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Pharmacology > B4 > Flashcards

B4 Flashcards

1
Q

List the component of tobacco smoke

A 
I) Phenol 
II) Nicotine 
III) Benzene 
IV) Tar 
V) CO
VI) Hydrogen cyanide
VII) Formaldehyde 
VIII) Arsenic
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2
Q

Explain the oral effect of tobacco use

A

A) Halitosis

B) Tooth discolouration

C) Inflammation of salivary gland

D) Increased buildup of plaque and tartar on the teeth

E) Increased loss of bone within the jaw

F) Increased risk of leukoplakia ( white patches inside the mouth )

G) Periodontal disease

H) Delayed healing process following tooth extraction , periodontal treatment or oral surgery

I) Lower success rate of dental implant procedure

J) Increased risk of developing oral cancer

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3
Q

Explain the MOA of nicotine and it’s effects to brain and peripheral nervous system

A

1) Nicotine binds on the nicotine acetylcholine receptor.
2) Depolarisation
3) Release several neurotransmitter

Effect to brain :

  • increase dopamine level - rewarding / addictive qualities
  • Increase Ach - enhanced cognition and attention
  • Increase NE - stimulation and arousal

Peripheral Nervous system

  • Increase release of adrenaline from the adrenal glands providing ‘hit’ or ‘ kick ‘ from each puff of a cigarette
  • Increase stimulation of the increase of BP , respiration and heart rate
  • decrease suppresses insulin output smoker are often in Hyperglycemic state
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4
Q

Explain the oral effect of nicotine

A
  • Increased plaque and calculus deposition
  • Ischemia
  • Gingival inflammation
  • Periodontal pockets
  • Gingival recession
  • Alveolar bone loss
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5
Q

Explain the oral effect of nicotine on periodontal disease

A

Local :

  • Cause peripheral vasoconstriction : local ischemia
  • increased pathogenic organism ( P. gingivalis , T. Forsythia)
  • Periodontal disease

Systemic

  • Decreased immunity ( decrease PMN chemotaxis / phagocytosis , Decrease IgG , IgA )
  • increased oxidant stress
  • Activation of inflammatory cascade TNF alpha , IL -6 , IL beta
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6
Q

List the smoking cessation technique

A

5 ‘A’
A) Ask
- Identify patients - Screening ( history taking , oral checkup , questionnaire , carbon monoxide breath test )

B) Advise to quit
- Explain the side effect ( general and oral side effect of taking nicotine

C) Asses willingness to make a quit
- Ask again if the patient is willing to quit . offer some counselling

D) Assist in the quit attempt. If the patient is willing to quit , choose a plan for them ( some may need pharmacology intervention )

E) Arrange
- Schedule follow (in person or by phone ) after one week after the quit date

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7
Q

Explain about the nicotine replacement therapy

A

1) Smaller amount of nicotine used to suppress withdrawal symptoms
2) desensitise the receptor by binding to nicotinic Ach receptor
3) Release of Dopamine will reduce cravings

A) Gum : Chewing gum
B) Patch : irritate oral mucosa
C) Lozenge : irritate oral mucosa
D) Inhaler

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8
Q

(………. ) is a specific nicotine receptor partial agonist help people stop smoking by a combination of maintaining moderate levels of dopamine to counteract withdrawal symptoms

A

(Varenicline) is a specific nicotine receptor partial agonist help people stop smoking by a combination of maintaining moderate levels of dopamine to counteract withdrawal symptoms

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9
Q

(…………) & (………) aids long term smoking cessation and independent of their antidepressant effect.

A

(Bupropion) & (Nortriptyline) aids long term smoking cessation and independent of their antidepressant effect.
Side effect : insomnia , dry mouth and nausea

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10
Q

Explain the MOA of penicillin

A
  • Inhibit bacterial growth by interfering with transpeptidation reaction of bacterial cell wall synthesis
    1) Beta- lactam antibiotics covalently bind to the active site of penicillin- binding proteins( PBP)
    2) This binding inhibits the transpeptidation reaction and halts peptidoglycan synthesis and the cell dies.
    3) Beta-lactam antibiotics kill bacterial cells only when they are actively growing and synthesising cell wall.
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11
Q

List the penicillin classification based on their antibacterial spectrum

A

1) Narrow spectrum penicillins
- Penicillin G
- Penicillin V

2) Antistaphylococcal penicillins
- Methicillin
- Cloxacillin , dicloxacillin
- Nafcillin
- Oxacillin

3) Extended spectrum penicillins
- Aminopenicillins - Ampicillin , Amoxicillin
- Antipseudomonal penicillins
A) Carboxypenicillins - Carbenicillin
B) Ureidopenicillins - Piperacillin

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12
Q

Explain the pharmacokinetics of penicillin G

A

*** - Does not penetrate into the CNS unless meninges are inflamed

  • Mostly unchanged drug appears in urine
  • Generally administered by I.m or iv route
  • 60% plasma bound
    • Primarily excreted by tubular secretion
  • Half life is 30 mins
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13
Q

Give some examples of drugs that are excreted largely unchanged in urine

A

100- 75 % : Furosemide , digoxin

75 - 50 % : Benzylpenicillin

50% - Propantheline

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14
Q

Explain the therapeutic uses of penicillin G

A

In dentistry : Vincent’s angina , necrotising gingivitis , periodontal infection ( either alone or with metronidazole )

: Streptococcal infection - Pharyngitis , Otitis media

: Tetanus & Gas gangrene - Along with anti-toxins

: Meningococcal infections

\: Gonorrhea : along with probenecid 
\:Syphilis 
\: Anthrax 
\: Trench mouth 
\: Rat bite fever
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15
Q

Explain the methods that prolonging duration of action of Penicillin G

A

1) Increasing the dose
2) Combination with probenecid ( probenecid will compete with penicillin for secretion )

3) Depot preparation
~1 day: Procaine
~2 day: Clemizole
~7-28 day: Benzathine

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16
Q

Explain the prophylactic use for penicillin G

A

A) Penicillin G ( benzylpenicillin )

  • Sub- Acute bacterial endocarditis - along with aminoglycoside ( Gentamicin )
  • Surgical infection - along with aminoglycoside

B) Benzathine penicillin ( can prolong to 4 weeks )

  • Rheumatic fever***
  • Gonorrhea & Syphilis

C) Procaine Penicillin
- Treatment & post exposure prophylaxis of inhalation of anthrax

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17
Q

Explain the pharmacokinetics of penicillin V ( phenoxymethypenicillin )

A
  • Oral form of penicillin
  • Acid resistant alternative to penicillin G
  • Antibacterial Spectrum same as Penicillin G ( narrow antibacterial spectrum )
    * * Less effective against Neissera spp
    * * Is indicated only in minor infections
    * * Milder infections of streptococcus ( example : otitis media , sinusitis , pharyngitis )
  • Relatively poor bioavailability
  • The need for dosing four times a day
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18
Q

Explain the therapeutic uses of Extended Spectrum Penicillin ( Aminopenicillins - Amoxicillin & Ampicillin )

A

1) In dentistry : Amoxicillin is used alone or with metronidazole in acute necrotizing ulcerative gingivitis , dentoalveolar abscess , osteomyelitis of mandible
2) Upper respiratory infections

3) Subacute bacterial endocarditis : Aminopenicillins in combinations with gentamicin .
: To prevent bacterial endocarditis in patients with valvular lesion before undergoing dental procedure

4) Urinary tract infections : Fluoroquinolones are the preferred anti microbial agents for urinary tract infections . Ampicillin can be used if organism is sensitive
5) Meningitis : Combination of ampicillin , vancomycin and third generation of cephalosporins

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19
Q

Explain the rationale for combining calvulanic acid with amoxicillin

A

Clavulanic acid

  • Contain beta lactam rings that interacts with lactamases
  • Beta-lactase inhibitors binds to lactamases and inactivated them
Clavulanic acid + Amoxicillin : with the addition of Clavulanic acid , the spectrum of Amoxicillin is increased to include all beta-lactamases producing strains of Amoxicillin covered organisms 
\: Prophylaxis of surgical infections
\: Skin & soft tissue infection 
\: Gonorrhea 
\: UTIs
\: Respiratory tract infection
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20
Q

Explain the adverse effect of penicillin

A

1) Hypersensitivity reaction :
- Characterised by skin rashes , urticaria , dermatitis , bronchospasm or anaphylactic reaction

2) Pain & sterile abscess at the site of IM injection
3) Prolonged use of IV penicillin G may cause thrombophlebitis

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21
Q

Explain the MOA of Cephalosporin

A

1) Inhibit bacterial growth by interfering with the transpeptidation reaction of bacterial cell wall synthesis
2) Beta-lactam antibiotics covalently bind to active site of penicillin-binding protein (PBP)
3) This binding inhibits the transpeptidation reactions and halts peptidoglycan synthesis and the cell dies
4) Similar to penicillin

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22
Q

List the 1 generation Cephalosporin and explain the antibacterial spectrum

A

Parental agents : Cephalothin , Cefazolin
Oral agents : Cephalexin , Cephradine ,Cefadroxil

Antibacterial spectrum :
A) Against gram positive organism ( Except enterococci & MRSA) : highly active
B) Against gram negative organism : less active ( E.coli , K. Pneumonia )
C) Anaerobes : Effective against oral cavity anaerobes ( except B. Fragilis)
D) Not effective against pseudomonas and salmonella

: Act as penicillin G substitutes
: MRSA are resistant
: Efficacy against beta lactamases producing organisms is poor.

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23
Q

List the 2 generation of Cephalosporins & explain the antibacterial spectrum

A

Parental agents : Cefuroxime , Cefoxitin , Cefotetan
Oral agents : Cefaclor , Cefuroxime axetil

Antibacterial spectrum :
A) Moderately active against gram positive organism except enterococci & MRSA

B) Moderately active against gram negative organisms (E.coli , K.pneumonia , **Proteus and H.influenza)

C) Effective against anaerobes including B.fragilis ( cefoxitin & cefotetan )

D)Not effective against pseudomonas & salmonella

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24
Q

List 3rd generation Of Cephalosporins and explain the antibacterial spectrum

A

Parental agents : Cefotaxime , Ceftizoxime , Ceftriaxone , Ceftazidime , Cefoperazone

Oral agents : Cefixime , Cefpodoxime , Cefdinir , Ceftibuten

Antibacterial spectrum :
A) Less actively against gram positive organism ( except enterococci & MRSA )

B) Highly actively against gram negative organism

C) Effectively against anaerobes including B. fragilis ( cefoperazone & ceftizoxine )

D) Effectively against pseudomonas ( cefoperazone and ceftazidime )

E) Effective against Salmonella ( ceftriazone & cefoperazone )

  • Cefotaxime , ceftriaxone , ceftazidimine , ceftrizome have good CNS penetration , thus indicated in Gram negative bacillary meningitis
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25
Q

List the 4th generation of Cephalosporins and explain the antibacterial spectrum

A

Parental agents : Cefepime , Cefpirome

Antibacterial spectrum
A) moderately active against gram positive organism ( except enterococci & MRSA)

B) Highly active against gram negative organism

C) Not effective against anaerobes ( B . Fragilis )

D) Effective against pseudomonas

E) Effective against salmonella

  • More resistant to beta lactamases than 3rd generation
  • mainly for serious Gram negative infections ( enterobacter , citrobacter , serratia)
  • Infections of CNS
  • Hospital acquired resistant infections
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26
Q

List the 5th generation Cephalosporins and explain the antibacterial spectrum

A

Parental agents : Ceftobiprole , Ceftaroline

Antibacterial spectrum
A) Highly active against gram positive organism

B) Highly active against gram negative organism

C) Effective against anaerobes

D) Effective against pseudomonas

E) Effective against Salmonella

: Greater stability against beta lactamases
: Broad gram positive and gram negative activity
: Extended coverage to P. aeruginosa ( ceftobiprole ) , extended-spectrum beta lactamases ( ESBL) producing Enterobacteriaceae & Acinetobacter baumanni

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27
Q

Explain the therapeutic uses of Cephalosporins

A

A) Odontogenic infections in dentistry : Cephalexin & cefadroxil can be used orally

B) Prophylaxis of bacterial endocarditis before dental procedure : Cephalexin / Cefadroxil / Cefazolin

C) Prophylaxis of surgical infections : Cefazolin

D) Sinusitis - Cefadroxil

E) Septicemias by gram negative bacteria - Cefuroxime , Cefotaxime ( used along with aminoglycoside )

F) H.influenza meningitis : Cefuroxime , Cefotaxime

G) Meningitis : Ceftriaxone , Cefotaxime

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28
Q

Explain the adverse effects of Cephalosporins

A

A) Hypersensitivity : Allergic reactions - Skin rashes , urticaria & rarely anaphylaxis .
Cross reactivity to penicillin is seen in patients.

B) Gastrointestinal disturbances : mainly diarrhoea , vomiting and anorexia

C) Pain at the site of I.M injection : cephalothin

D) Nephrotoxicity

E) Disulfiram like reaction : cefotetan & cefoperazone

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29
Q

List the types of tetracyclines

A

1) Doxycycline***
2) Oxytetracycline
3) Chlortetracycline
4) Minocycline
5) Demeclocycline

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30
Q

Explain the MOA of tetracycline

A

1) Actively taken up by susceptible bacteria
2) Bind reversible to 30 S ribosomal subunit
3) Prevent binding of aminoacyl tRNA to mRNA- ribosome complex.
4) Prevent addition of amino acid to the growing peptide chain
5) Inhibit bacterial protein synthesis ( Bacteriostatic )

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31
Q

Explain the uses of tetracycline of dentistry

A
  • broad spectrum antibiotics *
    1) Chronic periodontitis
    2) Doxycycline is useful for subgingival plaque :
    - gets concentrated in gingival fluid
    - inhibits collagen are enzyme and prevents destruction of connective tissue in gums
    3) Acute necrotizing gingivitis or periodontitis ( combination with metronidazole )
    4) Acne vulgaris : Doxycycline and microcycline

: first line of drugs for

  • Rocky Mountain fever , Typhus fever ( caused by Rickettsia )
  • Psittacosis , Granulomas inguinale , pneumonia caused by Chlamydia )

** Second line drug for amoebiasis , malaria , acne , peptic ulcer

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32
Q

Tetracyclines chelates with (…………….) hence it should not be given along because it reduce the absorption of tetracyclines

A

Tetracyclines chelates with ( calcium , magnesium , antacids , iron) hence it should not be given along because it reduce the absorption of tetracyclines

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33
Q

Explain the adverse effects of tetracycline

A

A) Superinfection : resulting in intestinal Candida albicans infection , whereas Staph. Aureus or Clostridium difficile overgrowth can lead to enterocolitis. Chronic use of tetracycline can cause fungal esophagitis. Treatment : Vancomycin

B) Staining of teeth and the retardation of bone growth occur when ( first trimester of pregnancy or if used in children under 10 years old )
- causes hyperplasia of dental enamel with pitting , cusp malformation , yellow or brown pigmentation and increase susceptibility to caries

C) Nephrotoxicity ( except doxycycline and minocycline )

D) Photosensitivity : Demeclocycline & doxycycline

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34
Q

List the example of macrolides

A

Erythromycin , clarithromycin , azithromycin , roxithromycin

35
Q

Describe the MOA of macrolides

A

1) Reversibly binding to the “P” site of 50 S ribosomal subunits of susceptible microorganism
2) Block peptidoglycan transferase , enzyme that catalyse the formation of peptide bond between the nascent peptide and the amino acid attached to the A site.
3) It induce dissociation of peptide transfer RNA ( tRNA) from the ribosome (inhibit translocation )
- Thus , RNA- dependent protein synthesis is suppressed and bacterial growth is inhibited

36
Q

Describe the therapeutic uses of macrolides

A

1) Used in patients who are allergic to the penicillins
- especially for prophylaxis against bacterial endocarditis in susceptible patients and as an alternate to penicillin in the treatment of syphilis

2) Respiratory tract infection caused by S, pyogenes or S . Pneumoniae
3) Listeriosis caused by Listeria monocytogenes
4) Respiratory tract infection due Mycoplasma pneumoniae
5) Pertussis a used by Bordetella pertussis
6) Diphtheria

37
Q

Explain MOA of macrolides in dentistry

A
  • treat orodental infections in patients allergic to beta-lactam antibiotics
  • Treatment as well as prophylaxis of dental infections ( gingivitis , periodontitis , orodental abscess , post-extraction infections )
  • Azithromycin is preferred because of wider spectrum of activity , high intracellular concentration , better tolerability and single daily dosing
38
Q

Explain the adverse effect of erythromycin

A

A) Epigastric distress : Motilin activation leads to contractions of the smooth muscles of the GI tract which manifests as abdominal discomfort and diarrhea

B) Cholestatic jaundice

C) Hypersensitivity

D) QT prolongation and ventricular arrhythmias

E) Erythromycin and clarithromycin are enzyme inhibitor and can increase the concentration of many drugs ( carbamazepine toxicity , Rhabdomyolysis by statins

39
Q

(………) have higher rate of causing pseudomembranous colitis than any other antibiotics

A

( Clindamycin ) have higher rate of causing pseudomembranous colitis than any other antibiotics

40
Q

List aminoglycosides

A

A) Genus micromonospora ( “ micin” )
- Gentamicin ( prototype) , Amikacin , sisomicin

B) Genus Streptomyces ( “ mycin”)
- Streptomycin , tobramycin , spectinomycin

41
Q

Explain the MOA of aminoglycosides

A

1) Aminoglycosides penetrate cell membrane through aqueous pores
2) Reach periplasmic space
3) Taken up by active transport into the cells
4) Bind 30s ribosome

5) Blocks initiation complex of protein synthesis
A) Cause misreading of mRNA - terminate protein synthesis . Addition of incorrect amino acids - abnormal synthesis of abnormal proteins

B) Block movement of ribosome —> interfere in assembly of polysome —>accumulation of non-functional ribosomes
42
Q

Explain the combination use of penicillin and aminoglycosides

A

Penicillin —> inhibit the transpeptidation enzymes - halts peptidoglycan synthesis
( inhibition of cell wall synthesis )

Then it will facilitate the penetration of aminoglycosides into the bacterial cell.

Therapeutic uses : Bacterial endocarditis ( caused by S. aureus , S viridans and enterococci which are susceptoble to both these drugs in high doses )

43
Q

Describe the adverse effects of aminoglycosides

A

A) Ototoxicity

  • aminoglycosides accumulated in endolymph or perilymph of inner ear —> damage to vestibular & cochlear hairs cells
  • due to VIIIth cranial nerve damage

B) Nephrotoxicity

  • it concentrated in renal cortex —> damage to the renal tubules —> rise serum creatinine levels or reduced creatinine clearance , low GFR and albuminuria
  • reversible
  • increases the risk with neomycin m gentamicin , amikacin , tobramycin but decrease with streptomycin
  • Concurrent use with loop diuretics ( furosemide , ethacrynic acid ) / nephrotic anti microbial agents ( vancomycin or amphotericin ) van potentials Nephrotoxicity

3) Neuromuscular blockade ( curaremimetic effect )
- Blockade of ‘NM’ type of receptors causes release of AcH from the motor nerve
- very high doses can cause respiratory paralysis
- Contraindicated in myasthenia gravis that will worsen symptoms
* * -can be reversed by an administration of I. V calcium glauconite or I.M neostigmine

44
Q

State the precaution in using aminoglycosides

A

A) Elderly patients

  • have ototoxic and Nephrotoxic potential
  • these patients have age related renal and hearing problems

B) Pregnancy
- Because of their ototoxic potential and capacity to reach the cochlea of the developing foetus ( highly polar compounds ) , they can damage the cochlea and vestibule of the inner ear of infant —> hearing problems at birth ( foetal ototoxicity )

45
Q

List Fluoroquinolones

A

1st gen : Nalidixic acid ( Narrow spectrum )
2nd gen : Norfloxacin , Ciprofloxacin ( Narrow spectrum )
3rd gen : Gemifloxacin ( broad spectrum )
4th spectrum : Moxifloxacin

46
Q

Describe the MOA of Fluoroquinolones

A

block bacterial DNA synthesis by inhibiting bacterial to topoisomerase II (DNA gyrase) in Gram negative and topoisomerase IV in gram positive organism

I) Gram negative organism
- inhibition of DNA gyrase prevents the relaxation of positively supercooled DNA that is required for normal transcription and replication

II) Gram positive
Inhibition of topoisomerase IV interfere with separation of replicated chromosome DNA into the respective daughter cell during cell division

: leads to DNA damage & ultimately causes bacterial cell lysis

47
Q

Describe the the therapeutic uses of Fluoroquinolones

A

1) Moxifloxacin - odontogenic infection as it has activity gram positive and some of the anaerobes

2) Ciprofloxacin
- active against gram -ve rods . Demonstrates minimal effect on streptococcus species , which are associated with periodontal health. This antibiotic is used to specifically target ( A. actinomycetemcomitans) , a slow growing but harmful bacterium that contributes to gum disease

3) Urinary tract infection
4) Typhoid Ciprofloxacin

48
Q

State the ADR of Fluoroquinolones

A

1) Newer Fluoroquinolones ( gemofloxacin , levofloxacin , Moxifloxacin ) prolong the QTc interval
2) CNS effect ( headache , dizziness )
3) Hypersensitivity
4) Arthralgias and joint swelling
5) GI tract

49
Q

Describe the MOA of Nitroimidazole

A

1) Metronidazole enter microorganism
2) Nitro group accept electron from pyruvate-ferrodoxin oxidoreductase ( bacteria )
3) Highly reactive nitroradical is cytotoxic to cell
4) Damages microbial DNA
5) Death of organism

  • Not effective in aerobic organism
    • In aerobic organism , highly reactive nitro radical x generated
50
Q

Explain the adverse effects of metronidazole

A

Frequent : Metallic taste , anorexia , nausea , vomiting and Epigastric disease

Disulfiram type reaction : if taken with alcohol

Allergic reaction

Prolong administration : peripheral neuropathy

51
Q

Describe the therapeutic uses of nitroimidazoles

A

1) Vincent’s angina ( acute ulcerative gingivitis ) : Metronidazole ( 200-400 mg three times daily for 7 days ) is highly effective in Vincent angina’s as it is secreted in saliva. Often used with penicillin
2) Treatment of alveolar abscess , pericoronitis , periodontitis. Often used in combination with penicillin
3) Amoebiasis : Useful in treatment of both intestinal and extra intestinal amoebiasis
4) Anaerobic brain abscess

52
Q

Explain the interaction of nitroimidazoles with alcohol ( Disulfiram-type reaction )

A

Ethanol is catalysed by alcohol dehydrogenase form acetaldehyde. But then metronidazole will inhibit aldehyde dehydrogenase which convert acetaldehyde to acetate.

  • Accumulation of acetaldehyde will cause flushing , headache , respiratory difficulty , nausea , vomiting , sweating , palpitation , dyspnoea
53
Q

Explain the Nitroimidazole derivatives

A 
Metronidazole 
\:  8 hours half life 
\: Nausea ,Epigastric distress , metallic taste 
\: Thrice daily for dosing frequency 
\: positive for Disulfiram like reaction 
Tinidazole 
\: 12-14 hours half life 
\:20 hours 
\: < Nausea ,Epigastric distress , metallic taste 
\: Once daily 
\: No Disulfiram like reaction 
\: 20 hours half life 
\:
54
Q

Classify the drugs used in acid peptic disease according to their MOA

A

A) Drugs which neutralise gastric acid ( Antacids ):

  • systemic antacids : sodium bicarbonate
  • non-systemic antacids : aluminium hydroxide , magnesium hydroxide

B) Drugs which reduce gastric acid secretion :
I) H2-receptor antagonists : Rantidine , Cimitidine
**II) Proton pump inhibitors (PPI) : Omeprazole , esomeprazole
III) Prostaglandin analogues : Misoprostol

C) Mucosal protective drugs : Sucralfate , bismuth subsalicylate

D) Anti-Helicobacter pylori drugs : Amoxicillin , clarithromycin , tetracycline

55
Q

Explain the MOA of antacids

A

Antacids are weak bases —> react with gastric HCL to form salt and water ( neutralise gastric HCL) —> increases the pH of stomach contents —> decrease the acid load delivered to duodenum —> reduction of intragastric acidity

56
Q

State the adverse effect of antacids

A
  • Diarrhoea ( with magnesium )
  • Constipation ( with calcium carbonate and aluminium )
  • Milk - alkali syndrome - hypercalaemia , renal insufficiency and metabolic alkalosis ( common with sodium bicarbonate and calcium carbonate )
57
Q

Explain the rationale of using antacid combination in acid peptic disease

A
  • Combination of two or more antacids is frequently used
  • Fast ( magnesium hydroxide ) and slow ( aluminium hydroxide ) acting components —> prompt as well as sustained effects
  • Magnesium salts are laxative , while aluminium salts are constipating ; combination may counteract each other’s action and bowel movement may be least affected
58
Q

Explain the MOA of H2 blocker

A

Rantidine —> blocks H2 receptor of gastric parietal cells —> prevents binding of histamine , which is released from enterochromaffin-like by gepastrin or cabal stimulation —> reduces the gastric acid secretion.

  • H2 blockers blocks more than 90% nocturnal acid
  • usually given twice daily basis : maintain at least 50% inhibition up to 10 hours
59
Q

State the therapeutic uses and adverse effects of H2 blockers

A

Therapeutic uses :
A) Gastroesophageal Reflux disease (GERD)
B) Peptic ulcer disease
C) Non ulcer dyspepsia
D) Prevention of bleeding from stress-related gastritis

Adverse effect
: headache , fatigue , myalgias , diarrhea

60
Q

** Explain the MOA of Proton Pump Inhibitors

A

Omeprazole is prodrug and weak bases —> get absorbed by passive diffusion across lipid membranes from intestine —> reach the parietal cell canaliculus —> undergoes a molecular rearrangement to an active “sulfenamide cation “ —> makes a covalent disulphide bond with the SH group of the proton pump ( H+/K+/ATPase) —> inactivates it irreversibly —> shutting off the gastric acid secretion

61
Q

Explain the therapeutic uses and adverse effects of Proton pump inhibitor

A
  • Gastroesophageal Reflux Diseas (GERD)
  • Peptic ulcer disease ( don’t give NSAID)
  • Non-ulcer dyspepsia
  • Gastrinoma (Zollinger-Ellison syndrome )

Adverse effects headache and abdominal pain

62
Q

Explain the MOA of sucralfate and misoprostol

A

Sucralfate :
- In gastric acid environment (pH<4 ) , Sucralfate polymerises by cross linking of molecules and forms a sticky like gel over ulcer crater , which acts as acid resistant physical barrier

Misoprostol :

  • is a prostaglandin (PGE1 ) analogue.
  • inhibits adenylate cyclase in parietal cell and decreases formation of cyclic AML reducing the gastric acid secretion
  • It enhances mucosal blood flow and stimulates the secretion of mucus and bicarbonates —> protection from gastric acidity
63
Q

Explain the drug interaction between antacid / H2 blocker / PPI and Sucralfate

A

Antacid / H2 blocker / PPI increase the intragastric pH —> Sucralfate cannot polymerise to form sticky-like gel over ulcer crater ( Sucralfate requires acidic pH to act ) —> decrease gastric mucosal protective effect of Sucralfate

64
Q

List the drugs for eradication of H.pylori

A
  • Lansoprazole 30mg / Omeprazole 20mg + amoxicillin 1000mg/ metronidazole 500mg + clarithromycin 500mg , all given twice daily for 2 weeks
65
Q

Classify the antiviral drugs based on their MOA

A

1) DNA polymerase inhibitors: Acyclovir , Ganciclovir , Adefovir , Idoxuridine
2) mRNA synthesis inhibitor : Ribavirin
3) Inhibitor of viral penetration & uncoating : Amantadine , Rimantadine
4) Neuraminidase inhibitors : Oseltamivir,Interferons , Palivizumab

66
Q

Explain the MOA of Acyclovir

A
  • prodrug that has to be activated to triphosphate form for its antiviral action.

Acyclovir ———> Acyclovir monophosphate —> Acyclovir diphosphate —> Acyclovir triphosphate
—->
I) Inhibition of viral DNA synthesis —> Inhibits viral DNA polymerase enzyme

II) Incorporate in viral DNA —> Termination of DNA strand growth

67
Q

List the therapeutic uses and adverse effect Acyclovir

A

Therapeutic uses

  • Genital Herpes
  • Herpes labialis
  • Ocular Herpes
  • Mucocutaneous Herpes simplex virus

Adverse effect

  • Stinging and burning sensation after topical application
  • Headache , nausea , malaise after oral administration
  • Rashes , hypotension , phlebitis , nephrotoxicity
68
Q

Explain the anti influenza drugs

A

I) Inhibitors of viral penetrations & uncoating ( M2 protein and hemagglutinin)
- Amantadine & rimantadine

II) mRNA synthesis inhibitors
- ribavirin

III) Neuraminidase inhibitors ** ( drug of choice )
- zanamivir , oseltamivir , peramivir

69
Q

List the antiretroviral drugs based on their MOA

A

A) Inhibit fusion and entry :
I) CCR5 inhibitors : Maraviroc
II) Fusion inhibitor : Enfuvirtide

B) Reverse Transcriptase :
I) NRTI : Zidovudine , Lamivudine , Emtricitabine
II) NNRTI “VIR” : Efavirenz , Nevirapine , Delavirdine

C) Integrase strand transfer
I) INSTI “tegra” : Raltegravir , Dolitegravir

D) Protease inhibitor
: “navir”
: Darunavir , Ritonavir , Lopinavir , Atazanavir , Indinavir

70
Q

Classify the antiemetic drugs

A

H1 antagonist : Promethazine , Diphenhydramine

AntiMuscarinic agents : Hyoscine ( scopolamine ) , dicyclomine

5-HT3 antagonists : Ondansetron, granisetron

Prokinetics - Metoclopramide

D2 blocker : Prochloperazine

Neurokinin-1(NK-1) receptor antagonist : Aprepitant

71
Q

Explain the MOA of scopolamine ( antimuscarinic agents )

A
  • blocks M1 receptor in vestibular apparatus —> blocks conduction of affecting nerve impulses from vestibular apparatus to vomiting centre and prevent vomiting in motion sickness
  • applied as transdermal patch ( mastoid area ) before travel
72
Q

Explain the superinfection with example

A
  • appearance of new infection as a result of antimicrobial therapy
  • normal microbial flora of GIT and oral cavity provides resistance to colonisation and limits the growth of other pathogenic flora.
  • Drug therapy ( broad spectrum antimicrobials / combinations of agents ) leads to alterations of normal microbial flora permitting the overgrowth of opportunistic specially fungi or resistant bacteria.

Example :
- Superinfection with Candida albicans —> Nystatin , clotrimazole treat

  • Clindamycin leads to Clostridium difficile —> metronidazole & vancomycin ( drug of choice )
73
Q

Describe chemoprophylaxis with example

A
  • use of antimicrobial agents in people who exposed to infectious disease to prevent infection by specific microorganism or to eridicate infection immediately before it become manifest
  • broad coverage should be avoided
  • proven efficacy
  • Example :
    Endocarditis —> Amoxicillin
    Surgical wound Infection —> Cefazolin
    Malaria —> Chloroquine
    Meningococcal disease —> Rifampin
74
Q

Explain the factor affecting the choice of antimicrobial agent (AMA)

A

Local host factor :
I) Presence of pus and secretion decrease the efficacy of drugs —> drain the pus
II) Presence of foreign body promotes biofilm formation
III) Anaerobic environment

B) Impaired host defence

C) Diagnosis on infecting organism —> need use broad spectrum drug then less likely to disturb normal microbial flora

D)Sensitivity of organism
- concentration of drug required to inhibit the growth of organism ( minimal inhibitory concentration (MIC))

75
Q

Classify the antifungal agents based on MOA

A

A) Polyene Antibiotics : Bind to fungal cell membrane ergosterol and increase permeability : Nyastin

B) **Azoles : Inhibition of ergosterol synthesis : Clotrimazole

C) Allyl amines : Inhibition of ergosterol + lanosterol synthesis : Terbinafine

D) Echinocandins : Inhibition of fungal cell wall synthesis : Caspofungin

E) Antimetabolite : Inhibiton of nucleic acid synthesis : Flucytosine

F) Inhibition of fungal mitosis

76
Q

Amphotericin B is well known for its ( ……. )
Nyastin is not used parentally because ( ……….)
Topical nystatin is drug of choice for treatment of ( ………..)

A

Amphotericin B is well known for its ( severe nephrotoxicity )
Nyastin is not used parentally because ( it’s high toxicity )
Topical nystatin is drug of choice for treatment of ( Candidal infections of oral cavity —> denture stomatitis )

77
Q

Explain the MOA of Nystatin and AMB

A

1) Binds to ergosterol present in the fungal cell membrane
2) Alters the permeability of the cell membrane by forming pores
3) Leakage of intracellular ions ( K+ , Na+ and Mg2+ )
4) Cell death

78
Q

Explain the MOA of Azole antifungals

A

1) Binds to CYP450 dependent 14-alpha-demethylase enzyme
2) Inhibits demethylation of lanosterol to ergosterol
3) Inhibits ergosterol synthesis
4) Damaged and leaky fungal cell membrane

79
Q

Azoles uses :
I) Ketoconazole —> ( ……)

II) ( ………..) —: Meningeal cryotococcosis

III) Itraconazole : Disseminated or chronic pulmonary histoplasmosis

IV) Voriconazole —> ( ……….)

A

Azoles uses :
I) Ketoconazole —> (inhibits CYP450 enzymes for oral pharyngeal candidiasis )

II) ( Fluconazole) —: Meningeal cryotococcosis ( attains high concentration of CSF

III) Itraconazole : Disseminated or chronic pulmonary histoplasmosis

IV) Voriconazole —> ( invasive aspergillosis)

80
Q

Explain the 5-HT3 antagonists

A
  • Ondansetron blocks 5-HT3 antagonists on vagal afferents in gut , CTS and NTS —> stop vomiting
81
Q

Which drugs is drug of choice of cancer chemotherapy induces , radiation induced and post surgery induced

A
  • 5-HT3 antagonists

— —> Ondansetron

82
Q

Explain the MOA of prokinetic agents

A
  • Metoclopramide , Domperidone
  • CNS :
  • It blocks D2 receptor in CTZ —> antiemetic action
  • At high concentration it blocks 5-HT3 receptor in CTZ

GIT

  • It activates 5-HT4 receptor present on excitatory interneurons —> enhances release of Ach from primary cholinergic ( myenteric motor) neutrons in myenteric plexus.
  • It blocks presynaptic D2 receptor in GIT —> dopamine loses its inhibitory control over Ach release —> more ACh is released from primary cholinergic
  • Increase lower esophageal (LES) tone , facilitates gastric peristalsis and speed up gastric emptying
83
Q

Explain the therapeutic uses of Prokinetics drugs

A

1) Domperidone : levodopa induced vomiting , vomiting in children and lactating women
- won’t block anti Parkinson effect of levodopa
- minimal adverse effect

II) Metoclopramide : post- operative vomiting , GERD , drug induced vomiting.

  • block anti-Parkinson effect of levodopa ( able to cross BBB)
  • induce extrapyramidal symptoms of Parkinson’s disease.
84
Q 
Motion sickness   ———>    ( ………..) 
Morning sickness ———>.  (…………) 
Vertigo ———-> ( ……… ) 
Cancer chemotherapy / radiation induced vomiting  ————> ( ………. ) 
Post operative vomiting ——> ( ………) 
Levodopa induced vomiting  ———>  (……….)
A

Motion sickness ———> ( Scopolamine )
Morning sickness ———>. ( Doxylamine )
Vertigo ———-> ( bethahistine)
Cancer chemotherapy / radiation induced vomiting ————> ( Ondansetron )
Post operative vomiting ——> ( Ondansetron )
Levodopa induced vomiting ———> ( Domperidone )

Pharmacology (4 decks)

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