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2a. BDS2 BAMS > x. General Lectures > Flashcards

x. General Lectures Flashcards

1
Q

L24: What is the major micoorganism associated with periodontitis?

A

P. gingivalis

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2
Q

L24: How many links are there in the chain of infection and what are they?

A

7:

  • Infectious agent (virulence factor);
  • Resevoirs;
  • Portal of Exit;
  • Means of Transmission;
  • Portal of Entry;
  • Susceptible Host.
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3
Q

L24: What does it mean when micro-organisms are highly virulent?

A

High ability to cause disease

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4
Q

L24: What are exotoxins?

A

A toxin released by a microorganism

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5
Q

L24: Give an example of an exotoxin.

A
  • Protease (from P. gingivalis);
  • Enterotoxin (S. aureus);
  • Leukocidin (S. aureus).
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6
Q

L24: What are endotoxins?

A

A component of a bacterial cell wall (are also pyrogens)

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7
Q

L24: Give an example of an endotoxin.

A

Lipopolysaccharide (from P. gingivalis and E. coli)

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8
Q

L24: What is an infectious dose (ID50)?

A

The number of microorganisms required to cause an infection

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9
Q

L24: Give an example of a reservoir.

A
  • Microbes ubiquitous in nature;
  • Humans;
  • Animals;
  • Environment;
  • Fomites (contaminated objects/ surfaces).
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10
Q

L24: From what reservoir do the most pathogenic microbes, to humans, come from?

A

Humans

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11
Q

L24: What is the incubation period (similar to latent period)?

A

The time between contamination and development of symptoms, varies widely for different infections

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12
Q

L24: What is the problem with longer incubation periods?

A
  • Longer time until onset of symptoms;
  • Unaware of infection;
  • More contact with humans;
  • Greater spread of the disease.
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13
Q

L24: What is the infectious period and does this overlap with the incubation period?

A

The time in which an infection can be transmitted between humans, this does overlap with the incubation period

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14
Q

L24: What is an asymptomatic carrier?

A

An infected person with no clinical evidence of disease, though signs and symptoms of the disease may have been evident earlier

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15
Q

L24: What is the difference between a colonisation and an infection?

A

A colonisation is the presence of a microorganism in a host, with growth and multiplication, but without overt expression (infection)

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16
Q

L24: Give an example of a colonisation, commonly carried in humans.

A

S. aureus (nose)

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17
Q

L24: What are endogenous reservoirs?

A

Disease caused bacteria/ microbes that are a normal part of a host’s flora, they can become displaces to another body site (e.g. brain or muscle) or invade deeper tissues (commensals)

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18
Q

L24: What are exogenous reservoirs?

A

Disease caused by bacteria/ microbes entering a host that are non-commensals (e.g. influenza)

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19
Q

L24: What is the portal of exit and what are the two main modes of exits?

A
  • Escape of microbes from a source to a new host;

- Natural and artificial.

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20
Q

L24: Provide an example of a natural portal of exit.

A
  • Coughing;

- Sneezing.

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21
Q

L24: Provide an example of an artificial portal of exit.

A
  • Blood donation;

- Dental handpick aerosols.

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22
Q

L24: What is the R0 number?

A

The number of cases one case generates on average over the course of its infectious period

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23
Q

L24: What does R0 < 1 mean?

A

The infection is likely to die out in the long run

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24
Q

L24: What does R0 > 1 mean?

A

The infection is likely to spread in the population

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25
Q

L24: What is the general relationship between R0 number and risk?

A

The higher the R0 number, the higher the risk and greater difficulty infection is to control

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26
Q

L24: What effects the R0 number?

A
  • Duration of infectivity;
  • Infectiousness (virulence);
  • Number of susceptible people.
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27
Q

L24: Where does the influenza virus primarily target?

A

Upper and lower respiratory tract (virus shed here)

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28
Q

L24: What is the incubation period of influenza?

A

2-3 days

29
Q

L24: When does influenza become infectious?

A

When symptoms appear, children are infectious for longer

30
Q

L24: Why does influenza also cause a fever, headache and fatigue?

A

Release of cytokines (IF and TNF)

31
Q

L24: What can ‘complicated’ influenza lead to?

A
  • Bacterial pneumonia;
  • Ear and sinus infections;
  • Worsening of chronic medical conditions (asthma, CVD).
32
Q

L24: Provide examples of direct contact for the portal of entry.

A
  • Respiration (aerosols);
  • Inhalation (all particles);
  • Contact (droplets).
33
Q

L24: Provide an example of in-direct contact for the portal of entry.

A

Settled particles (face touching)

34
Q

L24: For patients with underlying health conditions, what is their risk of death from flu compared to a healthy person?

A

18x more likely to die

35
Q

L24: Provide examples of susceptible hosts for flu.

A
  • Children aged 2-5;
  • Unvaccinated;
  • Elderly;
  • Pregnant;
  • Patients with underlying conditions.
36
Q

L89: How do local anaesthetics work?

A
  • Stop nerve conductions by blocking the voltage-gated Na+ channels;
  • Prevents Na+ influx;
  • ## Blocks AP generation and propagation;
37
Q

L89: What order of neutrons do LAs work on?

A

First order (peripheral nervous system), do not interfere with CNS

38
Q

L89: What are the different connective tissue layers of a neuron (outer to inner)?

A
  • Epineurium;
  • Perineurium;
  • Endoneurium.
39
Q

L89: What effects the rate at which nerve axons are anaesthetised from a site of injection?

A
  • Proximity to site;

- Number of membranes it has to pass.

40
Q

L89: After nerves are anaesthetised, which ones wean off first?

A

The ones that were first to be anaesthatised (usually)

41
Q

L89: What property makes LAs able to cross membranes?

A

Lipophilicity

42
Q

L89: What type of tissue helps to retain LA at the desired site?

A

Fat

43
Q

L89: In what order do different types of nerve fibres anaesthetise?

A
  • Ad;
  • c;
  • Ab;
  • Aa.
44
Q

L89: Why can patients still feel pressures under LA?

A

Aa fibres are last to be anaesthetised - responsible for proprioception (muscle sense)

45
Q

L89: Why is it important to avoid injecting LA into blood vessels?

A
  • LAs block Na+ channels in other excitable tissue, e.g. heart muscle;
  • Can cause bradycardia and hypotension.
46
Q

L89: LAs are organic molecules, what are the three components?

A
  • Aromatic region (hydrophobic);
  • Ester or amide bond;
  • Basic amine side chain (hydrophilic).
47
Q

L89: B.HCl is a term used to present LAs, what does B.HCl stand for?

A

B - base

HCl - hydrochloride

48
Q

L89: In what ‘form’ can LAs cross membranes?

A

Un-ionised

49
Q

L89: In what ‘form’ are LAs active?

A

Ionised

50
Q

L89: Describe the mechanism of action for a LA to cross a membrane:

A
  • Base and hydro dissociate to become diffusible (non-active);
  • Cross membranes as individual ions (B and H+);
  • Once inside neuron, bond to become active.
51
Q

L89: Why are small diameter axons more susceptible to LA block?

A
  • Number of Na+ channels relative to diameter of axon; - Small diameter axons, less Na+ channels to block to prevent action potential.
52
Q

L89: Are myelinated axons more or less susceptible to LA than non-myelinated axons?

A
  • Na+ channels concentrated at the NOR;

- Requires more energy as more channels.

53
Q

L89: It is very rare for patients to be allergic to LAs. If they ‘truly’ are, what component are they usually allergic to?

A

Preservative (as this often changes) or reducing agent

54
Q

L89: Give an example of an ester LA?

A

Benzocaine

55
Q

L89: Give an example of an amide LA?

A
  • Lignocaine (lidocaine);
  • Prilocaine;
  • Articaine;
  • Bupivacaine (surgery).
56
Q

L89: What are the two most common vasoconstrictors used in LAs?

A
  • Adrenaline;

- Felypressin.

57
Q

L89: What are the benefits of vasoconstrictors in LAs?

A
  • Prolong effects of LA;
  • Concentrates one area;
  • Reduces leak of LA;
  • Use of less LA;
  • Bloodless field to work in.
58
Q

L89: What are the disadvantages of vasoconstrictors in LAs?

A
  • Reduced blood flow;

- Sometimes need blood flow (perio/ gingival graft).

59
Q

L89: What receptors do vasoconstrictors in LAs target?

A
  • Adrenreceptors;
  • ADH receptors;
  • B2 receptors (vasodilation);
  • B1 receptors;
  • a receptors (vasoconstriction);
  • Vascular smooth muscle;
60
Q

L89: What receptors does adrenaline target on smooth muscle walls?

A

Alpha receptors (vasoconstriction)

61
Q

L89: Systemically, what receptors does adrenaline have a greater effect on?

A

Beta receptors (vasodilators - to lower TPR)

62
Q

L89: Why do patients sometimes experience palpitations, due to adrenaline?

A

Increase in HR and heart force

63
Q

L89: How are ester type LAs inactivated by the body?

A
  • ‘Washout’ from tissues by blood supply;

- Broken down by tissue esterases.

64
Q

L89: How are amide LAs inactivated by the body?

A
  • ‘Washout’ from tissues by blood supply;

- Broken down by the liver.

65
Q

L89: Before using an amide LA on a patient, what should you check?

A

Medical history of liver health/ disease

66
Q

L89: What does a % solution convert to? e.g. 3% prilocaine

A

3% = 3g/ 100mL = 30mg/ 1mL

67
Q

L89: How much prilocaine does a 2mL, 3% cartridge contain?

A

3g/ 100mL, 30mg/ 1mL, 60mg/ 2mL

68
Q

L89: How are vasoconstrictor strengths expressed in a LA?

A

Ratios: e.g. 1: 80,000 (1 part of adrenaline in 80,000 parts of liquid)

2a. BDS2 BAMS (10 decks)

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