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BDS 3 Sem 2 > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What is a good book to have for reference for pahrmacology?

A

Australian Medicines handbook

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2
Q

Why do we need to know about drugs?

A
  1. We prescribe them
  2. For the one we dont prescribe - patient may want to have info about them or drugs they are taking may affect your approach to their dental treatment
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3
Q

What is a pharmacopoeia?

A

It is a reference book containing direction for identification and purity standard of medicines

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4
Q

What is pharmacology?

A

It is a scientific discipline dealing with the interaction between living systems & drugs

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5
Q

What are the four right for drug prescribing?

A
  1. Right drug
  2. Right dose
  3. Right frequency
  4. Right duration and deprescribing
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6
Q

What does drug therapy hope to achieve?

A
  1. Prevent diseases
  2. Cure a disease
  3. Decrease mortality
  4. Decrease sickness
  5. Decrease symptoms of illness
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7
Q

What is a xenobiotic?

A

It is a substance that is not synthesized in the body but must be introduced into the body from outside.

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8
Q

How would you try to explain the relationships between substrates and their target molecules/active sites?

A

Lock & key relationship

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9
Q

What is pharmacodynamics?

A

It is the effect of drug on bod. Like paracetamol relieves pain and is antipyretic (lower body temp)

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10
Q

What is pharamacokinetics?

A

Effects of body on the drug. Like absorption and distribution and elimination. It looks at the how it is done and the rate at which it is done

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11
Q

What is the important of pharmacodynamics and pharmacokinetics?

A

It is the integration between those two key concepts that results in creation of appropriate drugs.

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12
Q

How can we classify drugs?

A
  1. Chemical makeup
  2. Function
  3. Target molecules
  4. International Nonproprietary names - i.e. the endings of similar drugs of function need to be simiar i.e. mevipicaine and lignocaine
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13
Q

What do we need to remember about drug nomenclature?

A

Always use the GENERIC NAME. Because that way when prescription is getting fulfilled - it is not dependent on the supply of a certain brand name.

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14
Q

What is a drug/medicine?

A

A drug is a substance that when introduced into the body alters the body’s function

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15
Q

Whatis the interaction between cliclosporin and Saint John’s wort?

A

Ciclosporin is an immunosupresant that is able to aid in organ transplants.

St John’s Wort is a over the counter herb that cna aid in depression.

St John’s Wort is able to trigger an increase production of an enzyme that metabolises ciclosporin.

Thus decreasing long term plasma concentration leading to transplant organ rejetion by the body.

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16
Q

What determines the osing regiment?

A

Pharmacokinetics control the dosage regiment.

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17
Q

What is the theraoetuic concentration range?

A

It is when the optimal concentration is reached, meaning the concentration of a medication is not too low to be ineffective and not too high to cause toxicity.

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18
Q

What is a therapeutic index?

A

The ratio of the dose that produces toxicity to the dose that produces a clinically desired or effective response.

Essentially drugs with a large therapeutic index are more safe and harder to get an overdose on.

Example of low therapeutic index - morphine 70:1 index

Example of high therapeutic index - remifantanil 33000:1

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19
Q

What is toxicology?

A

It is the discipline dealing with undesirable effects of xenobiotics.

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20
Q

What are some of the targets for drugs?

A
  1. Non-specific targets
  2. Proteins - the most common
  3. RNA/DNA
  4. Lipid cell membranes
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21
Q

What are some of the receptors that are targeted by medications?

A
  1. Ligand-gated ion channels (ionotropic receptors
  2. G-protein-coupled receptors (metabotropic)
  3. Hinase-linked receptors
  4. Nuclear receptors
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22
Q

How long does it take for ligand-gates ion channels to respond?

A

Miliseconds

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23
Q

What are some of the examples of ligand-gated ions channels? What are some of the drugs that bind to them?

A

Nicotinic receptors and ACh receptors.

Benzodiasapine like xanax

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24
Q

How long does it take for G-protein-coupled receptors (metabotropic) to respond?

A

Seconds

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25
Q

What are some of the examples of G-protein-coupied receptors (metabotropic)? What are some of the drugs that bind to them?

A

Muscarinic receptors, ACh receptors

Opiod agonists like morphine

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26
Q

How long does it take for Kinase-linked receptors to respond?

A

Hours

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27
Q

What are some of the examples of Kinase-linked receptors? What are some of the drugs that bind to them?

A

Cytokine receptors

Methotrexate

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28
Q

How long does it take for Nuclear receptors to respond?

A

Hours

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29
Q

What are some of the examples of Nuclear receptors? What are some of the drugs that bind to them?

A

Oestrogen receptors

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30
Q

Where are the targeted proteins usually found?

A
  1. Cell surface - membrane receptors, ion channels and carrier proteins
  2. Intracellular - enzymes, RNA/DNA and Proteins
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31
Q

What is affinity?

A

It is essentially the ability of the drug to be efficient in it’s function and it is highly dependent on the structure of said drug

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32
Q

What is a bad outcome of a drug having an affinity effect on 2 different receptors?

A

It increase the potential side effects that may occur from that drug

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33
Q

What kind of drugs do we use for reflux & indigestion?

A

Proton pump inhibitors

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34
Q

What doe NSAIDs target?

A

They inhibit the enzyme by the name of cyclooxygenase I and II

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35
Q

What are the two types of inhibition?

A
  1. Competitive inhibitor
  2. Irreversible inhibitor
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36
Q

What are the potential clinical consequences of this difference in inhibition for a patient requiring 3rd molar extraction?

A

Due to affect on platelets by aspirin, by irreversible inhibition of platelets, there needs to be extra caution in planing and use of extra tools such as mucoperiosteal flap use due to increase risk of inability to achieve adequate haemostasis.

Please ensure use of local haemostatic measures and remember that temporary interruption is not required.

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37
Q

Where in the body is ligand dated ion channel located?

A

Skeletal muscle. It’s blockage can result in inability to breath. This receptor is very very very quick.

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38
Q

What is the significance of the G Protein-Coupled receptors or the 2nd messengers receptors?

A

They have a very quick onset - basically minutes. And many drugs such as the opiods or anihistamines bind to them.

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39
Q

What is the significance of nuclear receptors?

A

It takes hours to reach them and the main objective of binding to them is to alter gene transcription stimulation.

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40
Q

What are the two types of asthma therapy medication?

A
  1. Relievers - slabutamol - quick effect by binding to beta-2 receptors
  2. Preventers - beclomenthasone - slow effect due to being a nuclear receptor
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41
Q

What are some of the side effects of salbutamol?

A

Due to an effect on beta-1 receptors aswell - they may cause heart palpatations.

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42
Q

What are the two functional types of meidctions?

A
  1. Agonists - drugs that elicit response
  2. Antagonist - drugs that bind but do not elicit response - essentially just occupy the space on the receptor by being competetive
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43
Q

What is potency?

A

It is the comparison between efficacy of different drugs and their dossages.

E.g. Drug A can reach the target of 30 units within 2mg and drug B can reach the target of 30 units within 10 mg. Therefore, drug A is 5 time more potent than drug B

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44
Q

How do you determine a full agonist on a logarithmic graph?

A

If the effect scale reaches 100% or max - it is a full agonist, if not it is a partial agonist.

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45
Q

What is the therapeutic index?

A

Difference between the minimal dose to achieve the 50% effect and toxicity of a substance.

It is a measure of drug safety!

An example of a drug with a wide therapeutic index - paracetamol only 500mg may need for in effect but the toxicity is around 15 grams (30 tablets)

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46
Q

Why are pharamacokinetics important?

A
  1. Adverse harmful effect to a medicine in people oftent due to altered pharmacokinetics - e.g. kidney disease
  2. Patient does not get better or gets worse on a medicine often due to altered pharamacokinetics 0 e.g due to genetic factor or taking other medicines
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47
Q

What is the important aspects of pharmacokinetics in prescription?

A

Same does does not suit all patient. There is a difference in doses due to age, weight, pregnancy, environment, diet and use of other medications.

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48
Q

Your prescribe the antibiotic metronidazole 200 mg twice a day for a spreading odontogenic infection and it has no effect. WHat could be a pharmacokinetic reason?

A
  1. Not dosing properly
  2. The drug is broken down too fast and it can not reach appropriate blood levels
  3. The drug is not being absorbed properly due to nausea and vomiting
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49
Q

Your prescribe the antibiotic metronidazole 200 mg twice a day for a spreading odontogenic infection and it has no effect. What could be a pharamacodynamic reason?

A
  1. Metronidozale can not affect the bacteria that is responsible for the odontogenic infection
  2. Bacterial resistance
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50
Q

How do we decide how to give medicine?

A
  1. Speed of response
  2. Chronic dosing of the drug
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51
Q

What are some of the ways we can introduce the drug to the organism?

A
  1. Enteral - through the intestine - oral, sublingual and rectal
  2. Parentral - everything else due to them being sensative to gastric juices or we need a quick effect - injections basically - intravenous, intramuscular or subcutaneous
  3. Other routes - inhalation, tranasal, topical, transdermal patches and other other like eyes, nose, ears drops
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52
Q

Why cant you give warfarin and miconazole together?

A

Miconazole can potentiate the actions of warfarin thus increasing International Normal Rate.

Thus make a patient more likely to bleed.

Miconazole is inhibiting hepatic microsomal cytochrome P-450 enzymes. increasing concentration of warfarin.

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53
Q

What are common routes of drug absorption?

A
  1. Gastrointestinal absorption - most common - from the lumen of the stomach through the enterocytes and into portal vein for systemic circulation - could be done through passive diffusion or though different transporters

2.

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54
Q

What are some of the factors that effect the gastrointestinal absorption?

A
  1. Blood flow
  2. Surface area of the intestines - remember stomach does not matter intestine is due to increased surface area of the intestine - microvilli and villi.
  3. Gastric emptying - e.g. codeine slows down the emptying of the stomach thus may increase the time that the drug may take to the site of absorption - water pormmotes stomach emptying 200ML OF WATER IS GOOD
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55
Q

Why do some medicine should be taken with food?

A
  1. To reduce side effects
  2. To reduce side-effects of stomach upset
  3. To treat heartburn/indigestion
  4. To ensure the medicine is absorbed into the blood stream: like very water soluble drugs
  5. To help process the meal - like for diabetes medication
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56
Q

Why do some drugs have bioavailability of less than 100%

A
  1. Insufficient time for absorption
  2. Decomposition in gut lumen
  3. Liver and first pass effect - portal vein passes through the liver thus the drug might be over processed there and it does not really reach systemic circulation
57
Q

What is drug distribution?

A

It is a reversible transfer of drug to and from the blood circulation.

There are different rates and extents of distribution.

It depends on: rate of blood flow to tissue/organ, ability to cross the cell membrane wall, binding to plasma and tissue proteins.

58
Q

What are the steps of drug distribution?

A
  1. Initially drug enters the blood stream and makes it to the capillaries around the organ tissue in the body
  2. Capillary endothelium is very “leaky” which means certain molecules can pass through. Exception: blood-brain barrier which is actually less permeable
  3. Drugs need to be lipid soluble to defuse into the target cell if not they can interact with receptors on the cell membrane
59
Q

What is drug elimination?

A

It is irreversible loss of drug from blood through use of metabolism (drug is converted to another chemical - done by liver) or excretion (loss of the chemically unchanged drug - done by kidneys)

60
Q

What kind of drugs are metabolised by the liver?

A

Lipid soluble drugs like local anaesthetics

61
Q

What kind of drugs are processed by the kidneys?

A

Water soluable drugs like anti-biotics

62
Q

What is drug clearance?

A

It is the measure of rate of elimination. Drugs could be totally cleared or partially cleared

63
Q

What are the steps to drug elimination in the kidneys?

A
  1. Afferent arteriole caries the blood to the glomerulus - drugs are than filtered as plasma water
  2. The plasma enters into the proximal tubules in which the drug is secreted via active pumps that pup the drug into the kidney lumen
  3. Lumen moves through the proximal tubule into the dital tubules and collecting duct where some rebasorption could occur but most emportantly water is removed and lipid soluble drugs will be diffused back into the blood stream - thus they need to metabolised by the liver
64
Q

How does the liver metabolise drugs?

A
  1. Enzymatic conversion of drug to another chemical form in order to make it more water soluble so kineys can excreate them
  2. Remember - liver processes most of the medication
65
Q

What are some of consequences of metabolism?

A

Usually, the metabolites have no pharmacological activity but:

  1. Some may act as parent drgus
  2. Some may be antagonistic - causing convulsions or nauses/vomiting

Concept - active metabolites is clinically important for elderly and patients with renal disease - because some patient may not be able to excrete the metabolite at the same rate thus the metabolite may have a toxic effect.

66
Q

What are 2 phases of metabolism?

A

Phase I: Oxidation - depends on Cytochrome P450 largley - binds the drugs and important in binding of steroid - essentially all drugs endogenous and exogenous - VERY IMPORTANT

Phase 2: Conjugation - polar chemical group is “added on or transferred” - Enzyme are called transferases

67
Q

What is the metabolic pathway of paracetamol and hepatotoxicity?

A
  1. Paracetamol enters the liver where 55% of it is turned into water soluble Paracetamol Glucuronide, 40% of it is turned into water soluble Paracetamol Sulphate and 5% is turned into Reactive Electrophilic metabolite
  2. This reactive electophilic metabolite than can turne into paracetamol glutathione and be excreted in the kidneys or it may bind with metabolite-proteins and cause hepatic cell death

Now in overdose:

  1. There is not enough sulphate to turn paracetamol into paracetamol sulphate so more paracetamol is trned into a reactive electrophilic metabolite thus increasing binding to metabolit-protein and cause more heaptic cell death
  2. The way to help a patient in this situation - measure blood and introduce a N-acetylcysteine (NAC) which will hel with conversion thus stop metabiolite-protein bindings
68
Q

What is a therapeutic dose of paracetamol

A

4 grams per day

69
Q

What paracetamol dose cause liver toxicity?

A

10-15 gram for young adults

8-12 grams for an older person

70
Q

Why might some people get an overdose with the “therapeutic dose” of paracetamol?

A

They taking paracetamol from different sources like regular paracetamol + Cough & Cold tablets + nurimol

71
Q

What are the four concepts we need to understand in pharmakokinectics?

A
  1. Clearance
  2. Half life
  3. Volume of distribution
  4. Bioavailability
72
Q

What does the shape of the curve of plasma concentration over time depend on?

A
  1. Dose
  2. Route of administration
  3. Single dose versus chronic dose
  4. Patients’ elimination and distribution rates
73
Q

Why does the concentration change with time?

A

Single does - the drug is being absorbed, distributed to tissues & organs

74
Q

What is bioavailability?

A

It is how much of the drug enters the blood stream and how much can actually be used.

Usually calculated by finding the difference of plasma concentration betwene oral ingestion and with use of IV

Good drugs - bioavailabiltiy 100%

Symbol on graphs - F

75
Q

What is the stead-state condition?

A

When we can achieve the balance between the rate of elimination and plasma concentration

76
Q

How do you calculate the clearance?

A

Rate of elimination divided by plasma concentration over time.

Clearance is considered to be the most important parameter in pharmakokinetics

77
Q

What is total clearance?

A

It is the addition of the renal clearance as well as hepatic clearance.

This is what regulators want to know when assessing medication.

78
Q

What does clearance rate determines?

A

It determines the dose rate.

It is important to know that clearance is an independent pharamakokinetic parameter.

If clearance is higher than concentration in the plasma should be higher.

If clearance is lower than concentration in plasma is higher.

79
Q

How do we know that we are at the steady state?

A

Half-life - time for blood concentration/amount of drug in body in half.

Half-life is very useful because it tells us when we are in the steady state. E.g. if half-life 97% is achieved in 5 doses - means it takes 5 half-lifes to get to the steady state.

It will also take 5 half-lifes to clear the drug.

80
Q

What is volume distribution?

A

Proportionality factor relating the concetration of drug in the blood with the amount of drug in the body.

It is useful because it helps us to determine a loading dose.

81
Q

What happens to drug clearance when kidney function declines?

A

Drug clearance declines in direct proportion to renal function decline.

Thus dosing regimen might need to decreased in order to reduce the probability of toxicity.

82
Q

What happens to drug clearance when hepatic disease occurs?

A

It results in lower clearance of drugs.

Dosing needs to decrease for some medication such as narrow therapeutic index. Example: paracetamol.

83
Q

What should you consider for prescription to a pregnant patient?

A

Avoid all drugs: unless benefit outweighs risk. Especially in 1st trimester.

Also remember that your GI mobility when pregnant is decreased/

84
Q

What is important to consider for prescription to paediatric patients?

A

They have increased renal & hepatic clearance thus the dosage could be higher per KG.

85
Q

What is important to consider geriatric patients?

A

They have higher pharmacokinetics due to declined liver and kidney function, gut function and polypharmacy.

Start low & go slow but don’t stay at a low dose if chronic dosing.

86
Q

What are some of the effects of cigarette smoke?

A

Increases the caffeine clearance

87
Q

What are some of the important aspects of Drug-Drug interactions?

A

Pharamacokinetic:
Interacting drug alters the plasma concentrations of index drug.

Usually also alters the hepatic clearance, could up or down shift it.

Commonly, renal clearance is down regulated.

Pharamacodynamically - some drugs may make the reaction to other drugs more potent

88
Q

What is drug enzyme induction?

A

When a drug stimulates gene transcritption that makes of a certain enzyme in general resulting in need in higher dose.

E.g. St Johns Wort

89
Q

A patient is taking some wafarin 3 mg daily and felodipine. They have candidiasis infection. You start them on fluconaole 100mg daily. Their candidiasis infection clears up but they starting to experience major gingival bleeding and bruising. Why?

A
  1. Fluconazole is an aenzyme inhibitor which prevents warfarin to be metabolised
  2. Thus decreasing the clearance of warfarin and increasing plasma concentration
  3. Increased plasma concentration results in toxicity which leads to increase in bleeding and bruising
90
Q

What is a triple wammy?

A

It is a pharmacodynamic problem which occurs with use of ACE inhibitor, diuretic and NSAID and can result in Acute Kidney Injury (AKI)

Process:

  1. ACE inhibitors preserve renal function and also cause constriction of efferent renal arteriole
  2. NSAID are able to increase the vasoconstriction of the afferent arteriole by inhibiting the production of prostoglandins - a potent afferent arteriole dilator
  3. Dirutetic drive the increase exertion of water through the renal system thus increasing the amount of blood that is carried to the glomerulus through the afferent arteriole
  4. All three factors compound and increase the pressure within the nephron in their own way and increase the risk of acute kidney injury due to increase pressure tearing the nephron
  5. Solution - avoid NSAIDs
91
Q

What other things can interact with the medication?

A
  1. Food - grapefruit juice and statin drugs - milk and antibiotics - green tea and fexofenadine (hayfever)
  2. Health products - St. John’s Wort and enzyme liver inducer - think about rejecting organs in transplants
92
Q

How to avoid drug interactions?

A
  1. Thorough history
  2. Check the list with the datatbases
  3. Remember of the over-the-counter and herbals
93
Q

What is an adverse drug reaction?

A

Any response to a drug which is unintended, harmful and which occurs at a dose usually given to humans for management of disease.

This does not include: Overdoes or Error in dosing

94
Q

What is an adverse drug effect?

A

An injury resulting from medical intervention related to a drug - includes wrong dose or device malfunction

95
Q

What is a drug side effect?

A

It is minor (sometime not so), insignificant and generally acceptable events that may occur if the drug is taken.

96
Q

How do you identify adverse drug reaction?

A
  1. Need to establish a link between adverse effect & drug
  2. Many ADRs detected years after marketing
97
Q

What are major types of ADRs?

A

Type A - Exaggerated response to medication even tho the dose is normal - it is usually predictable with dose decrease should fix it

Type B - BIZARRE effect - not predictable - high risk of death - need to stop the drug - ALWAYS ASK THE PATIENT IF THEY ARE ALLERGIC BEFORE ANY PRESCRIPTION ESPECIALLY WITH ANTI-BIOTICS

Type C - long term affects - tolerance like for caffeine

Type D - delayed effect - thalidomide with babies

Type other - unavoidable toxicity - cancer chemotherapy

98
Q

What drug should you not give to pregnant women?

A

Category C drug like ibuprofen.

Aloso Category D drugs but they are pretty rare!

99
Q

Who is more at risk of ADRs?

A
  1. Elderly
  2. Infats and children
  3. Women
  4. People with history of multiple allergies
  5. People with other diseases
  6. Certain ethnicity and pharmacogenetics
100
Q

What are some of the oral reaction to drgus?

A
  1. Local reaction such as chemical irritation or suppression of oral flora
  2. Systemic reaction like from bone marrow depressor or immune suppressors
  3. Stevens-Johnson syndrome - lots of ulcers - could be caused by ibuprofen
  4. Lichen planus - can be caused by allopurinol
  5. Gingival bleeding - SSRIs
  6. Xerostomia - polypharmacy
101
Q

What is a good principal of drug dosing for older patients?

A

SRTART LOW & GO SLOW

BUT DON’T STAY LOW if chronic dosing.

102
Q

What is MRONJ?

A

Medication-Related Osteonercrosis of the Jaw. Area of exposed bone in the jaw persisting for more than 8 weeks in a patient currently or previously treated with an antiresorptive or atiangiogenic drug who has not received radiation therapy to the craniofacial region.

103
Q

How do we ADRs in Australia?

A

Volunteer system, please go to TGA

104
Q

What is the cost of developing a medication?

A

US$2.5 billion dollars

105
Q

How are drugs discovered?

A
  1. Purification from natural sources through tradition medicine and chance observation - aspirin
  2. Screening of biological sources such as soil, microbes or marine organisms
  3. Chemical modification of active and known drugs
  4. Rational Drug Design depending on the disease - custom designs by manipulation or proteins etc - SSRIs
  5. Pure chance (Srendipity) - Aspartame
  6. New Indications from clinical observation
  7. Recombinant proteins - using bacteria to make endogenous proteins
106
Q

What are the steps of pre-clinical drug development?

A
  1. Laboratory tests in vitro - through use of high throughput screening
  2. Whole animal testing
  3. Phase I trials - is it immediatley safe?
  4. Phase II trials - trials in the target illness - can it work?
  5. Phase III trials - large scale clinical trials - is it effective?
107
Q

What is an example of potentiation effect of medications?

A

Warfarin and iboprofen/aspirin - increase bleeding significantly

108
Q

What are the steps of approval of a drug in Australia?

A
  1. Aims - to protect public from drugs that are: unsafe, ineffective and poor quality
  2. Process - TGA is presented data
  3. Evaluation of quality, safety and efficacy
  4. Registration
  5. Movement to the market
109
Q

What are the two types of products that are listed on the website of TGA known as the ARTG?

A

AUST L - listed produucts with little side effects - like sports supplements

AUST R - registered products with side effects - think all other proper medicines

110
Q

If a mouthrinse claims that is is for treatment of “gingivitis” but you can buy it at Woolworths, what type of listing is it and what type of schedule is it?

A

AUST R listing

Shedule 1 or unscheduled

111
Q

What are the schedules of drugs?

A
  1. Schedule 1 - unscheduled drugs - paracetamol
  2. Schedule 2 - Pharmacies only - Telfast
  3. Schedule 3 - Pharmacist Only medicines - Morning-after pill
  4. Schedule 4 - Prescription only - Antibiotics
  5. Skip all other schedules
  6. Schedule 8 - Drugs of addiction dependence - Morphine
112
Q

Define the following:

Infection

Colonisation

Bacteraemia

Septicaemia

Sepsis

A

Infection - invasion & multiplication of pathogenic microorganism in body tissue

Colonisation - localised presence of microorganisms

Bacteraemia - presence of viable bacteria in circulation

Septicaemia - systemic infection caused by microorganisms multiplying in circulation

Sepsis - multiple organ involvement from organisms

113
Q

What are antibiotics?

A

They are drugs that stop the spread and multiplication of bacteria in the body that are causing harm.

They come under general term of anti-infectives and antimicrobials.

114
Q

What some of the other anti-infective and anti-microbials?

A
  1. Antibacterials - bacteria
  2. Antivirals - viruses
  3. Antifungals - fungal infections
  4. Antimycobacterials - for TB
  5. Antiprotozals - malaria medication
  6. Anthelminitics - againts worms
115
Q

What is important to understand about antibiotics?

A

Antibiotics do not cure infections - our immune system does. Antibiotics just needed for their bactericidal or bacteriostatic functions.

Antibiotics give immune system more time to mobilise more effectivley

116
Q

How do antibiotics work?

A
  1. Inhibit metabolism of a bacteria (folic acid blockage) - trimethoprim - bacteriostatic effect
  2. Inhibit cell wall synthesis - penicillins - bacteriocidal effect
  3. Disrupt cell membrane - both bacteriostatic abd bacteriocidal
  4. Inhibit protein synthesis - metronidazole inhibits DNA synthesis
117
Q

How do antiobitcs have a bacteriostatic effect?

A

Sulfanilamide antibiotics have a bacteriostatic effect by targeting synthesis of folica acid - an important component of bacterial RNA and DNA

Sulfanilamide can completitivley inhibit enzymes that are used in production of folic acids, thus slotwing the synthesis thus slowing growth of bacteria due to reduced production of plasmids (circular DNA in bacteria).

118
Q

How do antiobtics have a bacteriocidal effect?

A

By inhibiting cell wall synthesis through rapid depolarization.

Beta-lactam - like amoxycillin - able to bind to bacterial cell walls causing repid depolirasation resulting in loss of membrane potential leading to inhibition of protein synthesis and destruction of DNA.

119
Q

What are the different efficacy of antibiotics?

A
  1. Narrow spectrum - a few species - benzylpenicillin
  2. Moderate spectrum - several species - amoxicillin
  3. Broad spctrum - many species - tetracyclines
120
Q

Why in general, narrow spectrum is better than broad spectrum anti-biotics?

A

Due to higher instance of unwanted harmful effect?

  1. Superinfections - gut flora inhibition and other opportunistic bacteria take over
  2. Antibiotic-associated colitis - inflammation of colon wall
  3. Elder patient are even more sensitives
  4. Increased potential of hypersensitivity reactions
  5. Increase in the number of bacteria that may become resitant to antibiotics
121
Q

What are the 2 concepts that determine anti-biotic efficacy?

A
  1. Time-dependent killing - time in the blood where drug is above MIC - MIC can change with resistence - penicillins
  2. Concentration-dependent killing - the higher the peak concentration the more it will kill - prologned duration of killing - aminoglycosides
122
Q

What are some of the resistance pathway for the bacteria?

A
  1. Bacteria produce enzymes that inactivate the drug
  2. Bacteria changes drug binding site
  3. Drug is pumped out of microbe
  4. Microbe makes alternative enzyme bypass pathway

Example: MRSA - multiresistant Staphylococcus aureus

123
Q

What are the different way to introduce antibiotics?

A
  1. Prophylaxis - only use before appropriate surgeries for appropriate patient with certain conditions - like rheumatic fever
  2. Empirical - when bacteria is not proven but assumed
  3. Directed - when bacteria is known
124
Q

What is the “creed” of antibiotic therapy?

A

M - microbiology guides therapy
I - indications should be evidence-based
N - narrowest spectrum required
D - dosage appropriate to the site & typ of infection

M - minimise duration of therapy
E - ensure monotherapy in most situations

125
Q

What are the principles of antimicrobial selection?

A
  1. Use narrowest antibiotic to treat disease
  2. Use the safest
  3. Avoid topical administration of a drug used systemically
  4. Don’t use combinations
  5. Don’t give prophylactically
  6. After considering all theses factors - choose lowest coast
126
Q

Form most odontogenic infections, how many days of antibiotic use, with appropriate dental treatment, is sufficient for treatment?

A

Less than 7 days

127
Q

What should the dentist put on the prescription sheet to make sure that pharmacist does not dispense too many antibiotic capsules?

A

Number of days and numbers of pills

128
Q

Do blood thinning drugs actually thin blood?

A

No - they affect the clotting cascade thus reducing the ability to clot. Old fashion warfarin for example affect Vitamin K which is an important clotting factor. To counter warfarin, just drink some Vitamin K

129
Q

What is the difference between the reliever and a dialator?

A

Preventer is taken before to lower the chance or severity of asthma through different vasodialating effect. Usually a low dose of corticosteroids

Reliever - is usually just use for quick relaxation of smooth muscles.

130
Q

Your patient has been prescribed enteric coated aspirin tablets for prophylaxis. How do these tablets work to prevent gastric irritation? Why would your patient be taking them? What are the dental implications?

A
  1. Aspirin may cause gastric bleeding thus if it coated in enteric coating it can travel the small intestine and not damage the stomach or be damaged by acidity of the stomach. The coating will be disolved in the small intestine as it is alkaline sensative
  2. Patient take prophylactic dose of aspirin in order to reduce the probability of heart attacks and blood clots as it affects the clotting cascade - higher doses are for pain relief
  3. Dental implication - aspirin induces bleeding, be careful with invasive procedures.
131
Q

Your patient seeks your advice as to why he has been told by his GP not to swallow his Anginine tablets but rather to allow them to dissolve under the tongue?

A

Anginine is a vasodialator for angina. It is put under the tongue for absorption in order to by pass the first pass effect as it is metabolised in the liver quite fast.

132
Q

Neostigmine is a competitive inhibitor of cholinesterase. Why is it useful in the treatment of Myasthenia Gravis?

A

Myasthenia Gravis is a auto-immune disease that affect acetylecholine receptors on skeletal muscles - thus affecting the contraction of said muscles. It is an inhibitor.

Neostigmine inhibits the enzyme acetylcholine esterase which breakswdown acetylcholine thus increasin it’s number in synaptic cleft.

this results in improvemenet in the condition due to greater numbers of acetylecholine.

133
Q

Which receptor does morphine bind to?

A

Opiod receptor

134
Q

Rank the following in terms of speed of onset action when an agonist occupis the receptor?

GABBA receptor

Opiod receptor

Glucocorticoid receptor

A
  1. GABBA receptor - inhibitory receptor in the nerve - very quick because it is an ion channel
  2. Opiod receptor - G protein-coupled receptors - moderatley quick
  3. Glucocoricoid receptor - nuclear receptor superfamily of transcription factors - very slow
135
Q

How would being a poor metaboliser of medicine alter a patient’s dosage ragime?

A

Lower maintanance dose needs to be administered to reduce the chance of toxicity

MD = CL x Css ; Css = MD/CL , lower CL increases the Css (steady state serum concentration)

136
Q
A
137
Q

How do we calculate the body clearance, renal clearance, and hepatic clearance?

A

Total clearance will be amount of drug in mg devided by the area undre the curve (do the conversion correctly)

Renal clerance - look at the percentage of the renal recovery than time it by total clearance

Hepatic clearance is body clearance minus leaver clearance

138
Q
A

BDS 3 Sem 2 (16 decks)

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