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Pharmacology > Pharmacology Finals > Flashcards

Pharmacology Finals Flashcards

1
Q

What are the four basic stages of pharmacokinetics?

A

Absorption
Distribution
Metabolism
Elimination

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2
Q

What protein in the blood would slow down the distribution process of a drug?

A

albumin

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3
Q

Distribution of drug in the body depends on four main factors.

The first is blood flow, what are the others?

A

Lipophilicity (is the drug lipid soluble?)

Capillary permeability (Liver is more permeable than brain, so drug goes to Liver)

Plasma and Tissue Binding (albumin)

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4
Q

What does the Volume of Distribution help predict?

A

Whether the drug will be concentrated in the blood plasma (eg. with albumin), or within the tissues.

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5
Q

What do these have in common?

Phenytoin

Carbamazepine

Rifampin

Alcohol (Chronic)

Barbiturates

St. John’s Wort

PCRABS

A

Inducers of some of the main enzymes in Phase I cytochrome P450 reactions.

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6
Q

What do these drugs have in common?

(CPACMAN)

Grapefruit

Protease inhibitors

Azole antifungles

Cimetidine

Macrolides (Except Azithromycin)

Amiodarone

Non-DHP CCBs (diltiazem and verapamil)

A

Inhibitors of some enzymes of cytochrome P450 pathway.

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7
Q

What are the mechanisms of antibiotics? (6)

A
  • inhibit cell wall synthesis
  • inhibit cell membrane synthesis
  • inhibit protein synthesis
  • inhibit folate synthesis
  • inhibit RNA polymerase
  • inhibit DNA gyrase
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8
Q

What four subgroup of antibiotics share the Beta-lactam structural ring?

(these antibiotics affect cell wall synthesis)

A

Penicillins

Cephalosporins (described by generations eg. 4th gen Cefepime)

Carbapenems

Monobactams

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9
Q

What four things can antimicrobial drugs target?

A
  • inhibiton of cell wall synthesis
  • disruption of cell membrane function
  • inhibition of nucleic acid synthesis
  • inhibition of protein synthesis
  • RNA synthesis
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10
Q

How are penicillins and Cephalosporins eliminated?

A

via the kidneys

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11
Q

Why aren’t cephalosporins routinally administered for chest infections?

A

Permit overgrowth of Clostrium difficile, and they alter normal flora in the gut (also the quinolones)

Also… insufficient activity against haemophilus influenzae

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12
Q

What kind of drug is gentamicin?

A

aminoglycoside

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13
Q

what is Gentamicin used for?

A

drug of choice for serious infections, eg. endocarditis, septicaemia, meningitis

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14
Q

What are some adverse effects from Gentamicin?

A
  • Nephrotoxicity
  • Ototoxicity (8th cranial nerve - irreversible vestibular and auditory toxicity)
  • neuromuscular paralysis
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15
Q

What are the Five Rights?

A

Right Patient

Right Drug

Right Time

Right Dose

Right Route

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16
Q

For women, what must you always ask?

A

Date of last menstrual bleed

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17
Q

Why are bactericidal drugs more favourable than bacteriostatic?

A
  • a faster microbiological response
  • less likely to elicit microbial resistance
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18
Q

Folate synthesis inhibitors (2)

A
  • sulfanomides
  • trimethoprim
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19
Q

What are the narrow-spectrum penicillins?

A

Penicillin G

Penicillin V

flucloxacillin

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20
Q

What are the extended-spectrum penicillins?

A

amoxicillin

ampicillin

piperacillin

ticarcillin

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21
Q

what does MRSA stand for?

A

methicillin resistant Staphylococcus aureus

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22
Q

Groups of antibiotics that are bacterial cell wall inhibitors (4)

A
  • penicillins
  • Cephalosporins
  • monobactam
  • others; vancomycin, fosfomycin
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23
Q

what is Ceftazidime?

Kef- ta -zid -i -me

A

cephalosporin antibiotic, used in hospitals.

Cephalosporins

-antibacterials. interrupt cell wall biosynthesis

Used for pseudomonas aeruginosa

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24
Q

Extended-spectrum penicillins are be subdivided into two groups, what are they?

A
  1. aminopenicillins (amoxcillin and ampicillin)
  2. antipseudomonal penicillins (piperacillin, ticarcillin)
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25
Q

What can amoxicillin treat on its own?

A
  • upper respiratory tract infections
  • community-acquired pneumonia
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26
Q

What is special about haemophilus influenzae and Moraxella catarrhalis?

A

These bacteria produce pencillinase , they need clavulanate combination.

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27
Q

What is vancomycin used for?

+ what happens if >> infusion rate?

A

MRSA (rem. staphlococcus) - given orally.

Adminstered parenterally to treat systemic infections.

>>> infusion rate = hypotension, erythematous rash on face/ upper body “red man syndrome”

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28
Q

What can be used to treat (some strains of) pseudomonas aeruginosa?

A

antipseudomonal penicillins (eg. piperacillin)

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29
Q

why do bacterial protein synthesis inhibitors work?

A

due to differences in structure and function of ribosomes in prokaryotic and eukaryotic cells.

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30
Q

What three mechanisms do bacteria exert resistance to Beta-lactam antibiotics?

A
  • inactivation of drug by Beta-lactamase enyzmes (main cause)
  • reduced affinty of PBP for the antibiotics
  • decreased entry od drugs into bacteria through outer membrane porins.
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31
Q

What is special about gram -ve bacteria and penicillins?

A

they are innately resistant to pencillins because if impermeable porins in outer membrane

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32
Q

What is doxycycline example of?

A

Doxycycline is a broad-spectrum antibiotic of the tetracycline class.

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33
Q

what is the most serious adverse effect of aminoglycosides? (2)

A

nephrotoxicity

ototoxicity

(most common cause of drug-induced renal failure)

rem. gentamicin, neomycin, stephomycin

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34
Q

name some groups of drugs that are bacteriostatic

A

Sulfonamides (block the synthesis of folic acid which is a cofactor for enzymes that synthesize DNA components and amino acids)

tetracyclines (because they reversibly inhibit bacterial protein synthesis)

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35
Q

way aren’t tetracyclines very popular?

A
  • because they are bacteriostatic.
  • increased resistance.
  • can cause discolouration of teeth if used by pregnant women or children under eight years old.
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36
Q

How do tetracycline antibiotics work?

A

Inhibitor of bacterial protein synthesis

(30s Ribosome subunit)

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37
Q

How do macrolide antibiotics work?

A

Inhibit bacterial protein synthesis

(affect the 50s ribosomal subunit)

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38
Q

both tetracyclines and macrolides affect bacterial protein synthesis. Which is other main group that also affects protein synthesis?

A

Aminoglycoside (eg. streptomycin, gentamicin)

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39
Q

Inhibitors of bacterial protein synthesis….. (3)

A

tetracyclines

macrolides

aminoglycosides

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40
Q

Which penicillins are anti-pseudomonal?

A

piperacillin/ tazabactum

ticarcillin/ clavulanic acid

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41
Q

IMPORTANT

Which drug groups (according to modus operandi) are bacteriocidal?

A

Those that target :

Cell Wall (van, pen, ceph)

or

Cell membrane (aminoglyc, polymyx)

or

DNA synthesis (metro, f/quin)

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42
Q

Name the six classes of bacteriostatic antibiotics

A
  • Tetracyclines
  • Sulphonamides
  • Macrolides
  • Chloramphenicol
  • Trimethoprim
  • Spectinomycin
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43
Q

Name the six classes that are bacteriocidal

A

All the b-lactam group

(penicilliins, cephalosporins, monobactams, carbapenems)

glycopeptides (vancomycin)

fluoroqinolones (ciprofloxacin)

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44
Q

There are THREE narrow spectrum penicillins, what are they?

A

Penicillin G (Benzylpenicillin)

Pen V (Phenoxymethylpenicillin)

Flucloxacillin

Unlike other penicillins, flucloxacillin has activity against beta-lactamase-producing organisms such as Staphylococcus aureus

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45
Q

Name THREE broad spectrum penicillins

A

Amoxicillin/ co-amoxiclav

ampicillin

piperacillin with Tazobactam (Tazocin)

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46
Q

Which penicillin can great Staphylococcus aureus?

A

flucloxacillin has activity against beta-lactamase-producing organisms such as Staphylococcus aureus as it is beta-lactamase stable

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47
Q

What are common side effects of penicillins?

A

nausea, vomiting, diarrhoea

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48
Q

Which drugs target gram -ve?

A

Aminoglycosides

(eg. gentamicin)

Carbapenems

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49
Q

What drug would you use for serious infections? Endocarditis, septicaemia, meningitis?

A

Gentamicin

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50
Q

Gram +ve is the largest group of bacteria, give some examples.

A

Staphylococcus

Stephtococcus

Clostridium

Enterococus

Listeria

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51
Q

Give some examples of gram -ve bacteria

A

E. Coli

Pseudomonas aeruginosa

N. gonorrhoea

chlamydia

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52
Q

Vancomycin belongs to which group?

and how do they work?

A

Glycopeptides

Inhibit bacterial cell wall synthesis

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53
Q

There are two groups that are bacteriostatic and inhibitor folate synthesis. One group is sulfanomides, what’s the other drug?

A

Trimethoprim

54
Q

Quinolones/ floroquinolones. bacteriostatic or cidal?

A

Bacteriocidal… they are inhibitors of DNA gyrase.

55
Q

What is flucloxacillin? And what makes it special?

A

Flucloxacillin is a narrow-spectrum beta-lactam antibiotic of the penicillin class.

It is used to treat infections caused by susceptible Gram-positive bacteria.

Unlike other penicillins, flucloxacillin has activity against beta-lactamase-producing organisms such as Staphylococcus aureus (not MRSA though)

56
Q

What drug would treat chlamydia?

A

tetracycline

57
Q

tetraycline cause teeth discolouration. What is another important adverse effect?

A

phototoxicity; need to be careful when sunbathing.

(safe after 18 weeks gestation)

58
Q

Both these groups are inhibitors of bacterial protein synthesis, but they are different. WHY?

aminoglycosides

(eg. gentamycin)

tetracyclines

A

tetracyclines are bacteriostatic because reactions with bacteria are reversible.

59
Q

Metronidazole

(nitroimidazole compound)

A

active against anerobic protozoa.

Also some anerobic bacteria; H.pylori, C. difficle

Drug of choice for amebiasis, giardiasis, trichomoniasis

60
Q

What is the main use for flucloxacillin?

A

It’s not inactivated by penicillinases, and thus effective in infections caused by penicillin-resistant staphylococci.

61
Q

Piperacillin and Ticarcillin belong to which class of penicillins?

A

antipseudomonal

62
Q

Name some macrolides

A

Clarithromycin

Erthromycin

Azithromycin

Telithromycin

63
Q

How do macrolides work?

A

inhibit protein synthesis

64
Q

Definition of pharmacodynamics

A

The study of the mechanism of action by which drugs produce their pharmacologic effects.

The effect of the drugs on the body.

65
Q

Definition of pharmacokinetics

A

How the body affects the drug

66
Q

What is efficacy of a drug?

A

The ability of a drug to initiate a cellular effect. Also called instrinsic activity. NOT directly related to receptor affinity.

a full agonist has maximal efficacy, partial agonists will never have the same efficacy as full agonist.

67
Q

What is potency?

A

a characteristic of drug action useful for comparing different pharmacologic agents.

68
Q

What is pharmacokinetics?

A

the study of drug disposition in the body. It focuses on the changes in drug plasma concentration.

Plasma concentration will change according to absorption, distribution and elimination.

69
Q

What is pharmacodynamics?

A

this is the study of the detailed mechanism of action by which drugs produce their pharmacologic effects.

70
Q

Trimethoprim

moa, indications, side effects

A

Antifolate drug.

Weak base that concentrates in acidic prostate tissues and vaginal fluids via ion trapping.

Often used for UTI.

SD: nausa, vomiting, epigastric distress, rashes, hepatitis, thrombocytopenia, leukopenia.

71
Q

Ciprofloxacin

A

Fluoroquinolone group

Effective for many gram -ve bacteria.

Used to treat anthrax - postexposure prophylaxis of inhalational anthrax.

serious adverse effects; tendonitis and tendon rupture.

alters blood glucose, phototoxicity, prolongation of QT interval

Contraindicated; children, adolescents, pregnant and lactating women.

72
Q

What is fluconazole?

A

Anti-fungal. Azole derivative

excreted in the urine, therefore can treat vaginal candidiasis

73
Q

What is metronidazole used for?

A

Metronidazole is used to treat a wide variety of infections caused by anaerobic bacteria and protozoa.

Metronidazole is commonly prescribed to treat an infection called bacterial vaginosis. It is also prescribed before gynaecological surgery and surgery on the intestines to prevent infection from developing. It can safely be taken by people who are allergic to penicillin.

Metronidazole is also used to get rid of Helicobacter pylori.

Metronidazole is available as a skin preparation also.

First episode of C. diff

74
Q

clarithromycin

A

macrolide

alternative to penicillin

indicated for chest infections, cellulitis, ear infections, H. pylori

75
Q

what macrolide is indicated for acne?

A

erthromycin

(if tetracyclines not effective - doxycycline)

76
Q

What are the characteristics of aminoglycosides, and give some examples.

A

Gentamicin, Tobramycin (very good for pseudomonas aeruginosa), streptomycin, neomycin (very nephrotoxic).

Bactericidal - interfer with protein synthesis.

Generally poorly absorbed from the gut, and thus adminstered parenterally.

They are not metabolised, they are excreted primarily by the renal glomerular filtration.

Dosage must be reduced in patients with renal impairment because clearance is proportional to GFR (and creatinine excretion)

Active against wide range of aerobic gram-negative bacilli.

Most important side effects; nephrotoxicity and ototoxicity. Aminoglycosides are one of the most common causes of drug-induced renal failure. They can cause acute tubular necrosis.

Ototoxicity; can be both vesicular and cochlear toxicity. Often there is a delay between drug adminstration and onset of symptoms, px may have left the hospital.

77
Q

What are the symptoms of vestibular toxicity that maybe associated with aminoglycosides?

A

dizziness, impaired vision, nystagmus, vertigo, nausea, vomiting, problems with postural balance and walking.

78
Q

What are the symptoms of cochlear toxicity that maybe associated with aminoglycosides?

A

tinnitus, hearing impairment, irreversible deafness.

79
Q

Some facts about cephalosporins

A

Third gen Ceftazidime (IV) is good for pseudomonas (HAP), 2nd gen cefuroxime can be used for CAP.

B-lactam group. 10% of px allergic to pencillin will be hypersenitive.

Renally excreted; dose reduction with renal impairment.

Can cause pseudomembranous colitis (swelling or inflammation of the large intestine) due to an overgrowth of Clostridium difficile.

80
Q

Which antiobiotics are good for C. difficile?

A

metronizaole

and

vancomycin (could put in NG tube if px very unwell)

81
Q

Key mechanism of Warfarin (coumarin compounds)

A

Vitamin K antagonist

Vitamin K is used to synthesis coagulation factors II (prothrombin), VII, IX, and X

82
Q

Can Warfarin be used in pregnancy?

A

No because it crosses the placenta

83
Q

Does Warfarin act immediately?

A

No because pool of circulating clotting factors needs to be depleted first.

Synthesis of new factors is then inhibited.

(takes 3-5 days to reach maximal effect)

84
Q

What’s the management of acute thromboembolic disorders?

A

LMWH (Low molecular weight heparin) plus warfarin, and then withdraw LMWH when warfarin is effective.

85
Q

Patient advise for Warfarin

A
  • Any signs of bleeding, including ecchymoses.
  • Contraindicated in pregnancy (fetal warfarin syndrome)
  • Avoid physical activities such as kick boxing
  • Don’t >>> green vegetables (vit K)
  • Avoid grapefruit juice, cranberry juice
  • Avoid major weight changes
  • Avoid aspirin, NSAIDs
86
Q

Some common uses of Warfarin

A

Long-term treatment of DVT

Patients with AF

Patients with artificial heart valves.

87
Q

Name three LMWHs

A

enoxaparin

dalteparin

tinzaparin

88
Q

Key mechanism of heparin

A

inactivates clotting factors by potentiating the activity of an endogenous anticoagulant (antithrombin III)

89
Q

Can Heparin be given orally?

A

No because heparin and related anticoagulants are not absorbed from the gut (large molecules) and so much be administered by IV.

90
Q

What is antithrombin?

A

an endogenous anticoagulant (potent inhibitor of coagulation)

91
Q

What is the principal component of fibrinolysis?

A

Enzyme plasmin

(generated from inactive precursor plasminogen)2

92
Q

What are the key adverse effects of Heparin?

A

Bleeding

thrombocytopenia

(hyperkalemia)

93
Q

What’s the antidote for warfarin-induced bleeding

A

Phytonadione (vitamin K1)

94
Q

Clinicial uses for Warfarin

A

Long term management of DVT, AF, and artificial heart values.

95
Q

What is the INR for recurrent embolization or artificial heart valves?

What is the INR for warfarin (generally)

A

3 - 4.5

2-3

96
Q

Name three LMWH

A

enoxaparin

dalteparin

tinzaparin

97
Q

How does Dabigatran work?

A

Direct thrombin inhibitor

(thrombin is used in the pathway of transforming fibrinogen to fibrin)

98
Q

How does LMWH compare to unfractionated heparin in it’s modus operandi?

A

Primarily deactive factor X

99
Q

What’s the advantages of LMWH compared to standard heparin?

A

can be administered subcutaneously.

more predictable anticoagulation activity (aPTT monitoring not required)

100
Q

What is HIT?

A

Heparin-induced-thrombocytopenia

101
Q

Tell me about HIT 1

A

occurs in 25% of patients. Direct interaction between heparin and platelets, leading to platelet aggregation. Mild and reversible.

102
Q

Tell me about HIT 2

A

less common, more serious.

Immunoglobulin mediated platelet inactivation.

High risk of thrombotic complications and mortality.

103
Q

How does Fondaparinux work?

A

Indirect Factor Xa inhibitor

It selectively binds to antithrombin (an endogenous anticoagulant)

which

inactivates Xa resulting in a strong inhibition of thrombin generation and clot formation.

104
Q

How Warfarin monitored?

A

Prothrombin Time (PT)

105
Q

What does INR stand for?

A

International normalized ratio

INR = (PT observed / PT control)

PT = prothrombin time

106
Q

What is the antidote to unfractionated heparin and LMWH?

A

Protamine sulfate

(+ve charged protein than combines with -ve charged heparin)

** measure aPTT to monitor **

107
Q

How do you monitor

(a) Heparin
(b) Warfarin
(c) Dabigatran

A

(a) Heparin - aPTT

(b) Warfarin - PT - Prothrombin Time (remember the INR equation for warfarin)

(c) Dabigatran - TT (thrombin clotting time)

108
Q

What initiates the formation of platelets along the vascular wall?

A

injury and the expose of the blood to extravascular collagen.

109
Q

What activates the intrinsic pathway?

A

surface contact with a foreign body or extravascular tissue (i.e. collagen)

110
Q

What activates the extrinsic pathway in the coagulation cascade?

A

a complex tissue factor called thromboplastin.

111
Q

Where does the intrinsic and extrinsic pathways converge?

A

Factor X - major rate-limiting step

112
Q

What does the activation of factor X lead to?

A

the formation of Thrombin

113
Q

What three factors combined often lead to thrombic changes?

A
  • sluggish blood flow
  • inflammation
  • abnormalities in vascular endothelium
114
Q

What’s the difference between arterial thrombi and venous thrombi?

A

arterial thrombi (white); more platelet aggrevation driven

venous thrombi (red); more coagulation driven

115
Q

Aspirin; clinical usages and action as an antiplatelet drug

A

Acute coronary syndrome

Thrombic strokes; acute and prophylaxis

shown to prevent MI with angina.

Artificial heart valves, percutaneous coronary angioplasty.

ACTION: inhibits the synthesis of prostaglandins from arachidonic acid.

116
Q

What’s the most important prostaglandin affecting platelet aggregation?

A

prostacyclin and TXA2

(prostaglandin I2 (PGI2)

Aspirin irreversibly inhibits cyclooxygenase; enzyme that catalyzes TXA2 synthesis.

117
Q

Adverse effects of aspirin

A

GI bleeding

hypoprothrombinaemia; therefore increased bleeding risks

118
Q

When is clopidogrel indicated?

A
  • px who can’t tolerate aspirin
  • used in COMBINATION with aspirin for ACS
119
Q

When are the representative drugs steptokinase, alteplase indicated?

A

intravenously to degrade thrombi in px with

MI, thromvotic stroke, PE

Primary means of restoring coronary blood flow if angioplasty facilities not available.

120
Q

Adverse reactions with aspirin?

A

GI irritation, bleeding,

hypersensitivity reactions,

tinnitus

121
Q

Adverse reactions to streptokinase

A

bleeding, hypersensitivity reactions,

and reperfusion arrhymias (of interest)

anaphylactic shock can occur with streptokinase, therefore cannot be used repeatedly on same patient.

122
Q

what is t-PA and give an example drug

A

Alteplase

drugs that are ‘recombinant forms of human tissue plasminogen activator’

tissue-Plasminogen Activator

123
Q

How do Rivaroxaban, Apixaban, Edoxaban work?

A

Direct Factor Xa inhibitor

124
Q

How does Dagibatran work?

A

Direct thrombin inhibitor.

125
Q

What’s best for arterial thrombosis? Anticoagulants or antiplatelets?

A

Antiplatelets

126
Q

Some advantages of NOACs/ DOACs

A
  • few interactions with food/ drugs
  • predictable anticoagulant effect
  • no need for routine monitoring
127
Q

Which pathway does Warfarin affect?

A

Both intrinsic and extrinsic

128
Q

MOA of Heparin

A

binds to body’s own anticoagulant (antithrombin III)

This complex inhibits factor Xa (and other factors)

129
Q

What is Dipyridamole?

What is it indicated for?

A

Dipyridamole a coronary vasodilator and a relatively weak antiplatelet drug.

Dipyridamole is used in COMBO with aspirin to prevent ischaemic stroke in px with history of thrombotic stroke, and persons experiencing TIAs.

130
Q

What is Dipyridamole?

A

Dipyridamole is an antiplatelet medication that also has vasodilating properties that can make it unsuitable for use in those with severe coronary artery disease, unstable angina, recent myocardial infarction.

Can be combined with aspirin as an option to prevent occlusive vascular events in patients who have had a TIA, or ischaemic stroke.

131
Q

What is prochlorperazine and what is it indicated for?

A
132
Q

What is prochlorperazine?

What are it’s indications?

A

D2 receptor antagonist ; this group acts primarily on the CTZ to inhibit stimulation of the vomiting centre.

Can also be given IV to treat unremitting migraine headache.

(rem that prochlorperazine is an anti-psychotic)

Pharmacology (13 decks)

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