Pharmacology in SRH Flashcards

1
Q

What are some examples of bactericidal antibiotics?

A

Beta-lactam antibiotics
Aminoglycosides
Fluoroquinolones
Metronidazole

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2
Q

How do bactericidal antibiotics work?

A

Inhibition of cell wall synthesis

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3
Q

How do bacteriostatic antibiotics work?

A

Inhibit bacterial protein synthesis pathway
Inhibit DNA replication
Limit growth of bacteria

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4
Q

What are some examples of bacteriostatic antibiotics?

A

Tetracyclines
Macrolides
Clindamycin

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5
Q

What are the classes of antibiotic relevant to SRH?

A
  1. Beta-lactam - includes subclasses of carbapenems, cephalosporins, monobactams, and penicillins
  2. Aminoglycosides
  3. Fluoroquinolones
  4. Macrolides
  5. Tetracyclines
  6. Other Abx that don’t fit classes - e.g. metronidazole and clindamycin
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6
Q

How does benzylpenicillin benzathine work (MOA)?

A

Inhibition of bacterial cell wall synthesis through a blockade of the penicillin-binding proteins (PBPs), such as transpeptidases

This results in a bactericidal action

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7
Q

What is the MOA of gentamicin (aminoglycoside)?

A

Forms a bond with bacterial 30S ribosomal subunits, which causes misreading of mRNA

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8
Q

What is the MOA of ofloxacin/moxifloxacin (fluroquinolones)?

A

Inhibits the supercoiling activity of bacterial DNA gyrase, halting DNA replication.

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9
Q

On what organisms do ofloaxcin/moxifloxacin act?

A

Broad spectrum activity on both gram +ve and gram -ve organisms

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10
Q

What organisms does clindamycin act upon?

A

Gram +ve aerobes and a wide range of anaerobic bacteria

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11
Q

What is the MOA of clindamycin?

A

Primarily bacteriostatic

Bind to the 50S subunit of the bacterial ribosome similarly to macrolides and inhibit the early stages of protein synthesis

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12
Q

What is a severe, but not uncommon complication associated with clindamycin?

A

Pseudomembranous colitis

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13
Q

With repeated doses in a pregnant woman, what may the amniotic concentration of clindamycin be relative to the maternal serum concentration?

A

30%

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14
Q

Which organisms does metronidazole act upon?

A

Anaerobic bacteria and protozoa

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15
Q

What is the MOA of metronidazole?

A

Not fully established, but ?blocking nucleic acid synthesis

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16
Q

What advice should be given re: metronidazole and alcohol?

A

No alcohol during metronidazole therapy and for at least 48 hours afterwards because of the possibility of a disulfiram like (antabuse effect) reaction

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17
Q

How does azithromycin work?

A

Protein synthesis inhibitor: 50S ribosome subunit

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18
Q

How does erythromycin work?

A

Protein synthesis inhibitor: 50S ribosome subunit

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19
Q

In whom is erythromycin contraindicated?

A

Long QT, or those at risk of long QT (e.g. those with electrolyte disturbance)
With certain medications, e.g. simvastatin

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20
Q

From where is erythromycin absorbed?

A

Small intestine

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21
Q

How does doxycycline work?

A

Protein synthesis inhibitor: 30S ribosome subunit

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22
Q

How does fluconazole/clotrimazole work?

A

Ergosterol synthesis inhibitor

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23
Q

How does ciprofloxacin work?

A

Targets DNA gyrase in gram negative organisms

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24
Q

What type of gene mutation are associated with azithromycin/macrolide resistance?

A

23sRNA gene mutations

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25
Q

What are the constituents of EMLA cream?

A

Lidocaine - 2.5%
Prilocaine - 2.5%

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26
Q

What can high doses of prilocaine cause?

A

Increase in methaemoglobin levels particularly in conjunction with methaemoglobin-inducing medicinal products (e.g. sulphonamides, nitrofurantoin, phenytoin, phenobarbital).

27
Q

Is EMLA cream considered safe in pregnancy and breastfeeding?

A

Yes

28
Q

The quality of the anaesthesia with EMLA cream depends on what?

A

Dose AND application time (time required to procedure reliable anaesthesia = usually 1-2 hours, apart from on the face, where due to increased blood flow, peak affect achieved after 30-60 minutes)

29
Q

What type of anaesthetics are lidocaine and prilocaine?

A

Amide-type

30
Q

What is the mechanism of action of EMLA cream?

A

They both stabilise neuronal membranes by inhibiting the ionic fluxes required for the initiation and conduction of impulses, thereby producing local anaesthesia

31
Q

1% lidocaine, contains how many mg of lidocaine per ml?

A

10mg per 1ml

32
Q

What is the maximum dose of lidocaine when infiltrated for anaesthetic?

A

4.5mg/kg

33
Q

Which drug may result in a slightly increased risk of Trisomy 21 if used within 3/12 of conception?

A

Colchicine

34
Q

What is Gardasil 9 indicated for?

A

Premalignant lesions and cancers affecting the cervix, vulva, vagina and anus

Genital warts

35
Q

What is the MoA of Gardasil 9?

A

Adjuvanted non-infectious recombinant 9-valent vaccine

It is prepared from the highly purified virus-like particles (VLPs) of the major capsid L1 protein

36
Q

Gardasil is expected to protect again the HPV types that cause approximately what?

A

90% of cervical cancers
95% of adenocarcinoma in situ (AIS)
75-85% of high-grade CIN
85-90% of HPV related vulvar cancers
90-95% of HPV related high-grade VIN 2/3
80-85% of HPV related vaginal cancers
75-85% of HPV related high-grade VaIN 2/3
90-95% of HPV related anal cancer
85-90% of HPV related high-grade AIN 2/3
90% of genital warts.

37
Q

What temp should Gardasil 9/Rhophylac/Engerix B/Twinrix be stored at?

A

2-8 degrees-C

38
Q

To when should vaccination with a live vaccine be delayed relative to the last anti-D injection?

A

3 months, as otherwise the efficacy of the live vaccine may be impaired

39
Q

What does Rhophylac contain?

A

Specific antibodies (IgG) against the Rh(D) antigen of human erythrocytes

40
Q

Do what degree can Rhophylac prevent Rh(D) immunisation?

A

Passive immunisation with anti-D immunoglobulin prevents Rh(D) immunisation in more than 99% of cases

41
Q

When does absorption of anti-D following injection reach a maximum?

A

After 2-3 days

42
Q

What is half life of anti-D?

A

3-4 weeks

43
Q

How do Engerix B vaccines work?

A

Engerix B induces specific humoral antibodies against HBsAg (anti-HBs antibodies)

Anti-HBs antibody concentrations ≥ 10m IU/ml correlate with protection to HBV infection

44
Q

What is the protective efficacy of Engerix B?

A

95-100%

45
Q

What are the dosing schedules of Twinrix?

A

0 - 1 - 6 months
0 - 7 - 21 days + 1 year boooster

46
Q

What factor may reduce the immune response to Hep A vaccination?

A

Obesity

47
Q

What factor may reduce the immune response to Hep B vaccination?

A

Older age
Male gender
Obesity
Smoking
Route of administration
Some chronic underlying diseases

48
Q

What is the seropretection rate against Hep after a course of Twinrix?

A

92% and 56% at 7 and 48 months respectively

49
Q

What is the seropositivity rate for anti-HAV antibodies after a course of Twinrix?

A

97% at both 7 and 48 months

50
Q

How may serum levels of anticonvulsant drugs - phenytoin, phenobarbital, primidone - be affect by folic acid adminsitration

A

Reduced

51
Q

Absorption of folic acid may be reduced by which drugs?

A

Sulfasalazine

Cholestyramine - folic acid 1 hour before or cholestryamine 4-6 hours after

Al/Mg anatacids - take 2 hours after folic acid

52
Q

How can folic acid affect the intestinal absorption of zinc?

A

Reduce it

53
Q

How is folic acid absorbed?

A

Mucosa of the duodenum and upper part of the jejunum, rich in dihydrofolate reductase, where folic acid absorbed

Once absorbed, folic acid rapidly reduced and then methylated to form tetrahydrofolic acid derivatives and transported to tissues

54
Q

What is the MOA of ENG in Nexplanon?

A

Etonogestrel is the biologically active metabolite of desogestrel. It is structurally derived from 19-nortestosterone and binds with high affinity to progesterone receptors in the target organs.

The contraceptive effect of etonogestrel is primarily achieved by inhibition of ovulation. Ovulations were not observed in the first two years of use of the implant and only rarely in the third year. Besides inhibition of ovulation, etonogestrel also causes changes in the cervical mucus, which hinders the passage of spermatozoa.

55
Q

How does ivermectin work?

A

High affinity with glutamate-gated Cl- channels present in invertebrate nerve and muscle cells

Binding to these channels promotes an increase in membrane permeability to Cl- ions = hyperpolarisation of the neural or muscle cell

This results in neuromuscular paralysis and may lead to the death of certain parasites

56
Q

How does aciclovir work?

A

Aciclovir is converted to aciclovir triphosphate in the presence of HSV

Aciclovir triphosphate then interferes with the viral DNA polymerase and inhibits viral DNA replication with resultant chain termination following its incorporation into the viral DNA.

57
Q

In whom is TXA contraindicated?

A

Active thromboembolic disease

History of venous or arterial thrombosis

58
Q

What is the MOA of TXA?

A

Competitively and reversibly inhibits the activation of plasminogen

The binding of plasminogen to fibrin induces fibrinolysis - by occupying the necessary binding sites, TXA prevents this dissolution of fibrin, thereby stabilizing the clot and preventing hemorrhage

59
Q

What is the MOA of mefenamic acid?

A

Binds the prostaglandin synthetase receptors COX-1 and COX-2, inhibiting the action of prostaglandin synthetase.

As these receptors have a role as a major mediator of inflammation and/or a role for prostanoid signaling, the symptoms of pain are temporarily reduced

60
Q

How do bisphosphonates work?

A

Inhibit bone resorption by attaching to hydroxyapatite binding sites on the bone, particularly in areas with active resorption
As osteoclasts resorb bone, the bisphosphonate embedded in the bone is released and impairs the osteoclast’s ability to continue bone resorption

61
Q

What is the MOA of denosumab?

A

Denosumab prevents RANKL from activating its receptor, RANK, on the surface of osteoclasts and their precursors.
Prevention of the RANKL/RANK interaction inhibits osteoclast formation, function, and survival, thereby decreasing bone resorption and increasing bone mass and strength in both cortical and trabecular bone

62
Q

How is denosumab administered?

A

S/C once every 6/12 into the thigh, abdomen or upper arm

63
Q

How does raloxifene work?

A

SERM
It occupies the same ER ligand binding site as estrogen - typically maintain the bone integrity by inhibiting the cytokines that recruit osteoclasts and oppose the bone-resorbing, Ca2+-mobilizing action of PTH
In contrast, estrogens promote osteoblast proliferation, augment the production of TGF-β3 and bone morphogenic proteins, and inhibit apoptosis

64
Q

How does teriparatide work?

A

Binding of teriparatide to PTH receptors on osteoblasts activates the downstream PKA- and PKC-dependent signaling pathways that promotes anabolic effects on bone