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Dentistry year 3: Semester 6 > ORAL SURGERY – PHARMACOLOGY & THERAPEUTICS > Flashcards

ORAL SURGERY – PHARMACOLOGY & THERAPEUTICS Flashcards

1
Q

Which receptors pick up pain superficially on our surfaces?

A

Nociceptors

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2
Q

Which nerve fibres detect the pain stimuli?

A

A-delta and C-fibres

a delta faster - myelinated

c - non myelinated

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3
Q

What limits the long-term use of NSAIDS’s?

A

Renal, Gastric and Cardiac complications

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4
Q

Complete the WHO analgesic ladder?

1

2

3

4

A
  1. Pain: simple analgesics (non-opioid)
  2. Pain: simple analgesics + NSAID’s
  3. Pain persisting or increasing: weak opioids
  4. Pain persisting or increasing: + strong opioid morphine +/- adjuvant
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5
Q

Aspirin has 4 therapeutic activity what are they?

A
  1. Anti-pyrexic
  2. Anti-platlet/thrombotic
  3. Anti-inflammatory
  4. Analgesic-mild/moderate
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6
Q

What is the mechanism of action for aspirin?

A

Aspirin works as a COX inhibitor (cox 1,2,3) .

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7
Q

What are the 7 functions of aspirin?

A
  1. Regulate BP
  2. Renal effects
  3. Inflammatory response
  4. Duration and intensity of pain
  5. Fever
  6. Gastric effects
  7. Inhibits platelet aggregation and thrombosis
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8
Q

Aspirin has a greater inhibition of cox 1 or cox 2?

A

Cox 1 (x100)

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9
Q

Which COX induces inflammatory sites?

A

COX-2

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10
Q

Which COX induces stomach, kidney, intestines, platelets, endothelium?

A

COX-1

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11
Q

What are the indications for Aspirin?

A
  1. Acute pain
  2. Dental pain
  3. Rheumatic fever
  4. Rheumatoid arthritis
  5. Other inflammatory disease
  6. Fever
  7. Acute coronary syndrome/ischemic stroke
  8. Anti-thrombotic
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12
Q

How quickly is aspirin absorbed?

A

5-16 mins

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13
Q

What is the half life of aspirin?

A

20-30 mins

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14
Q

Why is aspirin avoided in pregnancy?

A

Because it crosses the placenta

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15
Q

What are the contradictions for aspirin?

A
  1. Gastrointestinal
  2. Respiratory – AERD (What is aspirin-exacerbated respiratory disease)
  3. Renal (3x increase renal failure)
  4. Pregnancy
  5. Gout (increase in uric acid)
  6. Skin reactions
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16
Q

Prostaglandin inhibition comes as a result of taking aspirin through the COX 1 route. One of the side effects of long-term use of aspirin is ulcerogenesis, how does this effect the intestines?

A

The long-term use of aspirin results in the inhibition of prostaglandins.

Prostaglandins are responsible for mucus production. Taking aspirin reduces the amount of mucus that is produced, which in turn increases the acid production in the intestines. It increases the cell permeability for H+. this over time increases the development of ulcers.

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17
Q

What is the standard adult dose for aspirin?

A

Aspirin 300-900mg 4-6 hourly, maximum of 4g daily (preferably with food)

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18
Q

What is the standard adult dose for Ibuprofen?

A

oral 400mg TDS max 2.4g/day

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19
Q

What is the standard adult dose for diclofenac?

A

Oral 50mg TDS max 150mg/day

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20
Q

Aspirin is NOT advised for some groups without medical advice, who are these groups?

A
  1. Children under 16
  2. Asthmatics
  3. Women in the last trimester of pregnancy
  4. Heavy alcohol drinkers
  5. People with bleeding disorders
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21
Q

Why can’t/shouldn’t heavy alcohol drinkers take aspirin?

A

Mixing aspirin and alcohol can result in certain types of gastrointestinal distress. Aspirin can cause nausea and vomiting when mixed with alcohol. The combination can also cause or worsen ulcers, heartburn, or stomach upset.

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22
Q

Acetylsalicylic acid is known as?

A

Aspirin

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23
Q

What is antipyretic?

A

An antipyretic is a substance that reduces fever. Antipyretics cause the hypothalamus to override a prostaglandin-induced increase in temperature. The body then works to lower the temperature, which results in a reduction in fever.

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24
Q

Is aspirin a NSAID?

A

Yes

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25
Q

Is prostaglandin an inflammatory mediator?

A

Yes

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26
Q

Prostaglandins bind to which receptors?

A

Prostanoid receptor.

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27
Q

What can arachidonic acid be converted to in the event of cell damage or illness?

A

Arachidonic acid can be converted to prostaglandin H2, which then converts to prostaglandin E2.

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28
Q

What is the function of prostaglandin E2?

A

Initiate fever, cause pain and inflammation.

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29
Q

Which enzymes are responsible for the conversion of arachidonic acid into prostaglandin?

A

Cyclo-oxygenase 1 and Cyclo-oxygenase 2 (Cox-1, Cox-2).

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30
Q

Why is Cox-1 always active in the body?

A

To maintain homeostasis

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31
Q

Which Cox is active during stress, injury, and trauma?

A

Cox-2 (inflammatory)

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32
Q

Why is aspirin a non-specific NSAID?

A

Because it blocks both Cox-1 and Cox-2

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33
Q

In the event of an injury where you a bleeding, platelets work by forming a platelet plus to stop the bleeding. Arachidonic acid in platelets is converted to prostaglandin H2 through Cox-1. Prostaglandin H2 is then converted to what in PLATELETS?

A

Thromboxane A2 (this causes platelet aggregation).

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34
Q

COXIBS known as specific Cox inhibitor inhibits which Cox?

A

Cox-2

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35
Q

Aspirin, ibuprofen and naproxen are known as non-specific NSAIDS, meaning they influence both Cox1 and Cox2. What physiological effect do they have in the body?

A

They work as an antipyretic, analgesic and anti-inflammatory.

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36
Q

Cox-1 is normally active in the body and maintains homeostasis, particularly in the stomach and the kidneys. Why does inhibiting Cox-1 through the intake of aspirin have an affect on the stomach?

A

Cox-1 converts arachidonic acid in the stomach to prostaglandin H2, which then forms prostaglandin E2 and prostaglandin I2. These prostaglandins help reduce acid production in the stomach. So, by inhibiting Cox-1 in the stomach you are essentially allowing more acid to be produced in the stomach. Resulting in the long-term complications such as.

  1. Dyspepsia
  2. Nausea
  3. Vomiting
  4. Gastric ulceration
  5. Haemorrhage
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37
Q

Cox-1 is normally active in the body and maintains homeostasis, particularly in the kidneys and the stomach. Why does inhibiting Cox-1 through the intake of aspirin influence the kidneys?

A

Cox-1 converts arachidonic acid in the stomach to prostaglandin H2, which then forms prostaglandin E2 and prostaglandin I2. In the kidneys prostaglandin E2 and Prostaglandin I2 help maintain renal blood flow. Taking aspirin can cause nephritis and kidney injury.

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38
Q

What are the 4 ANTS by aspirin?

A
  1. Anticoagulant
  2. Antihypertensives
  3. Antidepressants
  4. Anti-epileptics
  5. NSAIDs
  6. Thrombocytes
  7. Steroids
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39
Q

There are hundreds of different types of antibiotics, but most of them can be classified into 6 groups. What are those groups.

A
  1. Penicillin’s
  2. Cephalosporins
  3. Aminoglycosides
  4. Tetracyclines
  5. Macrolides
  6. Fluoroquinolones
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40
Q

Antibiotics can be divided into two classes based on their mechanism of action that removes the bacteria, what are they?

A
  1. Bactericidal – damaging the bacteria’s cell wall
  2. Bacteriostatic – stalls bacterial cellular activity without directly causing bacterial death.
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41
Q

What type class does penicillin fall in to in reference to its structure?

A

Beta-lactam

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42
Q

Does penicillin work as a bactericidal or bacteriostatic?

A

Bactericidal affecting cell wall synthesis

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43
Q

Which class of bacteria has a thick peptidoglycan wall?

A

Gram positives

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44
Q

Which class of bacteria has an extra phospholipid bilayer outside of the cell wall?

A

Gram negative

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45
Q

Peptidoglycan walls in a bacteria is composed of chains of a amino sugars such as?

A

NAMS and NAGS

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46
Q

The NAMS and NAGS amino sugar chains are crosslinked together by which enzyme?

A

Transpeptidase enzyme.

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47
Q

Which protein does penicillin bind to in the cell membrane?

A

Penicillin binding protein, this activates the penicillin antibiotics.

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48
Q

What does the active penicillin antibiotics do to the peptidoglycan?

A

they bind and inactivate the transpeptidase enzymes, which results in the inactivation of the amino acids chains and the collapse of the cell wall.

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49
Q

Is penicillin a broad or narrow spectrum antibiotic?

A

Narrow spectrum

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50
Q

Penicillin is useless against organisms that produce what?

A

Beta lactamases

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51
Q

How is penicillin g administered?

A

Injection

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52
Q

Phenoxymethylpenicillin is known as what?

A

Penicillin v

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53
Q

What are the indications for penicillin g?

A
  1. Reserved for severe infection (IV)
  2. Oral route compromise (malabsorption syndrome or vomiting)
  3. Recent penicillin or prophylaxis of Rh fever, alternative
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54
Q

Of the antibiotics which have the highest propensity for hypersensitivity reactions?

A

Penicillin and Beta lactams

55
Q

What percentage of the population have a reaction to penicillin?

56
Q

What are the two common type of rash, experienced from an allergic reaction to penicillin V?

A

maculopapular or urticarial.

57
Q

The following reactions are immediate or delayed reactions to penicillin v hypersensitivity?

  1. Nausea/vomiting
  2. Pruritis
  3. Erythema/ urticaria/rash
  4. Wheeze
  5. Laryngeal oedema
  6. Angiodema
  7. Bronchospasm
  8. Hypotension
  9. Cardiovascular collapse
58
Q

The following reactions are immediate or delayed reactions to penicillin v hypersensitivity?

  1. Vesicular
  2. Maculo-papular
  3. Bullous
  4. Urticarial
  5. Scarlatiniform
59
Q

What are the risk factors for developing hypersensitivity to penicillin v?

A
  1. Multiple drug allergies
  2. Atopic disease
  3. Asthma
  4. Allergic rhinitis nasal polyps
60
Q

When an adverse drug reaction occurs, it is important to complete the?

A

Yellow card reporting mechanism.

61
Q

What is the dose/duration/frequency/route for penicillin v?

A
  1. Dose – 500mg
  2. Interval – 6 hourly
  3. Duration – 3-5 days
  4. Route – oral
  5. Loading dose – yes
  6. Food? – fasting
62
Q

What is the dose/duration/frequency/route for penicillin G

A
  1. Dose – 1.2g
  2. Interval – 6 hourly
  3. Duration – 3-5 days
  4. Route – IV
  5. Loading dose – no
63
Q

What are the 3 evasion mechanisms of penicillin v?

A
  1. Reduced drug binding to penicillin binding protein PBP (altering configuration)
  2. Hydrolysis of the drug by beta lactamase enzymes (this is the principal mechanism in most species)
  3. Development of a tolerance by disabling their autolysis mechanism (penicillin becomes bacteriostatic instead of bacteriocidal)
64
Q

Rapidly dividing bacteria are most affected by bacteriostatic or bacteriocidal antibiotic?

A

Bacteriocidal. Something to do with them dividing there cell walls and the antibiotic works by breaking these new forming walls. Meh

65
Q

How to NSAIDs increase the half life of penicillin?

A

They reduce the renal excretion

66
Q

What are the common/uncommon side effects of penicillin?

A
  1. Diarrhoea
  2. Nausea
  3. Skin rash

Uncommon

  1. Vomiting
  2. Urticaria & pruritis
  3. Arthralgia
67
Q

What are the alternatives to penicillin if you have an allergy to it?

A
  1. Metronidazole
  2. Clarithromycin
  3. Erythromycin
  4. Clindamycin
68
Q

what are the indications for prescribing penicillin v?

A

oral dental infections

69
Q

what is penicillin mechanism of action?

A

Cell wall inhibitor

70
Q

what is the half life of penicillin?

71
Q

What is metronidazole’s mechanism of action?

A

Inhibition of DNA replication

72
Q

Which antibiotic penetrates all cells equally?

A

Metronidazole (enzymatic reduction/oxidoreductase)

73
Q

Is metronidazole a bactericidal or bacteriostatic?

A

Bactericidal

74
Q

What is the spectrum of metronidazole spectrum of activity?

A
  1. Obligate anaerobes
  2. Gram-ve pathogens (anaerobes)
  3. Clostridium (c.diff)
  4. Fusobacterium spp
  5. Prevotella
  6. Peptostreptococcus
75
Q

What is the killing mechanism for metronidazole?

A

Concentration dependent

76
Q

What is the oral absorption rate of metronidazole?

A

Nearly 100 percent

77
Q

What is the half life of metronidazole?

78
Q

What is the peak serum time for metronidazole?

A

60-120 mins

79
Q

Which trimester is metronidazole to be avoided?

A

1st trimester

80
Q

How many metabolites of metronidazole is there and where is it metabolised in?

A

5 active metabolites and metabolised in the kidney.

81
Q

Metabolism of metronidazole is severely reduced in what patients?

A

Patients with severe hepatic function.

82
Q

What are the indications for metronidazole?

A
  1. Oro-dental infections
  2. Anaerobes suspected
  3. Acute necrotizing forms of gingivitis
  4. Pericoronitis (with systemic involvement)
  5. Dental abscess
  6. Beta-lctamase producing anaerobes
  7. Alternative to penicillin allergy
83
Q

Which enzyme pathway metabolises metronidazole?

A

Cytochrome P450 pathway

84
Q

The cytochrome P450 pathway increases the production of what for the reduction of the half life of metronidazole?

A

Phenobarbital and phenytoin.

85
Q

What are the main adverse effects of metronidazole?

A
  1. Gastrointestinal
  2. Nausea
  3. Vomiting
  4. Anorexia
  5. Diarrhoea
  6. Epigastric distress
  7. Abdominal cramping
  8. Constipation
86
Q

What are the rare adverse effects of metronidazole?

A
  1. Convulsive seizure
  2. Peripheral neuropathy (paraesthesia extremities)
  3. Also: dizziness, vertigo, incoordination, ataxia, irritability, depression, weakness and insomnia
  4. Prolonged or intensive
87
Q

What are the main oral adverse effects of metronidazole?

A
  1. Unpleasant taste (varied)
  2. Sharp/metallic
  3. Taste disturbances
  4. Furred tongue
  5. Glossitis
  6. Stomatitis
  7. Candida
88
Q

What are the rare reversible adverse effects of metronidazole on blood?

A
  1. Blood dyscrasias (any blood related disease)
  2. Temporary neutropenia
  3. Thrombocytopenia (deficiency of platelets in the blood.)
89
Q

What is the main mechanism method of resistance to metronidazole?

A

Chromosomal/plasmid mediated – reduction in the oxidoreductase

90
Q

What structural similarity does metronidazole have?

A

Tetraethylthiuram disulfide (drug taken for alcoholics) bad reaction.

91
Q

What is the chemical responsible for hangovers?

A

Acetaldehyde this is also experienced in metronidazole.

92
Q

What is the dosage for metronidazole?

A

200mg – 400mg

93
Q

What is the interval for metronidazole?

A

8-12 hourly

94
Q

What is the duration for metronidazole?

95
Q

What is the route for metronidazole?

96
Q

Do you need a loading dose for metronidazole?

97
Q

What are the two interactions you want to avoid with metronidazole?

A

Alcohol and warfarin

98
Q

Clindamycin derives from which antibiotic?

A

Lincomycin

99
Q

What is the spectrum of activity for clindamycin?

A
  1. G +ve / G-ve bacteria
  2. Penicillinase staph.
  3. Bacterioides
  4. Prevotella
  5. Porphyromonas, veilonella
  6. Peptostrep, actinomyces
  7. Eubacteria and clostridium
100
Q

What is the mechanism of action for clindamycin?

A

Inhibits protein synthesis by binding on the 50sribosomal subunit

101
Q

Is clindamycin bacteriostatic or bactericidal?

A

Its mechanism of action is dependant on its concentrations, it is bactericidal at higher concentrations, bacteriostatic at lower.

102
Q

What is the oral absorption of clindamycin?

103
Q

What is the half life of clindamycin?

104
Q

Where is clindamycin metabolised?

105
Q

Is clindamycin affected by food?

106
Q

How quickly can clindamycin reach peak serum time?

107
Q

Can clindamycin penetrate to the bone?

108
Q

Can clindamycin penetrate the CSF?

109
Q

What are the unwanted affects of clindamycin?

A
  1. Nausea/vomiting
  2. Abdominal pain
  3. Oesophagitis
  4. Glossitis
  5. Stomatitis
  6. Allergy
  7. Myelosuppression (reversible)
  8. Metallic taste
  9. Maculopapular rash
110
Q

What drugs significantly slow down absorption for clindamycin?

A

Anti-diarrhoeal drugs

111
Q

Clindamycin is regarded as a second line antibiotic drug, what are the indications for it?

A
  1. Oro-facial infections
  2. Penicillin allergy
  3. Refractory to penicillin(s)/metronidazole.
  4. Beta lactam resistance
112
Q

What are the contraindications for clindamycin?

A
  1. Allergy
  2. Clindamycin should not be used routinely
  3. No more effective than penicillin
  4. Cross resistance with erythromycin-resistant bacteria
113
Q

What is the dose for clindamycin?

114
Q

What is the interval for clindamycin?

115
Q

How long would you expect to take clindamycin for?

116
Q

What is the route for clindamycin?

117
Q

Do you need a loading dose for clindamycin?

118
Q

If you have diarrhoea whilst on clindamycin what should you do?

A

Cease immediately.

119
Q

What is acetaminophen?

A

Paracetamol

120
Q

The mode of action for paracetamol is quite vague, however there is strong evidence that paracetamol affects which COX pathway

121
Q

According to the WHO analgesic ladder, paracetamol is considered a what?

A

A first line analgesic, used for acute and chronic, mild to moderate pain. Also, an antipyretic.

122
Q

What affects does paracetamol have on platelet aggregation?

A

No effects

123
Q

What are positive negative effects that paracetamol has?

A
  1. Fewer adverse drug reaction
  2. Little effect respiratory
  3. Little effect cardiovascular
  4. Little or no gastric irritation
  5. No relevant impact on uric acid excretion
124
Q

What are the indications for paracetamol?

A
  1. First line for dental pain
  2. Non inflammatory conditions - where NSAIDs are contraindicated (asthmatics, gastric ulceration)
125
Q

What are the 3 methos of taking paracetamol?

A
  1. Tablet
  2. Suppository
  3. Iv
126
Q

What is the half life of paracetamol?

127
Q

What is the peak plasma for paracetamol?

128
Q

Where is the primary transformation of paracetamol?

129
Q

What are the contraindications/side effects for paracetamol?

A
  1. Blood dyscrasias (thrombocyte-, neuro, -leuco-penia)
  2. Hepatotoxicity
  3. Liver disease, alcohol, malnutrition, dehydration
130
Q

What is the dosage for paracetamol?

A

Standard adult dose: 10-15mg/Kg every 4-6 hours to a daily maximum of 4 grams (500mg = 1 tablet)

131
Q

What are the side effects of paracetamol – systematic review?

A
  1. Increased mortality
  2. Cardiovascular adverse events
  3. Gastrointestinal adverse effects
  4. Renal impairment
132
Q

What are the special considerations for paracetamol?

A
  1. Overdose and toxicity
  2. Toxic dose (20-30 tablets)
  3. Acute liver damage – 10-15g (8g)
  4. 25g fatal
  5. Maximal liver damage 3-4 days post ingestion
  6. Urgent hospital transfer
  7. Treatment for overdose – activated charcoal, acetylcysteine IV – 10-32 hours
133
Q

What is the function of inactivating glutathione?

A

It binds to the toxic metabolite NAPQI, of paracetamol, and inactivates it making it nontoxic.

Dentistry year 3: Semester 6 (16 decks)

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