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Phase 1 > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What is guided antibiotic therapy?

A

Antibiotic usage dependent on identifying the cause of infection and selecting the best antibiotic based on sensitivity testing.

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2
Q

What is antibiotic empirical therapy?

A

Best (educated) guess therapy based on clinical/epidemiological acumen. Used when therapy cannot wait for culture eg. meningitis or sepsis.

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3
Q

What is prophylactic therapy?

A

Used to prevent infection before it begins. For example healthy people exposed to surgery/injury/infectious agent or in immunocompromised individuals eg. transplantation/HIV.

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4
Q

What is nitrofurantoin?

A

A narrow spectrum antibiotic used to treat uncomplicated UTI.

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5
Q

Penicillin

A

A beta-lactam antibiotic that works on cell walls. Rapid bacterial killing and low toxicity.

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6
Q

Describe type I hypersensitivity reactions

A

Urticaria (hives), wheeze and anaphylaxis.

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7
Q

Describe type II hypersensitivity reactions

A

Haemolytic anaemia

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8
Q

Describe type III hypersensitivity reactions

A

Vasculitis

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9
Q

Describe type IV hypersensitivity reactions

A

Delayed hypersensitivity

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10
Q

Vancomycin

A

A glycopeptide that directly inhibits cell wall formation. Main use is in treatment of MRSA. Difficult to deliver, needs n IV infusion. Can cause renal toxicity, bone marrow toxicity, ototoxicity and red man syndrome. Cannot cross cell membranes so not useful against gram negative bacteria.

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11
Q

What are macrolides?

A

Antibiotics that are protein synthesis inhibitors, they inhibit the bacterial ribosome to prevent peptide chain extension. Usually bacteriostatic. Good activity against gram positive pathogens and respiratory gram negative pathogens. Highly concentrated intracellularly so useful against intracellular pathogens. Macrolides bind to and inhibit CYP-3A4. Has complex drug interactions with statins and warfarin.

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12
Q

What are aminoglycosides?

A

Gentamicin is an example. Gentamicin reversibly binds to 30S ribosome (bacteriostatic) but also has a poorly understood effect on the cell membrane (bactericidal) which is prominent at high concentrations and causes rapid killing.

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13
Q

What are quinolones?

A

DNA gyrase inhibitors that cause extensive DNA fragmentation and cell death. They are useful against a wide range of microorganisms but unfortunately resistance is becoming increasingly common.

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14
Q

Trimethoprim

A

A bacteriostatic agent that inhibits folate metabolism and terminates DNA synthesis. Principally used in UTIs. Causes (usually) mild renal toxicity- high K+.

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15
Q

What are the 3 principal mechanisms of resistance to antibiotics?

A

1) Mutation of target site. 2) Inactivating enzymes. 3)Limit access- reduced permeability or increased efflux. Genes mediating resistance can often be easily transferred.

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16
Q

How does beta lactam resistance occur?

A

1)Mutation of penicillin binding proteins. 2)Production of beta lactamases (irreversibly inactivate beta lactams enzymatically). 3) Altered outer membrane porins-reduced access of certain beta lactam to targets.

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17
Q

What are beta lactamases?

A

Enzymes that lyse and inactivate beta-lactam drugs. Commonly secreted by gram -ve bacteria and staphylococcus aureus. They confer a high level of antibiotic resistance.

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18
Q

What are beta lactamase inhibitors?

A

Drugs that effectively inhibit some beta-lactamases. They are often co-administered with penicillin antibiotics (ie. co-amoxiclav=clavulanic acid and amoxicillin) and so greatly broaden the spectrum of penicillin against gram -ve and S. aureus.

19
Q

What is co-amoxiclav?

A

Clavulanic acid, a beta lactmase inhibitor, co-administered with amoxicillin, a penicillin antibiotic.

20
Q

What is zero-order kinetics?

A

In drugs with zero-order kinetics the rate of elimination is constant and independent of plasma concentration- examples include ethanol and phenytoin (anti-epileptic).

21
Q

Advantages and disadvantages of intravenous drug routes

A

Advantages: rapid immediate onset, by-passes liver, permits titration. Disadvantages: increased risk of adverse effects, requires IV access, infection, pain.

22
Q

Advantages and disadvantages of intramuscular drug route

A

Advantages: rapid onset and shorter duration, by-passes liver. Disadvantages: absorption depends on blood flow, neurovascular damage, bleeding, pain, infection, delayed absorption in shock.

23
Q

Advantages and disadvantages of subcutaneous drug route

A

Advantages: prolonged effect, by-passes liver, constant and slow absorption. Disadvantages: absorption depends on blood flow, pain, infection and delayed absorption in shock.

24
Q

Advantages and disadvantages of enteral (oral or rectal) drug route

A

Advantages: convenient, safe, cheap, slower onset, prolonged but less potent. Disadvantages: Drug passes through liver, absorption rate can be highly variable, absorption is influenced by stomach contents, gastric acid interferes with absorption, uncooperative patients may not take them.

25
Q

What is a topical route of drug administration?

A

Placing a drug on a surface with a mucous membrane eg. sublingual, intranasal or skin.

26
Q

What is bioavailability?

A

Fraction of the administered dose of drug that reaches the systemic circulation. Expressed as letter F. Affected by drug factors- molecular weight/ ionisaition. Absorption pH, health of GI tract. First pass metabolism (hepatic)-phenytoin may reduce F. Grapefruit juice may increase F. F=1 for IV drugs.

27
Q

What is the loading dose?

A

Apparent volume into which a known amount of drug must be dispersed to give the measured plasma concentration. Relates the plasma concentration to the total amount of drug in the body. Used to determine loading dose amount and elimination half life (dosing interval). IV loading dose (mg)=Target C (mg/L) x V (L).
Oral loading dose= Target C x (V/F)

28
Q

What is the half-life?

A

Time required for serum plasma concentration to decrease by half. Determined by clearance and volume of distribution. Loading dose often use for drugs with a long half-life.

29
Q

What is clearance?

A

Theoretical volume of plasma “cleared” of drug per unit time eg. mlmin-1 or Lh-1.

30
Q

What is steady-state?

A

When the amount of drug administered is equal to the amount of drug eliminated within one dosing interval. Drugs with a short half life reach the steady state rapidly.

31
Q

What is ADME in relation to pharmacology?

A

Absorption, Distribution, Metabolism, Excretion.

32
Q

What is a drug?

A

A chemical entity which alters body function which we use for the prevention or treatment of disease. Two main types: small molecules and biologics.

33
Q

What is pharmacodynamics?

A

Study of the biochemical and physiologic processes underlying drug action.

34
Q

What is a drug receptor?

A

A macromolecular component of a cell with which a drug interacts to produce a response. This usually involves an effect on a signal transduction pathway/alters enzyme function.

35
Q

Define ‘affinity’

A

Measure of propensity of a drug to bind a receptor; the attractiveness of drug and receptor.

36
Q

Define ‘efficacy’ (or intrinsic ability)

A

Ability of a bound drug to change the receptor in some way that produces an effect; some drugs posses affinity but not efficacy.

37
Q

What is potency?

A

Relative position of the dose-effect curve along the dose axis.

38
Q

What is an agonist?

A

A drug that interacts with and activate receptors; they possess both affinity and efficacy. Can be full (maximal efficacy) or partial (less than maximal efficacy).

39
Q

What is an antagonist?

A

Drugs that interact with receptors but do not change the receptor. Two types: competitive (can be overcome by increasing agonist concentration) and non-competitive.

40
Q

What is the ED50?

A

Median effective dose; the dose at which 50% of the population or sample manifests a given effect; used with quantal dose response curves.

41
Q

What is the TD50?

A

Median toxic dose; the dose at which 50% of the population manifests a given toxic effect.

42
Q

What is the LD50?

A

Median lethal dose; the dose which kills 50% of the subjects.

43
Q

What is the equation for therapeutic index?

A

TD50 or LD50/ED50. The higher the therapeutic index the better the drug.

Phase 1 (13 decks)

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