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Year 2 > The Public - Semester 1 > Flashcards

The Public - Semester 1 Flashcards

1
Q

What is Public Health?

A

Prevention and management of disease/health condition through health promotion

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2
Q

What is epidemiology?

A

The study of the incidence, distribution and possible control of a disease

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3
Q

What is pathogenicity?

A

The ability of a microorganism to grow within an infected host - usually causes harm to the host

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4
Q

Define commensalism and symbiosis

A
  • Commensalism - Allowing microorganism growth without causing damage to the host (co-existence)
  • Symbiosis - A partnership in which the host and microorganism both benefit
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5
Q

What is the difference between opportunistic and obligate pathogens?

A
  • Opportunistic pathogens can survive outside of a host and be transmitted without causing disease
  • Obligate pathogens must infect a host and cause disease in order to survive
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6
Q

What are the methods of elimination of a pathogen?

A
  • Physical or internal removal
  • Starvation of nutrients preventing growth
  • Immune response
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7
Q

What are the methods of accumulation for a pathogen?

A
  • Adherence to host cells or tissues
  • Obtaining nutrients from host or other pathogens
  • Proliferation in the body
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8
Q

What affects human-pathogen interactions?

A
  • Host factors (e.g. health status)

- Pathogen factors (e.g. type of pathogen)

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9
Q

What are the two types of disease transmission?

A
  • Vertical (from mother to child)

- Horizontal (between members of a population)

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10
Q

What is an incubation period?

A

The period between infection and disease where the microorganism can grow

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11
Q

Define virulence

A

A measure of the pathogenicity of a microbe

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12
Q

What is the difference between disease and infection?

A
  • Infection - The establishment of a pathogen in the body

- Disease - Damage or injury that impairs host function

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13
Q

How can an infection develop?

A
  • Attachment to epithelial cells
  • Invasion of cells of the mucous membrane
  • Penetration of the epithelial cells allowing invasion of deeper tissues
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14
Q

Describe the microbiota of the oral cavity

A
  • High nutrient concentration provides a desirable environment for microorganisms
  • Acidic glycoproteins on the tooth surface allows bacterial colonisation, causing dental plaque
  • Bacteria produce acid the decalcifies tooth enamel and causes decay
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15
Q

Describe the anatomy and microbiota of the GI tract

A
  • Consists of stomach, small intestine and large intestine

- Natural gut flora responsible for absorption of nutrients from digested food

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16
Q

Describe the anatomy and microbiota of the respiratory tract

A
  • Upper RT = sinuses, nasopharynx, pharynx, oral cavity, larynx
  • Lower RT = Trachea, bronchi, lungs
  • If individual is healthy, only upper RT will be colonised
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17
Q

Describe the microbiota of the urogenital tract

A
  • Bladder is sterile but bacteria may be present in the urethra
  • If bacteria in urethra multiplies and becomes pathogenic it can cause an infection (e.g. UTIs)
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18
Q

How are acidic conditions maintained in the vagina?

A
  • Presence of Lactobacillus acidophilus

- Glycogen fermented to lactic acid which maintains acidic conditions

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19
Q

Explain the concept of chemotherapy and its relevance to antimicrobials

A
  • Chemotherapy - Selective toxicity to the invader
  • Closer the invading cells are to our cells makes selective toxicity harder
  • Bacterial differences make infections caused by them much easier to treat
  • Viruses and cancers are difficult to treat due to similarities to our cells
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20
Q

How was a treatment for Syphilis developed?

A
  • Paul Ehrlich - Using principles of selective toxicity to develop a treatment for Sleeping Sickness
  • Atoxyl (first development) ended up being a lead compound for Salvarsan which could be used to treat syphilis
  • Development of Neosalvarsan - More hydrophilic and less toxic than Salvarsan
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21
Q

What is Salvarsan and how does it work?

A
  • Pro Drug - Decomposes to oxophenarsine

- Oxophenarsine reacts with thiol groups on proteins causing denaturation

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22
Q

How is the therapeutic index of a drug related to selective toxicity?

A

Measurement between a drug being therapeutic and toxic (may be therapeutic to humans but toxic to microorganisms in a specific dose range)

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23
Q

What is Vancomycin used for?

A

Treatment of Strep. pneumoniae and MRSA infections

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24
Q

What are common drug targets in a bacterial cell?

A
  • Cell wall and membrane
  • Ribosomes (transcription and protein synthesis)
  • DNA synthesis
  • Metabolism
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25
Q

How do pathogens cause disease?

A
  • Virulence factors

- Toxicity and invasiveness can determine whether an infection is local or systemic

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26
Q

Describe a test for virulence and why it applies to 50% of a test group

A

LD50 - The amount of agent required to kill 50% of a test group

50% instead of 100% because the pathogen numbers for 100% are similar for all organisms

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27
Q

Define attenuation

A

Alteration of favourable growth conditions of an organism, resulting in reduced virulence

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28
Q

Define toxicity

A

A toxin released by an organism which inhibits host cell function or kills the cell - can be systemic

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29
Q

Define invasiveness

A

Growth of an organism to a density the inhibits normal host function and causes damage

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30
Q

In which systems can a pathogen invade the body?

A

Circulatory and lymphatic systems

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31
Q

Give two examples of anatomical virulence factors of a bacterial cell

A
  • Capsule - Protects bacterial cell and enhances ability to causes disease
  • Pili - Allows attachment of bacteria to host cells or is involved in DNA exchange between bacterial cells
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32
Q

What type of pathogen causes diphtheria, how does it present and how does it cause disease?

A
  • Non-Invasive Pathogen
  • Pseudomembrane on throat
  • Production of AB toxin inhibits EF2 which prevents protein synthesis and kills the cell
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33
Q

What type of pathogen causes whooping cough, how does it present and how does it cause disease?

A
  • Non-Invasive Pathogen
  • Violent cough, mucous present in throat
  • Produces pertussis exotoxin, tracheal cytotoxin and invasive adenylate cyclase toxin
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34
Q

What type of pathogen causes cholera, how does it present and how does it cause disease?

A
  • Non-Invasive Pathogen
  • Infects small intestine causing rice water stools
  • Cholera toxin increases adenylate cyclase activity which causes excess salt and water movement into the lumen of the small intestine, death by dehydration
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35
Q

Give an example of a disease caused by a partially invasive pathogen and describe it

A
  • Shigellosis
  • Blood and pus in diarrhoea
  • Shiga toxin produced
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36
Q

How do primary invasive pathogens spread?

A

Enter lymphatic system from a primary infection site

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37
Q

Give an example of a disease cause by an invasive pathogen and describe it

A
  • Enteric Fever (Typhoid)
  • Infects small intestine and then enters system through epithelial cells
  • Causes constipation/diarrhoea and a fever
  • Spread through contaminated people/foods
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38
Q

Give an example of disease without colonisation

A

Food Poisoning

  • Neurotoxin produced from Clostridium botulinum
  • Entertoxin produced from Staphylococcus aureus
  • Emetic and enterotoxins produced by Bacillus cereus
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39
Q

Describe the structure and function of gram positive and negative cell walls

A
  • Positive: Thick layer of peptidoglycan outside cell membrane, teichoic acids in membrane (maintains iodine stain)
  • Negative: Two membranes with a thin layer of peptidoglycan in between
  • Function: Shape and structure, prevents rupture due to osmotic pressure
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40
Q

Why is it difficult to stain Nocardioform bacteria?

A
  • Gram positive BUT

- Peptidoglycan covalently linked to arabinogalactan which is esterified to lipids, making it resistant to staining

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41
Q

Describe the structure of peptidoglycan

A
  • Alternating NAM and NAG residues
  • Branched peptide chains
  • Peptide chains cross link to form peptidoglycan sheets
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42
Q

Describe the structure and function of the Beta Lactams

A
  • Lactam ring present in structure
  • Possibly constructed from valine, cysteine and phenylalanine residues
  • Lactam ring binds transpeptidase/carboxypeptidase enzymes to prevent cross-linking in the cell wall
  • Cell wall weakened causing cell to rupture
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43
Q

What four factors affect the efficacy of a Beta Lactam?

A
  • Ability to penetrate cell wall
  • Affinity to peptidase enzymes
  • Resistance to stomach acid
  • Bacterial resistance
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44
Q

What are the 5 main penicillins and how susceptible are they to Beta Lactamases?

A
  • Amoxicillin and Penicillin G - Susceptible to Beta Lactamase degradation
  • Ampicillin - Resistant to class 1 Beta Lactamases
  • Methicillin and Flucloxacillin - Resistant to all Beta Lactamases
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45
Q

What are the generations of Cephalosporins?

A
  • 1st, 2nd and 3rd
  • 1st not widely used anymore
  • Gram negative activity
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46
Q

What are carbapenems?

A
  • Broad spectrum beta lactam antibiotics

- Resistant to beta lactamases

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47
Q

What are monobactams and which one is in use?

A
  • Gram negative beta lactams

- Only aztreonam in use

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48
Q

Describe the structure and mechanism of action of Vancomycin

A
  • Glycosylated structure made of amino acids
  • Non-ribosomal peptide
  • Crystal structure fits between peptidoglycan sheets, preventing cross-linking
  • Cannot penetrate gram negative cell wall therefore only exhibits gram positive action
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49
Q

Give an alternative to Vancomycin

A

Teicoplanin - A glycopeptide

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50
Q

How does immunology help us understand drug mechanisms?

A

Drugs generally work synergistically with the immune system for an effective response

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51
Q

What are the benefits and disadvantages of the immune system?

A
  • Benefits: Protection, removal of infected cells

- Disadvantages: Discomfort as a result of inflammation, damage to host cells (autoimmunity)

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52
Q

What is the difference between the innate immune system and the adaptive immune system?

A
  • Innate: Rapid, first line of defence but does not vary between pathogens
  • Adaptive: Slower activation but initiates a specific response to each pathogen. Response stored in immunological memory for a faster secondary response
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53
Q

List 4 innate defence mechanisms

A
  • Anatomical and physiological barriers
  • Phagocytosis
  • Vasodilation
  • Increased capillary permeability
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54
Q

How does the epithelia protect the body from infection?

A
  • Prevents entry of bacteria

- Locally produced antibiotics and intraepithelial lymphocytes kill bacteria at the surface

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55
Q

What are the components of the innate immune system and what are their functions?

A
  • Lysozymes - Split the cell wall of bacteria
  • Acute Phase Proteins - Opsonization, attraction of phagocytes, increased blood flow
  • Complement System - Opsonization
  • Interferons - Antiviral resistance
  • Macrophages - Engulf and break down cells to present them to the immune system
  • Natural Killer Cells - Recognise changes in cell surface of infected cells
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56
Q

What are the granulocytic cells of the immune system?

A

Cells with a multi lobed nucleus

  • Neutrophils: Destruction through lysosomes
  • Basophils: Contains granules containing toxic chemicals which are secreted when in contact with a microorganism, release of histamine in allergic reactions, bind complements C3a, C3b and C5a
  • Eosinophils: Release toxins from crystalloid granules at the site of parasitic infection/allergic reaction
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57
Q

What are the monocytes cells of the immune system?

A

Cells with one large nucleus

  • Macrophages - Breakdown cells and present antigens to immune system, repair damaged tissues, remove infected cells
  • Dendritic Cells - Bring antigen to lymphoid organs
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58
Q

How do NK cells know which host cells are infected?

A
  • Virus suppression of MHC Class 1

- MHC Class 1 is expressed on healthy cells and stimulates inhibitory receptor of NK cells

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59
Q

What is the complement pathway?

A
  • Mast cells are activated causing vasodilation and increased capillary permeability to bring immune cells to the site of infection
  • Phagocytes then engulf and present microorganisms for opsonisation
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60
Q

List four evasion mechanisms of pathogens

A
  • Resistance to phagocytosis
  • Resistance to the complement pathway
  • Resistance to reactive oxygen intermediates in phagocytes
  • Resistance to locally produced peptide antibiotics
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61
Q

How does immunological memory work?

A

Structure of antigen and antibody produced is stored in the immunological memory, faster antibody production if infected again

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62
Q

What are the cells of the adaptive immune system and what are their functions?

A
  • Th Cells: Recognise antigens presented on MHC class 2 (type 1, cell mediated immunity, type 2, humoral immunity)
  • Tc Cells: Recognise antigen on MHC class 1, triggering apoptosis of the infected cell
  • B lymphocytes: Differentiate to plasma cells which produce antibodies (stimulated by cytokines)
  • Interactions between T and B cells ensure correct antibody is produced
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63
Q

Describe the structure and function of antibodies

A
  • 2 light and 2 heavy peptide chains
  • N terminal binds to antigen and C terminal binds to specific immune cell
  • Functions include opsonisation, neutralisation, complement activation and antibody-dependent cytotoxicity
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64
Q

What increases in a secondary immune response?

A
  • The speed of response

- The antibody titre

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65
Q

What are vaccines and why are they used?

A
  • A suspension of a dead, attenuated or modified microorganism
  • Provide immunological memory for a disease without contracting it
  • Prophylaxis
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66
Q

What are the three characteristics of vaccinations?

A
  • Immunogenicity: Ability to induce antibodies
  • Efficacy: Reduction in incidence between those who have been vaccinated and those who haven’t
  • Effectiveness: The ability of a vaccine to protect a community
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67
Q

Describe the 5 different types of vaccines

A
  • Killed Virulent Organism: Pathogen killed but antigen intact
  • Live Attenuated: Strain doesn’t cause disease but still elicits an immune response
  • Modified Toxins: Toxin treated with heat/chemicals, no symptoms experienced but immune response is triggered
  • Isolated Antigens: Antigen injected to elicit immune response
  • Genetically Engineered Antigens: Antigen is isolated and genetically engineered
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68
Q

What affects the response to a vaccine?

A
  • Antigen content (e.g. live vaccines have higher content)
  • Protein content (results in increased antibody content)
  • Adjuvants present
  • Type of antigen
  • Dosage intervals - Longer intervals = more MHC interaction
  • Genetics
  • Age
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69
Q

Describe the structure of bacterial ribosomes

A
  • About 55 proteins and 3 RNA strands

- Up to 30% of dry cell weight

70
Q

Why are ribosomes a good antibacterial target?

A
  • Up to 40% of total energy consumption is from protein synthesis
  • Even slow growing cells require protein synthesis so it targets all bacterial cells
71
Q

What are tetracyclines and how do they work?

How are bacteria resistant?

A
  • Synthesised from acetate by various Streptomyces
  • Binds nucleic acids and proteins but ribosomal inhibition is the main inhibitor of cell function
  • Usually cell membrane modifications cause resistance but mutations in the S10 ribosomal protein also cause resistance (prevent binding)
72
Q

Give some examples of tetracyclines and their indications

A
  • Chlortetracycline: Feline conjunctivitis
  • Oxytetracycline: Acne, Foulbreed in honey bees
  • Demeclocycline: Lyme Disease
  • Doxycycline: Prophylaxis of malaria
  • Lymecycline: Acne (more soluble than tetracycline)
  • Minocycline: Treatment of Neisseria meningitis infections
73
Q

Describe the structure and function of aminoglycosides

A
  • Several sugar rings + min. one amino group
  • Bind to 16S RNA in the 30S ribosomal subunit, preventing aminoacyl-tRNA binding to A site
  • Gram negative action, appears to disrupt cell wall
74
Q

How does tobramycin work?

A

Binds to both ribosomal subunits to prevent them combining

75
Q

Give some examples of aminoglycosides and the diseases they treat

A
  • Streptomycin - TB
  • Tobramycin - Pseudomonas aeruginosa
  • Gentamycin - Pseudomonas aeruginosa (less preferred)
  • Amikacin (Kanamycin derivative) - Hospital acquired gram negative infections
  • Paramomycin - Visceral and cutaneous leishmaniasis
76
Q

What type of drug is Linezolid and what is its method of action?

What is it used for?

A
  • Oxazolidinone
  • Binds to 23S RNA in 50S subunit, preventing 30S subunit binding
  • Secondary treatment of gram positive infections and MRSA infections
77
Q

What are macrolides used for and what is their mechanism of action?

A
  • Gram positive infections
  • Deep seated infections
  • Inhibit protein synthesis so can be used as a penicillin alternative - exit tunnel blocked
78
Q

What enzyme metabolises erythromycin and what can this result in?

A
  • CYP3A4

- Drug interactions

79
Q

What happens when macrolides are taken with food and why?

A
  • Can experience nausea, vomiting, diarrhoea

- Macrolides are gut motility agonists

80
Q

What is the difficulty of using macrolides in paediatric preparations?

A

They have a bitter taste which is not easily masked

81
Q

What is the difference between first and second generation macrolides?

A
  • More acid resistant
  • More hydrophobic
  • More favourable pharmacokinetics
82
Q

Give an example of a ketolide

A

Telithromycin

83
Q

How have bacteria developed resistance to macrolides?

A
  • Modification of L22 protein (exit tunnel structure)
  • Macrolide efflux pumps
  • Methylation of adenine 2058 in 23S RNA
84
Q

What is convergent synthesis?

A

The process of making a multi-step synthesis more efficient

85
Q

What is Chloramphenicol? Describe its structure and explain why it is used topically

A
  • Broad spectrum growth inhibitor produced by fungus
  • Molecule with 2 chiral centres (therefore 4 isomers, only one of which is active)
  • If used internally it can cause aplastic anaemia
86
Q

Give two examples of lincosamides and explain how they work

A
  • Clindamycin
  • Lindamycin
  • Assumed same action as macrolides due to same methylation resistance method
87
Q

What can clindamycin be used for?

A
  • Anaerobic infections (mainly)
  • TSS treatment, in combination with vancomycin
  • Treatment of protozoa infections (in combination with chloroquine/quinine)
88
Q

What is fusidic acid and how does it work?

A
  • Terpenoid produced from fungus
  • Used for treatment of gram positive infections - usually as eye drops but sometimes tablets
  • Binds an EGF-GTP complex which then binds a ribosome, hydrolysis of GTP then prevents the complex from leaving ribosome so protein synthesis is inhibited
89
Q

What are the meninges?

A

Protective membrane surrounding the brain - inflammation of the meninges from infection is meningitis

90
Q

How does meningococcal disease progress?

A
  • Organ failure and death can occur less than 12 hours after showing symptoms
  • Meningococcal septicaemia can cause coagulopathies to form in peripheral tissues
  • Can cause limb loss through gangrene and ischaemia
91
Q

Describe the structure of meningococci bacteria

A
  • Gram negative diplococci

- Capsule, which defines what type of meningococci (12 types but B, C, W, Y are most common)

92
Q

Which form of bacterial meningitis is most common?

A

Meningitis caused by capsular type B

93
Q

How is the meningococcal C vaccine licensed and how was the efficacy tested?

A
  • Licensed on immunological memory

- Efficacy data from HiB conjugate trial

94
Q

What is pneumococcal disease and what are the causes of death?

A
  • Invasive Strep. pneumoniae infection

- Septic shock, empyema and meningitis

95
Q

Describe the structure of Streptococcus bacteria and the form of the vaccines

A
  • Gram positive cocci with a capsule
  • Conjugate Vaccine: (with diphtheria protein) made from capsular polysaccharides from 13 common serotypes
  • Polysaccharide Vaccine: Capsular polysaccharide with 23 serotypes
96
Q

What are the symptoms of haemophilus influenzae type B commonly mistaken for?

A

Bacterial meningitis

97
Q

Describe the characteristics of a Norovirus virion

A
  • Single stranded RNA
  • No envelope
  • Low infectious dose - less than 10 virions
  • Variable
  • Extremely stable to temperatures, disinfection and high sugar concentrations
98
Q

What is gastroenteritis?

A

‘Winter vomiting virus’ caused by a norovirus

99
Q

What are the symptoms of norovirus and how long do they last?

A
  • Nausea and vomiting
  • Watery diarrhoea
  • Abdominal cramps
  • Headaches
  • Slight fever
  • Myalgia or malaise

Last around 72 hours - short term

100
Q

How is norovirus transmitted?

A
  • Direct contact

- Fecal-oral route

101
Q

What is viral shedding?

A
  • Expulsion of a virus from a cell
  • Movement to another area of the body
  • Shedding into the environment
102
Q

What causes diarrhoea as a symptom of norovirus?

A
  • Small intestine microvilli damaged

- Leads to nutrient malabsorption and enzymatic dysfunction at brush border

103
Q

What causes vomiting in norovirus?

A
  • Changes in gastric motility

- Delayed gastric emptying

104
Q

How is the spread of norovirus prevented?

A
  • Hand washing
  • Ward closures in hospitals following outbreaks
  • General hygiene measures
105
Q

What is the main worry surrounding symptoms of norovirus?

A

Dehydration due to diarrhoea and vomiting - consider dioralyte treatment

106
Q

Why is folate metabolism important?

A
  • Tetrahydrofolate is the active substance but it cannot enter cells
  • 1-carbon metabolism in the body depends on tetrahydrofolate
107
Q

What enzyme is an antibacterial target in the tetrahydrofolate pathway?

A

Dihydropteroate synthetase

108
Q

Why did the diethylene glycol elixir of sulfanilamide cause deaths?

A
  • Diethylene glycol oxidised to toxic aldehyde by liver

- Elixir wasn’t tested in humans before use

109
Q

What was used as a prodrug for sulfanilamide?

A

Protosil - a red dye

110
Q

How does sulphanilamide work and what are its limitations?

A
  • Mimics para-aminobenzoic acid which is used by the enzyme dihydropteroate synthetase in the tetrahydrofolate pathway
  • Difference in pKa means ionisation isn’t ideal and reduces its potential as a drug
111
Q

How are sulfanilamides made more acidic?

A

Substitutions within the molecule

112
Q

Give an example of a substituted sulphanilamide and what it’s used for

A
  • Sulfapyridine
  • Gram positive infections
  • Pneumonia
113
Q

What is folate metabolism essential for?

A
  • DNA/RNA synthesis

- C1 metabolism in mammals

114
Q

Describe the pathway of tetrahydrofolate biosynthesis in bacterial cells, including the enzymes in evolved in each step

A 
- Para-aminobenzoic acid + Pteridine
(Dihydropteroate Synthetase)
- Dihydropteroic Acid
(Dihydrofolate Synthetase)
- Dihydrofolic Acid
(Dihydrofolate Reductase)
- Tetrahydrofolic Acid
115
Q

Why is Trimethoprim an effective antibacterial despite inhibiting the enzyme present in the mammalian pathway (dihydrofolate reductase)?

A

It has a higher affinity for the bacterial enzyme than the mammalian enzyme

116
Q

What are the indications for Trimethoprim?

A
  • Antimalarial

- Treatment of cystitis (UTIs)

117
Q

What type of combination treatment is used for blocking folate metabolism and what effect does it have?

A
  • Sequential blocking

- Has a synergistic effect due to drug resistance

118
Q

Give a combination treatment for the inhibition of the folate pathway and why it is used

A
  • Trimethoprim and Pyrimethamine

- Prevent drug resistance

119
Q

What are the characteristics of Pyrimethamine?

A
  • More hydrophobic
  • More active in protozoa
  • Antimalarial action
120
Q

What is methotrexate used for and how does it work?

Why doesn’t it work in bacterial cells?

A
  • Anticancer treatment or IBD/rheumatoid arthritis at low doses
  • Targets dihydrofolate reductase preventing folate metabolism and therefore DNA synthesis
  • Too polar to act on bacterial cells
121
Q

What are the downsides of methotrexate use?

A
  • Moderately toxic

- If used concomitantly with penicillin, elimination is inhibited (overdose)

122
Q

Why are travel vaccinations important?

A
  • Risk to health of disease present in other areas
  • Prevent spread of infection
  • Check immunisation status of patients
  • Decrease the risk of reintroduction of an eradicated disease
123
Q

How is Cholera spread? Describe the vaccine type and regimen

A
  • Contaminated water, food and faeces
  • Killed cell vaccine, administered orally
  • 2 doses required within 6 weeks
124
Q

What is Hepatitis A and how is it spread? Describe the vaccines

A
  • Viral spread/Faecal-Oral spread
  • Infection of the liver
  • Either short-term immunisation from immunoglobulin vaccine or I/M injection of inactivated virus
125
Q

What is Japanese Encephalitis? Describe the vaccine

A
  • A virus spread through a vector
  • Inactivated virus - aluminium adjuvant enhances immune response
  • I/M administration
126
Q

Describe the meningococcal vaccine and the distribution of meningococcal disease

A
  • Capsular polysaccharides conjugated to proteins

- Different capsular serotypes more prevalent in different parts of the world

127
Q

What is rabies? Describe the vaccine

A
  • Virus transmitted through an infected animal bite

- Embryonated egg inactivated vaccine - Virus for vaccine grown in fertilised hens eggs

128
Q

What is tick-borne encephalitis? Describe the vaccine

A
  • Virus transmitted through infected tick bites

- Inactivated vaccine given as an I/M injection

129
Q

What is typhoid and how is it spread? Describe the vaccines

A
  • Invasive bacterial pathogen
  • Transmitted through contaminated food/water
  • Live attenuated vaccine given as an EC capsule or I/M injection of conjugated polysaccharide
130
Q

What is yellow fever and how is it spread? Describe the vaccine

A
  • Arbovirus
  • Transmitted through mosquitoes (vector)
  • Live attenuated vaccine administered I/M
131
Q

Which malarial parasites are most harmful to humans? How are they transmitted?

A
  • Plasmodium falciparum and Plasmodium vivax

- Female anopheles mosquito

132
Q

Describe the life cycle of the malarial parasite

A
  • Invasion and differentiation in hepatocytes, then released into blood
  • Merozoites multiply in red blood cells
  • Some merozoites differentiate into gametocytes which are taken up by the mosquito
  • Sporozites enter mosquito salivary glands and are then transmitted between humans when bitten
133
Q

What are the symptomatic stages of a malarial infection?

A

Cold stage, hot stage and sweating stage

134
Q

Why is an Artemisinin combination treatment used when the malarial parasite is unknown?

A
  • Artemisinin quickly removes most of parasite

- Partner compound removes remainder

135
Q

How can malaria be avoided?

A
  • Prevention of bites using DEET, long-sleeve clothing and mosquito nets treated with permethrin
  • Prophylactic medication starting 1 week before and finishing 4 weeks after
  • Monitor for symptoms for up to a year after return
  • Avoid travelling in pregnancy
136
Q

What is natural immunity?

A

Immunity that develops when living in an area where the disease is prevalent - this can be diminished when the area is left for a long time

137
Q

What are the two types of chemoprophylaxis used in malaria? Describe them and how they work

A
  • Suppressive Prophylaxis - Directed against red blood cell stages, treatment for 4 weeks
  • Causal Prophylaxis - Directed against hepatocyte stages, treatment for 7 days
138
Q

How is the Zika virus spread and how does it affect pregnancy?

A
  • Transmission through mosquito bites

- Can cause foetal abnormalities

139
Q

Describe the structure of the Herpes virus

A

dsDNA, lipid envelope surrounding virion

140
Q

What do Herpes Simplex 1 and 2 cause and how does it infect a human?

A
  • 1 = Cold sores (oral)
  • 2 = Genital herpes
  • Virus enters through a break in the skin
141
Q

Why is herpes a life long virus?

A
  • Remains in sensory nerve ganglion, evading the immune system
  • Travel back to the body surface can cause reactivation of the virus
  • Reactivation is more common in type 2
142
Q

How can herpes lead to systemic infections?

A

Viraemia can cause the virus to spread systemically

143
Q

How is Herpes Simplex treated and how can it be avoided?

A
  • Aciclovir or similar antiviral

- Use of condoms (HSV2) or wearing gloves when handling lesions caused by HSV1

144
Q

What is the Varicella-Zoster virus and how does it present?

A
  • Herpes virus causing chickenpox and shingles
  • Causes systemic lesions
  • Can cause nerve damage and blindness in eye lesions
145
Q

How is Varicella-Zoster treated?

A

Aciclovir

146
Q

What is the Epstein Barr virus and how does it present?

A
  • Glandular fever caused by a herpes virus
  • Fever, sore throat, fatigue, swollen glands
  • Can remain asymptomatic if controlled by T cells
147
Q

Describe the vaccine for Varicella Zoster and explain why dead vaccines are not as effective

A
  • Live attenuated vaccine given in 2 doses (adults) or a single dose (children)
  • Immunoglobulins produced from dead vaccine eventually broken down by the body
148
Q

What is the function of DNA gyrase?

A
  • Induces left-handed supercoiling in duplex DNA to allow it to fit into the cell
  • Through cutting, passing through and rejoining
149
Q

Why is DNA gyrase a good antibacterial target?

A

Only bacteria supercoil their DNA

150
Q

How do Quinolones work?

A
  • Inhibit A subunit of DNA gyrase, interfering with DNA breakage and joining
  • Broad spectrum activity so can be used if penicillin-resistant
151
Q

What is nalidixic acid and what is it used for?

A
  • First generation quinolone
  • Broad spectrum but mainly gram negative infections
  • UTI treatment
152
Q

What are fluoroquinolones and how do they differ from first generation quinolones?

A
  • Second generation quinolones for treatment of gram positive infections
  • Fluorine substitutes hydrogen in an aromatic ring, difference in electronegativity alters properties
153
Q

What are the indications of Ciprofloxacin?

A
  • Respiratory/Urinary tract infections
  • Gonorrhoea
  • Anthrax
  • Prophylaxis of meningococcal meningitis
154
Q

Describe the pharmacokinetics of Ciprofloxacin

A
  • Good absorption/distribution
  • Renal excretion without modification
  • Modified by CYP1A2 - can lead to interactions with warfarin and caffeine
155
Q

What are the problems relating to Ciprofloxacin?

A
  • Absorption reduced by antacids
  • Concomitant use with NSAIDs causes CNS disturbances
  • Can cause cartilage damage
  • Reactions are more severe than with other antibiotics
156
Q

What are third generation quinolones and what are they used for?

A
  • Broad spectrum antibiotics

- Treatment of Streptococcus infections and UTIs

157
Q

How do DNA strand breakers work?

A
  • Reduction of Nitro groups in the molecule (in low oxygen conditions) causes the formation of radical anions
  • Radical anions extract a hydrogen radical from DNA, causing cleavage of the sugar-phosphate backbone
158
Q

What types of DNA strand breakers are there?

A

Nitrofurans and Nitroimidazoles

159
Q

What is Nitrofurantoin used for?

A

Treatment of UTIs

160
Q

What are nitroimidazoles used for? List one side effect

A
  • Anaerobic bacterial and protozoal infections

- Alcohol intolerance

161
Q

How do C. difficile infections occur and what are the symptoms?

A
  • Strains acquired from hospital
  • Broad spectrum antibiotic treatment diminishes normal microflora, promoting overgrowth of C. difficile
  • Symptoms include diarrhoea, abdominal pain, fever, nausea
162
Q

How are C. difficile infections treated?

A
  • Metronidazole = First line

- Vancomycin

163
Q

How are C. difficile infections prevented?

A
  • Good hygiene practice
  • Use of narrow spectrum antibiotics
  • Patient isolation if suspected C. difficile
164
Q

What are the symptoms of chlamydia and how is it treated?

A
  • Generally asymptomatic
  • Can cause pain during urination and discharge
  • Abdominal pain and irregular bleeding in women
  • Pain in testicles
  • 1g Azithromycin (single dose), 100mg Doxycycline BD 7/7, 500mg Erythromycin BD 14/7
165
Q

What are the symptoms of urethritis (gonococcal and non-gonococcal) and how is it treated?

A
  • Urethral inflammation
  • Discharge (white, yellow or green)
  • Swelling and pain in genitals
  • Pain when urinating
  • Gonococcal Treatment: 1g Azithromycin + Ceftriaxone (500mg I/M or 400mg PO)
  • Non-Gonococcal Treatment: 1g Azithromycin (single dose), 100mg Doxycycline BD 7/7, 500mg Erythromycin BD 14/7
166
Q

What are the causes and symptoms of bacterial vaginosis and how is it treated?

A
  • Overwashing causing a build up of anaerobic bacteria
  • Fishy smell
  • Grey/white discharge
  • 400mg Metronidazole or 300mg Clindamycin BD 7/7
  • Also some vaginal gel formulations
167
Q

What are the symptoms of trichomoniasis and how is it treated?

A
  • Odorous, yellow discharge
  • Pain during urination/sex
  • Itching
  • 2g Metronidazole (single dose) or 400mg Metronidazole BD 7/7
168
Q

What are the symptoms of genital herpes and how is it treated?

A
  • Fluid-filled blisters

- 200mg Aciclovir or Aciclovir 5% cream 5 times a day 5/7

169
Q

What are the symptoms of syphilis and how is it treated?

A
  • First stage: Chancre (painless ulcer, may not be visible)
  • Second stage: Non-irritating rash
  • Third stage: Much later on, can present as neurological symptoms/cardiovascular disease
  • Treated with penicillin or 100mg Doxycycline BD 14/7
170
Q

What are the causes and symptoms of genital warts and how is it treated?

A
  • Caused by HPV
  • Itching but painless
  • Can be recurrent
  • Podophyllotoxin 0.5% applied BD 3/7 or imiquimod 5% applied 3 times weekly
171
Q

What is TB and how is it transmitted?

A
  • Bacterial infection caused by M. tuberculosis
  • Air-bourne, infects lungs
  • Only contagious if showing symptoms

Year 2 (6 decks)

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