system Respiratory sustem CVS ANS CNS GIT Endocrine Autocoides Blood Anticancer drugs

4. Pharmacodynamics  What the drug does to the body Physiological and biochemical effects of drugs Their mechanism of action at organ system Pharmacokinetics  What the body does to the drug Absorption Distribution Biotransformation (metabolism) Excretion of the drug

5. Pharmacodynamics deals with Effect of drugs on body Effect of body on drugs Absorption of drugs Metabolism of drugs

6. Pharmacodynamics deals with Effect of drugs on body Effect of body on drugs Absorption of drugs Metabolism of drugs

7. Pharmacokinetics includes study of all except - a) Absorption b) Distribution c) Adverse effects d) Excretion

8. Pharmacokinetics includes study of all except - a) Absorption b) Distribution c) Adverse effects d) Excretion

9. Pharmacodynamics includes - a) Drug elimination b) Drug excretion c) Drug absorption d) Mechanism of action

10. Pharmacodynamics includes - a) Drug elimination b) Drug excretion c) Drug absorption d) Mechanism of action

11. Factors affecting absorption 1. Aqueous solubility 2. Formulation 3. Concentration of drugs 4. Lipid solubility 5. Surface area 6. Motility of GIT 7. Presence of other substances in GIT 8. Vascularity of the absorbing surface 9. Ionization of drugs and local pH

12. HA  H + + A - BOH  B + + OH - Unionized form  A bsorbed Ionised form  Excreted

13. For absorption  Same pH is required Weakly acidic drugs  unionize/absorbed more at  acidic Ph (Stomach) Weakly basic drugs  unionize/absorbed more at  basic pH (intestine) For excretion  O pposite pHis required Weakly acidic drugs  ionize/excreted more at  basic pH (Alkaline urine) Weakly basic drugs  ionize/excreted more at  acidic pH (Acidic urine)

14. Remember Alkalinization of urine  done by IV infusion of sodium bicarbonate Acidification of urine  done by IV infusion of arginine hydrochloride followed by ammonium chloride (NH4Cl)

15. Acetyl salicylate & phenobarbitone are better absorbed from stomach because they are- a) Weak acids remain non-ionic in gastric pH b) Weak acids remain ionic in gastric pH c) Strong acids fully ionised in gastric pH d) Weak bases which are ionised at gastric pH

16. Acetyl salicylate & phenobarbitone are better absorbed from stomach because they are- a) Weak acids remain non-ionic in gastric pH b) Weak acids remain ionic in gastric pH c) Strong acids fully ionised in gastric pH d) Weak bases which are ionised at gastric pH

17. Acidic drug is more ionized at – a) Alkaline b) Acidic pH c) Neutral pH d) None

18. Acidic drug is more ionized at – a) Alkaline b) Acidic pH c) Neutral pH d) None

19. About acidic drug true is - a) Best absorbed in acidic medium b) Best absorbed in alkaline medium c) Not absorbed in acidic medium d) Binds to alpha glycoprotein

20. About acidic drug true is - a) Best absorbed in acidic medium b) Best absorbed in alkaline medium c) Not absorbed in acidic medium d) Binds to alpha glycoprotein

21. Which is the best way to manage a patient present with aspirin poisoning: Make urine acidic with NH4Cl Make urine alkaline with NaHCO3 Treat with N-acetyl cysteine Do gastric lavage

22. Which is the best way to manage a patient present with aspirin poisoning: Make urine acidic with NH4Cl Make urine alkaline with NaHCO3 Treat with N-acetyl cysteine Do gastric lavage

23. Aspirin is an acidic drug; it readily crosses any acidic medium. To treat this toxicity, make the urine alkaline with NaHCO3. Now, this acidic drug can't be reabsorbed from the basic medium, and it readily gets excreted from the body.

24. Alkalinization of urine is done for: (a) Weak acid drugs (b) Weak basics drugs (c) Strong acidic drugs (d) Strong basic drugs

25. Alkalinization of urine is done for: (a) Weak acid drugs (b) Weak basics drugs (c) Strong acidic drugs (d) Strong basic drugs

26. Bioavailability It is a measure of the fraction (F ) of administered dose of a drug that reaches the systemic circulation in the unchanged form.

27. Route of Administration General characteristics Bioavailiabilty Intravenous Onset of action is fastest 100% Intramuscular Painful 75-100% Subcutaneous Lesser volumes can be given compared to intramuscular route 75-100% Per oral Most convenient from patients perspective MC used route 5% to <100% First pass metabolism limits blood levels Per rectal Less first pass metabolism than peroral 30 to <100% Transdermal Very slow absorbtion Lack of first pass effect Prolonged duration of action 80-100%

28. Bioavailability of drug injected I.V. is 100% Bioavailability after oral ingestion is lower because  (a ) Drug may be incompletely absorbed. (b ) Absorbed drug may undergo first pass metabolism

29. AUC tells about the extent of absorption of the drug. T max tells about the time to reach maximum concentration, i.e. rate of absorption C max is the maximum concentration of a drug that can be obtained

30. It is calculated as Area under curve (AUC) of time and plasma concentration.

31.   PRODRUGS A ll A CE inhibitors (except captopril and lisinopril P refer P rednisone P roton pump inhibitors P roguanil D oing D ipivefrine M M ercaptopurine M ethyldopa M inoxidil D L evo -dopa I n I rinotecan C linical C yclophosphamide C lopidogrel C arbimazole S ubjects S ulfasalazine

32. All are prodrug EXCEPT: Aspirin Levodopa Dipivefrin Captopril

33. All are prodrug EXCEPT: Aspirin Levodopa Dipivefrin Captopril

34. Biotransformation (Metabolism) Biotransformation means chemical alteration of the drug in the body It is needed to convert nonpolar (lipid-soluble) compounds to polar (lipid insoluble) So that they are not reabsorbed in the renal tubules and are excreted

35. Classification of Biotransformation Nonsynthetic / Phase I / Functionalization reactions Synthetic/ Phase II / Conjugation reactions

36. Phase I reaction (Non polar  polar) Convert parent drug to a more polar metabolite by introducing or exposing a functional group (chemically reactive group), such as -OH, - NH7, -SH2, (hydroxyl, amine and thiol respectively) Oxidation Reduction Hydrolysis Cyclization Decyclization

37. Phase II reaction (Non polar  polar) It is coupling between drug and an endogenous hydrophilic substrate such as glucuronic acid, sulfuric acid etc. to create more polar conjugates Thus conjugation enhances drug hydrophilicity. Glucuronide conjugation Glycin conjugation Glutathion conjugation Sulfate conjugation Methylation Acetylation

38. Acetylation MNEMONIC- CHIPS – ABC C lonazepam (sedative) H ydralazine (anti HTN) I soniazid (anti TB) P rocainamide (anti-arrhythmic) S ulfonamides (dapsone) A cebutalol , Amrinone, ASA B enzocaine C affeine

39. All drugs are metabolized by acetylation EXCEPT: Phenytoin Isoniazid Procainamide Hydralazine

40. All drugs are metabolized by acetylation EXCEPT: Phenytoin Isoniazid Procainamide Hydralazine

41. Mechanism of metabolism The drug metabolising enzymes are divided into two types: Microsomal enzymes Non Microsomal enzymes

42. Microsomal enzymes Induction Inhibition

43. Microsomal Enzyme Inhibition One drug can competitively inhibit the metabolism of another if it utilizes same enzyme Occurs by direct effect on the enzyme  fast (within hours) Precipitate toxicity of object drug

44. Microsomal Enzyme Induction Increase the synthesis of microsomal enzyme protein (cytochrome P-450 and glucuronyl transferase) Many drugs interact with DNA  Slow Decreased intensity and duration of action of object drugs

45. Hofmann elimination Inactivation of the drug in body fluids by spontaneous molecular rearrangement without the agency of any enzyme e.g. Atracurium

46. All are enzyme inhibitors EXCEPT: Carbamazipine Cimetidine Valproate Ketoconazole

47. All are enzyme inhibitors EXCEPT: Carbamazipine Cimetidine Valproate Ketoconazole

48. Which of the following drug is an enzyme inducer: a. Rifampicin b. Isoniazid c. Ketokonazole d. Erythromycin

49. Which of the following drug is an enzyme inducer: a. Rifampicin b. Isoniazid c. Ketokonazole d. Erythromycin

50. Which is Cyt . P450 inhibitor - a) Ketoconazole b) Rifampicin c) Phenytoin d) INH

51. Which is Cyt . P450 inhibitor - a) Ketoconazole b) Rifampicin c) Phenytoin d) INH

52. Hofmann elimination is - a) Inactivation of drug by metabolizing enzyme b) Unchanged excretion by kidney c) Excretion in feces d) Inactivation by molecular rearrangement

53. Hofmann elimination is - a) Inactivation of drug by metabolizing enzyme b) Unchanged excretion by kidney c) Excretion in feces d) Inactivation by molecular rearrangement

54. Excretion Excretion is the passage out of systemically absorbed drug

55. Rate of Elimination Rate of Elimination is the amount of drug eliminated per unit time

56. Clearance (CL) The clearance of a drug is volume of plasma from which the drug is completely removed in unit time Clearance is the measure of the body's ability to eliminate the drug

57. It is the ratio of rate of elimination to the concentration of drug.

58. Order of Kinetics Rate of Elimination α (Plasma Concentration) order Zero order kinetics First order kinetics

59. Zero order kinetics  Rate of Elimination α (Plasma Concentration) (Plasma Concentration ) = 1 Rate of elimination is independent of plasma concentration

60. Rate of elimination is constant. CL decreases with increase in concentration A constant amount of the drug is eliminated in unit time

61. First order kinetics Rate of Elimination α (Plasma Concentration) 1 Rate of elimination is proportional to plasma concentration for drugs

62. CL remains constant A constant fraction of the drug present in the body is eliminated in unit time.

63. Zero order kinetics ( Plasma Concentration) = 1 Rate of elimination is constant. CL decreases with increase in concentration A constant amount of the drug is eliminated in unit time First order kinetics ( Plasma Concentration) 1 Rate of elimination is proportional to plasma concentration for the drugs CL remains constant A constant fraction of the drug present in the body is eliminated in unit time.

64. MNEMONIC Z ero - Z ero order kinetics shown by W - W arfarin A - A lcohol and Aspirin T - T heophylline T - T olbutamide P ower - P henytoin

65. True about zero order kinetics: Rate of elimination is independent of plasma concentration Rate of elimination is dependent on plasma concentration Clearance of drug is always constant Half-life of drug is constant

66. True about zero order kinetics: Rate of elimination is independent of plasma concentration Rate of elimination is dependent on plasma concentration Clearance of drug is always constant Half-life of drug is constant

67. Pharmacology Pharmacokinetics Pharmacodynamics Antimicrobial drugs Renal system Respiratory sustem CVS ANS CNS GIT Endocrine Autocoides Blood Anticancer drugs

68. All receptors have 2 properties  Affinity Intrinsic activity

69. Affinity Ability of a drug to combine with the receptor If a drug has no affinity, it will not bind to the receptor.

70. Intrinsic activity After binding to the receptor, the ability of drug to activate the receptor is called its intrinsic activity It varies from -1 through zero to +1

71. Based on their intrinsic activities  Drugs may be divided into 4 types Agonist Partial agonist Antagonist Inverse agonist

72. Agonist  IA is +1  B ind to the receptor and activate it maximally similar to that of physiological signal molecule Partial agonist  IA between 0 and +1  It bind with receptor and activates it submaximally similar to that of the physiological signal molecule  Antagonist  IA is 0  Binds to receptor but produces no effect  But now agonist is not able to bind to the receptor because these are already occupied by the antagonist  it decreases the action of the agonist but itself has no effect. Inverse agonist  IA is -1  bind to receptor and produce opposite effect

73. Dose Response Curve ( DRC) It is a graph between the plasma concentration of drug (on X-axis) and the effect/ response produced by the drug (on Y-axis) Generally, the intensity of response increases with increase in dose and the dose-response curve is a rectangular hyperbola

74. DRC is usually hyperbola in shape. As curved lines cannot give good mathematical comparisons, so usually the dose is converted to log dose to form log DRC , which gives a sigmoid shaped curve

75. Important parameters determined from DRC Potency Efficacy Slope Therapeutic index and Therapeutic range

76. Potency Measure of amount of a drug needed to produce the response (x axis) Drugs producing the same response at lower dose are more potent whereas drugs requiring large dose are less potent In DRC, more a drug is on left side of the graph, higher is its potency and a drug is on right side of the graph, lower is its potency

77. Efficacy It is the maximum effect produced by a drug (y axis) In DRC  More peak of the curve greater is the efficacy.

78. Which is more important??? Efficacy is clinically more important than potency Efficacy is a more decisive factor in the choice of a drug

79. Remember The position of DRC on the dose axis (X axis) is the index of drug potency which refers to the amount of drug needed to produce a certain response The upper limit of DRC (Y axis) is the index of drug efficacy and refers to the maximal response that can be elicited by the drug

80. QUESTIONS???

81. Question 1

82. Compare Drug A and C ?

83. POTENCY  'A' is more is potent than 'C’ EFFICACY  Drug 'A' and 'C' have equal efficacy

84. Compare Drug A and B ?

85. POTENCY  Drugs 'A' and 'B' are equipotent EFFICACY  A is more efficacious than B

86. Compare Drug B and C ?

87. POTENCY  Drug ‘B' is more potent than C EFFICACY  Drug ‘C’ is more efficacious than B

88. Question 2

89. Compare Drug A and B ?

90. POTENCY  Drug B is less potent than drug A EFFICACY  Drug B equally efficacious as drug A.

91. Important parameters determined from DRC Potency Efficacy Slope Therapeutic index and Therapeutic range

92. Slope S teep slope indicates that a little increase in dose will markedly increase the response (dose needs individualization) Flat slope implies that little increase in response will occur over a wide dose range

93. Important parameters determined from DRC Potency Efficacy Slope Therapeutic index and Therapeutic range

94. Therapeutic index/Safety margin Gap between the therapeutic effect DRC and the adverse effect DRC

95. Median Effective Dose (ED50 ): It is the dose that will produce the half of the maximum (50%) response. More is ED50, lower is the potency and vice a versa. Median Lethal Dose (LD50): It is the dose that will result in death of 50% of the animals receiving the drug. More is LD50 safer is the drug.

96. Therapeutic Index (T.I) is a measure of the safety of a drug. Drugs having high T.I are safer whereas those having low T.I are more likely to be toxic.

97. Therapeutic range / Therapeutic window Dose which produces minimal therapeutic effect and the dose which produces maximal acceptable adverse effect

98. Drugs which have low Therapeutic range / Therapeutic window Plasma concentration has to be monitered regularly Therapeutic Dose Monitoring (TDM)

99. MNEMONIC TDM is required for A - A minoglycosides (e.g. gentamicin) D rug - D igitalis P ossessing - P henytoin (anti-epileptics) L ow - L ithium T herapeutic - T ricyclic antidepressants I ndex - I mmunomodulators

100. Pharmacology Pharmacokinetics Pharmacodynamics Antimicrobial drugs Renal system Respiratory sustem CVS ANS CNS GIT Endocrine Autocoides Blood Anticancer drugs

101. Antimicrobials  Based on Mechanism of action Inhibit cell wall synthesis Cause leakage from cell membranes Inhibit protein synthesis Interference with nucleic acid synthesis

102. Antimicrobials  Based on Mechanism of action Inhibit cell wall synthesis Cause leakage from cell membranes Inhibit protein synthesis Interference with nucleic acid synthesis

103. Antimicrobials  Based on Mechanism of action Inhibit cell wall synthesis Cause leakage from cell membranes Inhibit protein synthesis Interference with nucleic acid synthesis

104. Beta-Lactam Antibiotics Antibiotics having a β-lactam ring. 1  Thiazolidine ring 2  Beta lactam ring

105. Classification Penicillins Cephalosporins Carbapenems Monobactam

106. Mechanism of action Interfere with synthesis of bacterial cell wall

107. Cell wall consist of  UDP-N-acetylmuramic acid ( NAM )  pentapeptide UDP-N-acetyl glucosamine ( NAG )

108. Normally UDP- NAM and UDP- NAG Peptidoglycan residues linked together forming long strands and UDP is split off Final step is cleavage of terminal D-alanine of peptide chains by transpeptidases Energy so released is utilized for establishment of cross linkages This cross linking provides stability and rigidity to cell wall

109. β-lactam antibiotics β-lactam antibiotic Inhibit the transpeptidases cross linking does not take place cell wall deficient (CWD) forms produced CWD forms swell and burst Bacterial lysis Bactericidal action

110. Bactericidal Active against multiplying organisms only Penicillin  higher susceptibility for gram-positive bacteria In gram-positive bacteria  cell wall consists of thick layer of peptidoglycan and extensively cross linked In gram-negative bacteria  cell wall consists of thin layer of peptidoglycan with little cross linking

111. Gram-negative bacteria Gram-positive bacteria

112. Mechanism of Antimicrobial Resistance 1. Decreased Permeability across the Cell Wall  by modifying their cell membrane porin channels 2. Efflux Pumps  expulsion of the drugs from the cell, soon after their entry  preventing intracellular accumulation of drugs

113. 3. By Enzymatic Inactivation  Eg . β- lactamase, penicillinase Most common mechanism β-lactamase enzymes Hydrolyze β-lactam rings (active site) of β-lactam antibiotics Deactivate their antibacterial properties

114. 4. Altered PBPs that lacks the binding affinity for penicillin  MRSA  Target site of penicillin i.e. penicillin binding protein (PBP) Gets altered to PBP-2a Do not sufficiently bind to β- lactam antibiotics Prevent them from inhibiting cell wall synthesis

115. Classification Penicillins Cephalosporins Carbapenems Monobactam

116. Penicillins First antibiotic to be used Discovery of penicillin  Alexander Fleming Natural penicillin is obtained from a fungus Penicillium notatum and Penicillium chrysogenum .

117. Penicillins Natural penicillin Semisynthetic Penicillins β- lactamase inhibitors CST Benzyl penicillin (Penicillin G) Phenoxymethyl Penicillin (Penicillin V) Acid resistant Alternative to Penicillin G Cloxacillin Oxacillin Nafcillin Dicloxacillin Methicillin Penicillinase resistant Penicillin CONDOM Extended spectrum Penicillins Mezlocillin Azlocillin Piperacillin Ureido Penicillin MAP Clavulanic acid Sulbactam Tazobactam Amino Penicillins AA Ampicillin Amoxycillin Carboxy Penicillins CT Carbenicillin Ticarcillin

118. Benzyl Penicillin or Penicillin G Limitations in its clinical use  Not effective orally  because of breakdown by acid in stomach Susceptibility to penicillinase  Penicillinase hydrolyze β-lactam rings (active site)  Deactivate their antibacterial properties Narrow spectrum of activity  covering mainly gram positive bacteria.

119. Adverse effects 1. Local irritancy 2. Hypersensitivity reactions 3. Jarisch-Herxheimer reaction  Penicillin injected in a syphilitic patient sudden release of spirochetal lytic products Produce shivering, fever, myalgia, exacerbation of lesions, even vascular collapse. Lasts for 12–72 hours Does not need interruption of therapy, Aspirin and sedation for relief of symptoms.

120. Uses Theuraptic Uses  LAST MAN DP Prophylactic uses  RAB

121. Theuraptic Uses LAST MAN DP L - Leptospira A - Actinomyces S – Streptococcus, Staphylococcus (non-penicillinase-producing) T – Treponema, Tetanus (and Gas gangrene) M - Meningococcus AN – Anthrax, Actinomycosis D – Diptheria P _ pnemococcus

122. Prophylactic uses RAB R heumatic fever  Benzathine penicillin 1.2 MU every 4 weeks till 18 years of age or 5 years after an attack, whichever is more. A granulocytosis patients B acterial endocarditis  Dental extractions, endoscopies, catheterization, etc. cause bacteremia which in patients with valvular defects can cause endocarditis.

123. Penicillins Natural penicillin Semisynthetic Penicillins β- lactamase inhibitors CST Benzyl penicillin (Penicillin G) Phenoxymethyl Penicillin (Penicillin V) Acid resistant Alternative to Penicillin G Cloxacillin Oxacillin Nafcillin Dicloxacillin Methicillin Penicillinase resistant Penicillin CONDOM Extended spectrum Penicillins Mezlocillin Azlocillin Piperacillin Ureido Penicillin MAP Clavulanic acid Sulbactam Tazobactam Amino Penicillins AA Ampicillin Amoxycillin Carboxy Penicillins CT Carbenicillin Ticarcillin

124. Semisynthetic Penicillins Aim  to overcome the shortcomings of PnG , 1. Poor oral efficacy due to acid succeptibility 2. Susceptibility to penicillinase . 3. Narrow spectrum of activity

125. Penicillins Natural penicillin Semisynthetic Penicillins β- lactamase inhibitors CST Benzyl penicillin (Penicillin G) Phenoxymethyl Penicillin (Penicillin V) Acid resistant Alternative to Penicillin G Cloxacillin Oxacillin Nafcillin Dicloxacillin Methicillin Penicillinase resistant Penicillin CONDOM Extended spectrum Penicillins Mezlocillin Azlocillin Piperacillin Ureido Penicillin MAP Clavulanic acid Sulbactam Tazobactam Amino Penicillins AA Ampicillin Amoxycillin Carboxy Penicillins CT Carbenicillin Ticarcillin

126. Phenoxymethyl penicillin (Penicillin V) It differs from PnG only in that it is acid stable. Oral absorption is better Peak blood level is reached in 1 hour Plasma t½ is 30–60 min.

127. Acid-resistant penicillins  V - Penicillin V O- Oxacillin D- Dicloxacillin K- Cloxacillin A - Amoxycillin and Ampicillin

128. Penicillins Natural penicillin Semisynthetic Penicillins β- lactamase inhibitors CST Benzyl penicillin (Penicillin G) Phenoxymethyl Penicillin (Penicillin V) Acid resistant Alternative to Penicillin G Cloxacillin Oxacillin Nafcillin Dicloxacillin Methicillin Penicillinase resistant Penicillin CONDOM Extended spectrum Penicillins Mezlocillin Azlocillin Piperacillin Ureido Penicillin MAP Clavulanic acid Sulbactam Tazobactam Amino Penicillins AA Ampicillin Amoxycillin Carboxy Penicillins CT Carbenicillin Ticarcillin

129. Penicillinase-resistant Penicillins Have side chains that protect the β-lactam ring from attack by penicillinase

130. Methicillin Highly penicillinase resistant ie . resistant to β- lactamases But it is not acid resistant  must be injected

131. MRSA MRSA have emerged in many areas. MRSA have altered PBPs which do not bind penicillins . These are insensitive to all penicillinase-resistant penicillins All MRSAs  multidrug resistance DOC  vancomycin, linezolid and teichoplanin

132. Penicillins Natural penicillin Semisynthetic Penicillins β- lactamase inhibitors CST Benzyl penicillin (Penicillin G) Phenoxymethyl Penicillin (Penicillin V) Acid resistant Alternative to Penicillin G Cloxacillin Oxacillin Nafcillin Dicloxacillin Methicillin Penicillinase resistant Penicillin CONDOM Extended spectrum Penicillins Mezlocillin Azlocillin Piperacillin Ureido Penicillin MAP Clavulanic acid Sulbactam Tazobactam Amino Penicillins AA Ampicillin Amoxycillin Carboxy Penicillins CT Carbenicillin Ticarcillin

133. Extended Spectrum Penicillins 1. Aminopenicillins 2. Carboxypenicillins 3. Ureidopenicillins

134. 1. Aminopenicillins This group has an amino substitution in side chain Ampicillin is the prototype Acid stable Not resistant to penicillinase or β- lactamases Spectrum  It is active against all organisms sensitive to PnG . In addition, many gram-negative bacilli  e.g. H. influenzae, E. coli, Proteus, Salmonella , Shigella and Helicobacter pylori are inhibited.

135. 2. Carboxypenicillins This group has an carboxy substitution in the side chain Carbenicillin is the prototype It is not acid resistant (inactive orally) It is not penicillinase-resistant Spectrum  Active against Pseudomonas aeruginosa and Proteus which are not inhibited by PnG or aminopenicillins. Platelet aggregation affected

136. 3. Ureidopenicillins Piperacillin is the prototype Spectrum  8 times more active for pseudomonas than carbenicillin. Activity against Klebsiella, many Enterobacteriaceae and some Bacteroides.

137. Penicillins Natural penicillin Semisynthetic Penicillins β- lactamase inhibitors CST Benzyl penicillin (Penicillin G) Phenoxymethyl Penicillin (Penicillin V) Acid resistant Alternative to Penicillin G Cloxacillin Oxacillin Nafcillin Dicloxacillin Methicillin Penicillinase resistant Penicillin CONDOM Extended spectrum Penicillins Mezlocillin Azlocillin Piperacillin Ureido Penicillin MAP Clavulanic acid Sulbactam Tazobactam Amino Penicillins AA Ampicillin Amoxycillin Carboxy Penicillins CT Carbenicillin Ticarcillin

138. Beta-lactamase Inhibitors Three inhibitors of β-lactamases enzyme  Clavulanic acid (combined with amoxicillin) Sulbactam (combined with ampicillin) Tazobactam (combined with piperacillin)

139. Mechanism of action β –lactamase enzyme produced by various organisms Hydrolysis of β -lactam ring of penicillins ( β -lactam antibiotics) Reduces their effectiveness

140. β - Lactamase inhibitors have a β -lactam ring It binds to β - lactamase Inhibits them Protect β -lactam antibiotics from destruction Increase the effectiveness of β -lactam antibiotics

141. Remember β- lactamase inhibitors themselves are not antibacterial But augment the activity of penicillins against β- lactamase producing organisms

142. Penicillins Natural penicillin Semisynthetic Penicillins β- lactamase inhibitors CST Benzyl penicillin (Penicillin G) Phenoxymethyl Penicillin (Penicillin V) Acid resistant Alternative to Penicillin G Cloxacillin Oxacillin Nafcillin Dicloxacillin Methicillin Penicillinase resistant Penicillin CONDOM Extended spectrum Penicillins Mezlocillin Azlocillin Piperacillin Ureido Penicillin MAP Clavulanic acid Sulbactam Tazobactam Amino Penicillins AA Ampicillin Amoxycillin Carboxy Penicillins CT Carbenicillin Ticarcillin

143. The following is not a penicillinase resistant penicillin- a) Methicillin b) Ampicillin c) Oxacillin d) Nafcillin

144. The following is not a penicillinase resistant penicillin- a) Methicillin b) Ampicillin c) Oxacillin d) Nafcillin

145. Acid Labile penicillin is- Cloxacillin Ampicillin Methicillin Phenoxy Methyl penicillin

146. Acid Labile penicillin is- Cloxacillin Ampicillin Methicillin Phenoxy Methyl penicillin Acid-resistant penicillins  V - Penicillin V O- Oxacillin D- Dicloxacillin K- Cloxacillin A - Amoxycillin and Ampicillin

147. Which among the following is not a beta lactamase resistant Penicillin? Methicillin Carbenicillin Nafcillin Oxacillin

148. Which among the following is not a beta lactamase resistant Penicillin? Methicillin Carbenicillin Nafcillin Oxacillin

149. All of the following are therapeutic uses of penicillin G, except a) Bacterial meningitis b) Rickettsial infection c) Syphilis d) Anthrax

150. All of the following are therapeutic uses of penicillin G, except a) Bacterial meningitis b) Rickettsial infection c) Syphilis d) Anthrax

151. All of the following are beta lactamase inhibitors except- Clavulanic acid Sulbactam Tazobactam Aztreonam

152. All of the following are beta lactamase inhibitors except- Clavulanic acid Sulbactam Tazobactam Aztreonam

153. True regarding clavulanic acid is Deactivates beta lactamase Decreases renal excretion of amoxycillin Potentiates action of penicillin Decreases the side effects of amoxicillin

154. True regarding clavulanic acid is Deactivates beta lactamase Decreases renal excretion of amoxycillin Potentiates action of penicillin Decreases the side effects of amoxicillin

155. Some gram-negative bacteria produce an enzyme that blocks the action of beta lactam antibiotics in periplasmic space. Which arrow in the structural diagram of Penicillin G denotes the site of action of this enzyme? A B C D

156. Some gram-negative bacteria produce an enzyme that blocks the action of beta lactam antibiotics in periplasmic space. Which arrow in the structural diagram of Penicillin G denotes the site of action of this enzyme? A B C D

157. THANK YOU BEST OF LUCK