PHARM; Lecture 31, 32 and 33 - Antibiotics, Antifungals and Anticonvulsants Flashcards Preview

Y2 LCRS 1 - Pharm, Endo, Reproduction > PHARM; Lecture 31, 32 and 33 - Antibiotics, Antifungals and Anticonvulsants > Flashcards

Flashcards in PHARM; Lecture 31, 32 and 33 - Antibiotics, Antifungals and Anticonvulsants Deck (35)
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1
Pharm

What are bacteria and their 3 categories?

x

2
Pharm

What are the 4 types of prokaryotic protein synthesis?

PABA->THF then leads to DNA synthesis;

after DNA gyrase (=topoisomerase) helps in DNA/RNA synthesis;

RNA polymerase is present within bacterial cells to produce RNA;

proteins produced in ribosomes (different from eukaryotic ones)

3
Pharm

Which drugs target the 4 types of protein synthesis in the bacterium?

  • Sulphonamide (not used by itself anymore) and trimethroprim are used together, reducing DNA synthesis which prevents the bacteria from replicating.
  • Quinolones target DNA gyrase preventing loosening of DNA, which prevents DNA replication, killing the cells.
  • Rifamycins inhibit RNA polymerase, causing cell death.
  • Ribosomes are targeted by 4 types -> macrolides (erythromycin is very important, affecting enzymes and causes a lot of drug interactions)

4
Pharm

How is the bacterial wall synthesised - 3 steps?

x

5
Pharm

What are the bacterial wall inhibitor drugs?

Vancomycin used more now as last chance, due to resistance.

Polymyxins are quite old but have started to be used again in emergency situations as resistance hasn't built up (bad side effect profile)

6
Pharm

What are the causes of antibiotic resistance?

  • Unnecessary prescription
    • ~ 50% of antibiotic prescriptions not required
  • Livestock farming
    • ~ 30% of UK antibiotic use in livestock farming
  • Lack of regulation
    • OTC availability in Russia, China, India
  • Lack of development
    • No new antibiotic drug classes in years

7
Pharm

What are the 5 Antibiotic resistance mechanisms? (HADED)

  1. Additional target: Bacteria produce another target that is unaffected by the drug (E. coli produce different DHF reductase enzymes making them resistant to trimethoprim);
  2. hyperproduction: bacteria significantly increase levels of enzymes (DHF reductase, so in E. coli trimethoprim less effective);
  3. Alteration in target enzymes: alteration to enzyme targeted by drug, with enzyme still effective but drug is ineffective (S.Aureus);
  4. Alterations in drug permeations: reductions in AQP and increased efflux systems (primarily important in gram -ve bacteria);
  5. Production of destruction enzymes

8
Pharm

How can you classify fungal infections?

Can be classified in terms of tissue/organs: Superficial - Outermost layers of skin Dermatophyte - Skin, hair or nails Subcutaneous - Innermost skin layers Systemic - Primarily respiratory tract

9
Pharm

What are the 2 most common categories of anti-fungals?

NB: azoles inhibit CYP450 which will slow down the metabolism of any drug that uses CYP450 for metabolism

10
Pharm

SAQ

x

11
Pharm

What is the structure of viruses?

Need cells to replicate -> parasites; have genetic material, with capsid protecting it. Also can have a lipid envelope with proteins

12
Pharm

What is viral hepatitis and its treatment?

  • HBV - not curable, with people catching hep B via sexual conditions/blood exchange - some people host infection for rest of their lives or clear it as soon as infected - tenofovir prevents progression of disease causing liver cirrhosis/hepatocellular carcinoma development.
  • HCV -> Peginterferon not used anymore as it had bad side effects

13
Pharm

What is the goal of HCV treatment?

x

14
Pharm

What is the HIV life cycle?

Chronic NOT curable disease

15
Pharm

Which drugs block HIV attachment and entry?

x

16
Pharm

Which drugs block replication of HIV?

Zidovudine - AZT (not really used anymore because it has a poor side effect profile)

17
Pharm

Which drugs block integration of HIV?

DNA integration Viral integrase inserts viral DNA into host DNA Integrase inhibitors Raltegravir - first of 3 licensed integrase inhibitors

18
Pharm

Which drugs block assembly and release of HIV?

NB: ritonavir isn't a real drug anymore; just used as a booster for saquinavir

19
Pharm

What is herpes simplex virus and what can you treat it with?

Acyclovir most used drug to treat it -> made by guanosine, blocking viral DNA formation; can also be used for chicken pox, shingles

20
Pharm

What is influenza and what can you treat it with?

Oseltamivir (tamiflu) prevents release of new viruses from the cell -> but doesn't block all the release

21
Pharm

What is a general seizure and what are the types?

Begins simultaneously in both hemispheres of brain -> affects the whole brain.

Genetic disorder, so more common in younger patients

Types of general seizure include:

  • Tonic-clonic seizures
  • Absence seizures
  • Myoclonic seizures

22
Pharm

What is a partial/focal seizure and what are the types?

Begins within a particular area of brain and may spread out

May be the result of an injury or insult to the brain.

More common in adults.

Types of seizure include:

  • Simple (maintains consciousness)/ complex (loses conciousness) partial
  • Temporal lobe epilepsy

23
Pharm

How can you measure brain activity?

Brain activity can be measured using techniques such as:

  • Electroencephalography (EEG)
  • Magnetoencephalography (MEG)
  • Functional magnetic resonance imaging (fMRI)

24
Pharm

What is the normal activity of brain - normal wave types?

  • Distinctive firing patterns associated with certain activities (high to low Hz):
  • Gamma: awareness - hyperactive
  • Beta: awareness - thinking
  • Alpha: awareness - relaxed
  • Theta: drowsiness, meditation
  • Delta: deep-sleep

25
Pharm

What is the brain activity in seizures?

Irregular/ asynchronous firing patterns due to neuronal over-activity - red box is EEG during seizure, green is normal brain

26
Pharm

How does neurotransmission occur across a glutamatergic synapse?

>10 types of glutamate receptors

27
Pharm

What are 2 types of VGSC inhibitors and what are their pharmacokinetics?

  • In inactive state, channel isn't fully open or closed -> inhibitors lock channel in inactive state, so channel can't be activated when action potential comes along.
  • Carbamaxepine is a CYP450 enzyme inducer (!!!); also HLA-B*1502 is concentrated in Chinese region of Asia, can cause Stevens-Johnson syndrome

28
Pharm

Give an example of a VGKC enhancer

Retigabine: Potassium channel opener specific for KV7 alpha subunit

Only licensed for adjunctive treatment

Fast onset (30mins); ~ 10h half-life (2/3x a day)

29
Pharm

Give an example of VGCC blocker

  • Ethosuximide
    • T-type Ca2+ channel antagonist (L-type is for cardiac problems, found on blood vessels;
    • T-type found in CNS, found in brain)
    • Mainly used for absence seizures
    • Long half-life (50 hours)
  • Gabapentin
  • Thought to inhibit alpha 2 delta subunit (auxillary subunit) Indicated for partial seizures

30
Pharm

What drugs target glutamate exocytosis and their receptors?

Want drugs to have fast onset and long duration

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