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Medicine 1 > Anatomy - Pneumonia > Flashcards

Anatomy - Pneumonia Flashcards

1
Q

What is volume of distribution?

A

Apparent volume in which drug is dissolved in body = amount in body / conc. = dose / conc. at t=0

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2
Q

What is clearance?

A

Volume of plasma cleared of drug in unit time (ml/min or L/h) = renal + hepatic clearance (eGFR)

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3
Q

What does a first order elimination graph look like?

What is the equation?

A

Rate of elimination = proportional to drug concentration

Ct = C0e-kt

Ct = conc. at t=t

C0 = conc. at t=0

k = rate constant (per minute or per hour)

t = time

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4
Q

What does the rate constant (k) stand for?

A

Fraction eliminated per unit time = clearance / Vd

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5
Q

How do you work out half-life using equation?

A

t1/2 = loge2 / k

k = loge2 / t1/2

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6
Q

What are the properties of IV infusion?

A

Administration of drug at constant rate (0 order)

Steady state = elimination (first order graph plateau) = infusion rate

Input = output = Css

Maintenance dose = amount removed Infusion rate = clearance X Css

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7
Q

What is aminophylline and its properties?

A
  • Used for severe asthma
  • Bronchodilator
  • Given intravenously
  • Is salt of theophylline (80% of aminophylline is theophylline)
  • Infusion rate = (CL X Css) / 0.8
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8
Q

What does and oral dosing graph look like and its properties?

A
  • Curve = influenced by rate of dissolution and rate of absorption
  • Rise to peak = absorption + elimination
  • After peak = just elimination
  • Functional half-life = prolonged absorption super-imposed on elimination (slow oral)
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9
Q

How do you work out bioavailability?

How do you work out dose given?

A

Bioavailability = F = fraction absorbed = AUC oral / AUC iv

Dose given = amount needed / F

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10
Q

What are the properties of repeated oral dose?

A
  • Each dose is independent of each-other if given far apart enough from each-other
  • Aim = to reach stead-state
  • Takes 5 half-lives (approx..) to reach steady state
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11
Q

What is the dose calculation equation?

What does ‘tau’ stand for?

What does doubling the dose do?

A

tau = dosage interval

Double dose = double concentration

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12
Q

What do you need for designing dosage regimens?

A
  • Measure therapeutic window
  • Loading dose large initial does to rapidly increase plasma conc. to therapeutic window range = target level X V/F
  • Elimination half-life
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13
Q

What are the properties of gentamicin dosaging?

A

Have period where dose is subtherapeutic and below therapeutic window to reduce damage done to kidneys and ears

Given via IV boluses

+ clearance renally

CL = CLcreatinine

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14
Q

What does the Hartford nomogram for gentamicin llok like and how do you find correct dose?

A

Use sampling

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15
Q

What is anti-microbial chemotherapy and it’s targets?

A

The use of drugs to selectively kill bacteria (and viruses / fungi) without affecting the host.

Targets:

  • Bacterial cell wall
  • Bacterial ribosomes
  • Bacterial folate metabolism
  • Bacterial DNA gyrase

Antibiotics

  • Produced by an organism to attack other organisms eg penicillin

Antibacterials

  • Man-made chemicals
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16
Q

What type of antibiotic are penicillins and what are it’s properties?

A

‘Beta’-lactam antibiotic

  • Inject with enzyme penicillin if suspected meningitis
  • Beta-lactam ring gives chemistry of drug
  • Inhibit bacterial cell wall synthesis à irreversibly bind to a transpeptidase which cross-links peptidoglycans in cell wall
  • Only effective against dividing organisms
  • Bactericidal, causing bacterial lysis
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17
Q

What are the properties of beta-lactamases?

A
  • Secreted by resistant bacteria
  • Deactivates some penicillins
  • Other penicillins are resistant to them
  • Inhibited by clavulanic acid + other agents –> Co-amoxiclav
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18
Q

What are the properties of a penicillin allergy?

A
  • Penicillins are immunogenic
  • Allergic reaction develops upon repeat exposure
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19
Q

What type of antibiotic are cephalosporins and how do they work?

A

‘Beta’-lactam antibiotics

  • Act in similar way to penicillin
  • Inhibit transpeptidases which cross-link peptidoglycan chains
  • Cross-reactivity - penicillin allergy = cephalosporin allergy in small no. of people
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20
Q

How do glycopeptides work and give an example?

A

Vancomycin

  • Inhibit bacterial cell wall synthesis by inhibiting peptidoglycan chain growth
  • Largely bactericidal
  • Used for superbug infections
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21
Q

Give and example of a tetracycline and how do they work and properties?

A

Tetracycline

  • Inhibit protein synthesis by binding to 30S subunit of bacterial ribosome
  • Prevent tRNA binding to acceptor site (A site)
  • Actively accumulate in bacterial cells
  • Are bacteriostatic
  • Decreased use from resistance increase
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22
Q

Give an example of a macrolides and how do they work and properties?

A

Erythromycin

  • Prevent translocation of 50S subunit of bacterial ribosome along mRNA
  • Prevent protein synthesis
  • Are bacteriostatic
  • Used as penicillin alternative for those with allergies
  • Are cytochrome P450 inhibitors and associated with + drug interactions
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23
Q

Give an example of an aminoglycoside and how do they work and properties?

A

Neomycin

  • Irreversibly bind to 30S subunit of bacterial ribosomes, causing misreading of mRNA
  • Interfere with protein synthesis
  • Are bactericidal
  • Used to manage Gram-negative bacteria
  • Complicated use due to toxicity
  • Have complex regimens
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24
Q

Give an example of a quinolone and how do they work?

A

Ciprofloxacin

  • Inhibit bacterial DNA gyrase (topoisomerase ll) and topoisomerase lV
  • Gram-negative bacteria = inhibit supercoiling of bacterial DNA, essential for DNA repair and replication à DNA gyrase is target
  • Gram-positive bacteria = interfere with separation of DNA strands during replication à Topoisomerase lV is target
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25
Q

What is trimethoprim and what are it’s properties?

A
  • Structurally related to folate
  • Is a folate antagonist
  • Inhibits bacterial dihydrofolate reductase which converts folate to tetrahydrofolate
  • Less potent against human form of enzyme
  • Are bacteriostatic
  • Used for UTIs
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26
Q

What are the properties of sulphonamides?

A
  • Analogues of p-aminobenzoic acid (PABA)
  • Inhibit growth of bacteria by competitively inhibiting dihydropteroate synthase (involved in folate synthesis from PABA)
  • Reduction of DNA and RNA precursors
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27
Q

What are the properties of metronidazole?

A
  • Pro-drug that’s activated by anaerobic bacteria to cytotoxic products
  • Damage DNA helical structure, protein and cell membrane
  • Used against anaerobic bacteria and protozoa
  • Can’t drink alcohol
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28
Q

What are the steps of antibiotic selection?

A
  • Guided by sensitivity of organisms
  • Broad spectrum antibiotics
  • Resistance
  • “Complete the course”
  • Allergies
  • Pharmacokinetics:
  • IV for rapid effects
  • Oral route: depends on bioavailability
  • Drug interactions
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29
Q

What is the most important antibiotic feature?

A

Selective toxicity

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30
Q

What are the differences in gram positive and negative bacteria?

A
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31
Q

What are the properties of an upper respiratory tract infection?

A
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32
Q

Who is community acquired pneumonia more common in?

A

Men

Elderly

Alcoholics

Chronic disease sufferers

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33
Q

What are the main symptoms of pneumonia?

A
  • Sputum
  • Coughing
  • Coughing up blood
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34
Q

What microbes cause community acquired pneumonia?

A
  • Conventional bacteria (60-80%)
  • ‘atypical’ bacteria (10-20%) (mycoplasma and legionella)
  • Viruses (10-20%)
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35
Q

What are the steps for community acquired pneumonia investigation?

A
  • Confirm diagnosis
  • Assess disease severity
  • Identify aetiological agent
  • Identify somplications
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36
Q

What tests do you do to confirm diagnosis of CAP?

A
  • Temperature
  • Full blood count
  • U rea, electrolytes and LFT
  • CXR
  • Arterial por capillary blood gases
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37
Q

What are the microbiological investigations for CAP?

A
  • Sputum culture and sensitivity
  • Blood cultures
  • Urine for pneumococcal antigen
  • Investigation for legionella if suspected
  • PCR/immunofluorescence for atypical organisms and viruses
  • Pleural fluid for microscopy, culture and antigen detection
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38
Q

What are the 3 steps for CAP management?

A
  • Correction of respiratory failure
  • Correction of haemodynamic compromise
  • Specific antimicrobial therapy
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39
Q

What tests and values determine the severity of CAP?

A
  • Confusion –> mini-mental test = 8
  • Urea –> > 7mmol/l
  • Respiratory rate > 30 bpm
  • Blood pressure –> sys < 90 mmHg dia < 60 mmHg
  • Older than 65
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40
Q

What are the 3 basis for antimicrobial chemotherapy?

A
  • Assessment of likely pathogen
  • Severity of illness
  • Likelihood of drug resistance
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41
Q

What is the treatment for low severity CAP (score0-1)?

A

Amoxicillin 500mgs qds / 5 days OR doxycycline 200mgs loading them 100mg od

Unable to take oral therapy = iv amoxicillin 500mgs tds OR iv cefuroxime 1.5g tds if mild penicillin allergy

Sever penicillin allergy = ciprofloxacin 400mgs bd + vancomycin

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42
Q

What is the treatment for moderate severity CAP (score 2)?

A

Amoxicillin 500mgs – 1g tds 7 days + clarithromycin 500mgs bd for 7 days OR doxycycline 200mgs loading then 100mg od

Unable to take oral therapy = iv amoxicillin or benzylpenicillin (cefuroxime 1.5 g tds if mild penicillin allergy) + iv clarithromycin 500 mgs bd

If severe allergy to penicillin ciprofloxacin 400 mgs bd + vancomycin

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43
Q

What is the treatment severe CAP (score >3)?

A

Co-amoxiclav 1.2 g tds +clarithromycin 500 mgs bd iv for 10 days

If severe allergy to penicillins or likely MRSA:

Levofloxacin 500 mgs bd + vancomycin 1 g bd

Treat for 10 days - extending to 14-21 days for legionella, staphylococcal or Gram neg pneumonia

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44
Q

What are the properties of hospital acquired pneumonia?

A
  • HAP is defined as pneumonia that occurs more than 48 hrs after hospital admission or within 10 days of a previous admission
  • HAP is the second most common infection acquired in hospital
  • Candidate organisms include: E.coli, Klebsiella spp., proteus spp., S. pneumoniae, S. aureus (MSSA or MRSA)
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45
Q

What are the treatments for mild and severe HAP?

A

Mild: co-amoxiclav 625 mgs (as co-amoxiclav 375 mgs plus amoxicillin 250 mgs) po tds

Severe: augmentin 1.25 g iv tds plus gentamicin 5 mgs/kg stat

46
Q

Whats puts people at higher risk of MRSA?

A
  • Previous MRSA infection
  • Long-term urinary catheter
  • Treated as inpatient within last 6 months
  • Resident of nursing home with skin breaks
  • Indwelling line
47
Q

What is the treatment for aspiration pneumonia?

A

Co-amoxiclav 625 mg po tds OR co-amoxiclav 1.2 g tds iv plus gentamicin 5 mgs/kg iv if ?MRSA

If allergic to penicillins levofloxacin 500 mgs po od + metronidazole po 400 mgs tds for 5 – 7 days

48
Q

When does mycoplasma pneumonia usually occur and treatment?

A
  • Young patient
  • Long prodrome
  • Patchy consolidation on CXR
  • Prominent extra-pulmonary disease
  • Use tetracyclines for at least two weeks
49
Q

When does legionellosis pneumonia usually occur and treatment?

A
  • Severe CAP? outbreak
  • Multi-lobe involvement on CXR
  • Hyponatraemia
  • Focal neurological disease
  • Check legionella antigen and use high dose macrolide (up to 4 g erythromycin per day) with rifampicin 600 mgs bd
50
Q

When does S.aureus pneumonia usually occur and treatment?

A
  • CAP during an influenza outbreak may be caused by S. aureus
  • Flucloxacillin at a dose of 2 g iv qds must be added to standard regimens
  • PVL S. aureus in young previously healthy cause of necrotising haemorrhagic pneumonia
51
Q

What are the properties of mycobacterium tuberculosis?

A
  • Obligate aerobes - grow in tissues with a high O2 content
    • (i.e. the lungs).
  • Facultative intracellular pathogens - usually infecting mononuclear phagocytes (e.g. macrophages).
  • Slow growing (generation time of 12 to 18 hours; 20-30 minutes for Escherichia coli).
  • Hydrophobic - high lipid content in the cell wall. Less permeable to usual bacterial stains (e.g. Gram stain).
  • Known as “acid-fast bacilli” because, once stained, the cells resist decolourisation.
52
Q

What is the pathophysiology of TB?

A
  • TB is spread by airborne droplet nuclei (1-5 mm).
  • Nuclei can remain airborne after coughing for several hours.
  • Droplets are inhaled, lodge in alveoli and the organism is taken up by alveolar macrophages.
  • Slow replication and spread (via lymphatic system) to hilar lymph nodes.
53
Q

How does TB infection develop once in a human?

A
  • In most individuals – cell-mediated immunity (CMI) develops 2-8 weeks after infection (associated with the development of a positive tuberculin skin test).
  • Activated T lymphocytes and macrophages form granulomas that limit further replication and spread.
  • Bacterial cells remain (sometimes viable) in centre of necrotic ‘caseating’ granulomas.
  • Most individuals are asymptomatic (latent infection) and never develop active disease (unless a subsequent defect in CMI occurs).
54
Q

What are these parts called?

A
55
Q

What are the clinical features of TB?

A
  • Non-specific –> fever, weight loss, night sweats
  • Respiratory symptoms –> cough, SOB, haemoptysis, chest pain
  • Mainly pulmonary
  • Extrapulmonary more common in HIV
  • CNS disease –> TB meningitis, space-occupying lesions (tuberculomas)
56
Q

What are the TB sites of infection in skin / soft tissue?

A
  • Commonest type of non-pulmonary disease
  • Cervical lymphadenitis (firm, discrete, painless lymph nodes)
  • Diffuse swelling in neck (‘cold’ abscess)
57
Q

Where in bone and joints does TB mainly infect?

A

Spine

Pott’s disease

58
Q

What are the effects of TB infection in genitourinary tract?

A
  • Prostatitis, orchitis, or renal lesions
  • May cause infertility in women
  • Sterile pyuria (WBC in urine but no growth)
59
Q

What is disseminated disease in TB and its properties?

A

Many organs involved simultaneously – ‘miliary’ pattern MAY be seen on CXR

May result from primary progressive disease or reactivation of latent infection

60
Q

What is the arrow pointing at?

A

Cerebral tuberculoma

61
Q

What type of TB is this?

A

Miliary TB

62
Q

What samples are required for TB diagnosis?

A
  • Sputum (requires decontamination)
  • Bronchoalveolar lavage
  • Pus / tissue
  • Urine –> 3 X 24 hour collection
  • Cerebrospinal fluid
63
Q

What stain is used for TB diagnosis and why?

A

Zeihl-Neelsen stain

Rapid, cheap, simple, robust, moderate specificity and sensitivity

64
Q

What are the properties of TB cultures?

A
  • Slow –>2-8 weeks
  • Requires specialised media (Lowenstein-Jensen slope in shatter-proof glass)
  • Performed in category 3 facility
65
Q

What are the properties of rapid TB cultures?

A
  • 1-2 weeks
  • Liquid media (Kirchner’s liquid medium)
  • Automated system (MGIT)
66
Q

What is the treatment for pulmonary TB?

A
  • Initial phase: 2 months of 4 drugs (rifampicin, isoniazid, pyrazinamide, ethambutol)
  • Continuation phase: 4 months of rifampicin and isoniazid
  • If resistance is suspected, 5 drugs may be used initially. For confirmed resistant strains, longer courses are required with second line agents
67
Q

What are the properties of URTIs and examples of some?

A

Very common; often viral in aetiology.

Secondary bacterial (or fungal) infections are common.

  • Rhinitis
  • Otitis media
  • Sinusitis
  • Pharyngitis
  • Laryngitis
  • Epiglottitis.
68
Q

What are examples of coryza (common cold) viruses?

A
  • Rhinoviruses (>100 serotypes)
  • Parainfluenza viruses 1-4
  • Coronaviruses
  • RSV
  • Adenoviruses
  • Enteroviruses (coxsackie, echo)
  • May predispose to 2o bacterial infection
  • sinusitis, otitis, bronchitis, pneumonia
69
Q

What is pharyngitis and what can cause it?

A

Tonsillitis

Adenoviruses

Strep pyogenes

70
Q

What is infectious mononucleosis and its symptoms?

A

Syndrome

  • Pharyngitis, lymphadenopathy (cervical, generalised), fever, malaise
  • Atypical mononuclear cells in peripheral blood
  • Epstein-Barr virus, cytomegalovirus, toxoplasmosis, HIV seroconversion
71
Q

What are the properties of epiglottitis?

A
  • Bacterial
  • Potentially life-threatening
  • Haemophilus influenza type b
72
Q

What are the proeprties of croup?

A
  • Young children
  • Inspiritory stridor from narrowed airways
  • Viruses (paraflu, RSV)
73
Q

What are examples of lower respiratory tract infections?

A
  • Influenza viruses
  • Respiratory syncytial virus
  • Rare:
    • Varicella zoster virus (adults)
    • Measles virus (giant cell pneumonia)
    • Cytomegalovirus (immunocompromised)
    • MERS (and SARS) coronaviruses
74
Q

What are the genetic properties of influenza?

A
  • Segmented -ve ssRNA genome
  • 8 segments encode 11 proteins
  • TYPES – A, B, or C
    • On basis of internal proteins NP, matrix
  • SUBTYPES – A only
    • On basis of surface proteins, HA, NA
    • 16 HA, 9NA known – each differs by >20% sequence
  • Respiratory tract symptoms (rhinitis) and systemic symptoms (fever)
75
Q

What are these parts called?

A
76
Q

What is the pathogenesis of influenza?

A
  • Pneumotropic virus –> infects cells lining RT down to alveoli
  • Infection = lytic –> strips off respiratory epithelium
  • Removes 2 innate defence mechanisms –> mucus secreting cells and cilia
  • Interferon production –> circulates in blood (virus doesn’t)
77
Q

Why do these same cell types appear different?

A

First = exfoliated respiratory epithelial cells

Second = flu infected respiratory epithelial cells

78
Q

What are the complications of influenza?

A
  • Pneumonia
  • Primary viral pneumonia: mononuclear cell infiltrate
  • Secondary bacterial pneumonia: PMNL infiltrate
  • Cardiovascular complications (myocarditis)
  • CNS complications (encephalitis)
79
Q

Whos is at risk of influenza?

A
  • Risk groups identified incl. patients with pre-existing
    • Lung disease
    • Cardiac disease
    • Renal disease
    • Endocrine disease
    • Immunodeficiency
    • Liver disease
  • Anyone >65 years
  • Pregnant women
  • Children
80
Q

What is the epidemiology of influenza?

A
  • Annual seasonal (winter) epidemics
  • Unpredictable worldwide epidemics with high mortality
  • Pandemics and inter-pandemic epidemics
  • Caused by antigenic drift and antigenic shift
81
Q

What are the properties of antigenic drift?

A
  • Occurs in both influenza A and B viruses
  • Random spontaneous mutation in viral genes encoding HA and NA –> 1% aa sequence change
  • Mutations clustered within key epitopes in HA and NA ie true Darwinian evolution Accounts for interpandemic epidemics ie year-on-year recurrence of infection
82
Q

Where are influenza A reservoirs?

A
  • Wild aquatic shore birds
  • Humans and animals
  • Pigs
83
Q

What are the properties of antigenic shift?

A
  • Occurs only in influenza A viruses
  • Genetic reassortment between human and non-human viruses leading to new subtypes
  • >20% aa differences, hence emergence of new pandemic strains against which the population has no pre-existing immunity
84
Q

What is respiratory syncytial virus?

A
  • Enveloped paramyxovirus
  • – ve ssRNA encodes 9 polypeptides incl. 2 surface proteins F,G
  • Highly seasonal infection (winter)
  • Extremely common - global infection by age 2
85
Q

What are the properties of RSV?

A
  • Causes LRTI in infants – bronchiolitis, pneumonia
  • High hospitalisation rates
  • Low mortality (<0.5%) unless
    • congenital heart disease
    • congenital lung disease (incl prematurity)
    • immunodeficiency (congenital or acquired)
  • Requires rapid diagnosis and appropriate infection control measures
  • Re-infection occurs throughout life - antigenic drift
86
Q

What is the tunica intima?

A

Innermost layer consisting of:

  • A simple squamous epithelium
    lining the lumen
  • An adjacent layer of connective tissue
87
Q

What is the tunica media?

A

Middle layer consisting of:

  • Smooth (or cardiac) muscle, mainly circular
  • Varying amounts of elastin, mainly in sheets in the interspersed connective tissue
88
Q

What is the tunica adventitia?

A

Outermost layer consisting of:

  • Connective tissue with varying amounts of interspersed elastin fibres

and smooth muscle cells, mainly longitudinal

89
Q

What are these 3 layers?

A

Red = endocardium - tunica intima

Orange = myocardium = tunica media

Black = epicardium = tunica adventitia

90
Q

What are the properties of the tunica media?

A

Much thicker than intima

Thick with spirally arranged smooth muscle cells (dark brown) and elastic lamellae, sheets of elastin (black wavy lines)

91
Q

What are the properties of the tunica adventitia?

A

Mostly loose connective tissue with vasa vasorum (=blood vessels of the blood vessels)

No elastic lamellae, just a few smooth muscle cells.

Bordered by a simple squamous epithelium

92
Q

What are the properties of elastic arteries?

A

Close to the heart

Experience plulsating blood flow which is met by the lamellae of elastin woven into the media

93
Q

What are the properties of muscular arteries?

A

Help distribute the bulk of blood to the site of need, for example to the leg muscles when cycling and to the intestinal system during resting periods such as sleep

94
Q

What are the properties of tunica intima of muscular artery?

A

Simple squamous epithelium (endothelium) bordering the lumen

Internal elastic membrane forming border to media

Loose connective tissue in between

All in folds because the smooth muscle of the media has contracted during tissue processing

95
Q

What are the properties of tunica media in muscular artery?

A

A thick layer of circumferentially arranged smooth muscle cells with interspersed collagen and very few elastic lamellae

Bordered by the sheet-like external elastic membrane which starts to disappear more distally

In sections from routinely processed samples, the muscle cells are fully contracted, which generates nicely round cross sections

96
Q

What are the properties of tunica adventitia in artery?

A

More longitudinal strings of elastin, fading out in the periphery

Mostly connective tissue, often loose

Border into adjacent connective tissue structures not defined

Recogniseable vasa vasorum.

97
Q

How do you spot an artery or arteriole from a cross section?

A

Perpendicular pattern

98
Q

What is the main site of blood pressure regulation?

A

Arterioles

99
Q

What are the properties of arterioles?

A
  • Site with + resistence
  • No internal elastic membrane
  • Don’t require vasa vasorum as can rely on diffusion
100
Q

What is this pointing at?

A

Capillaries

101
Q

What are these parts called?

A
102
Q

What is the difference between continuous and fenestrated capillaries?

A

Continuous = lumen lined by continuous, uninterrupted layer of single endothelial cells, linked by cell-cell contact of tight and adherens junctions

Fenestrated = numerous pores in endothelial cells and barrier to interstitium is basement membrane

103
Q

What are sinusoids?

A
  • Found in liver and spleen
  • Beds of wide capillaries with diameters of several erythrocytes
  • Holes in endothelial cells and basement membranes, allowing plasma to reach cells fast
104
Q

What is the function of venules and small veins and their properties?

A

Collect blood from capillary beds

  • 10-100 um diameter
  • Large lumen
  • No muscle cells
  • Tunica intima often pericytes
  • No media or barely any adventitia
105
Q

What is the muscle pump?

A

‘Second heart’

rhythmic muscle contraction pushing venous blood toward heart, due to valves

106
Q

What are vein-artery-vein triplets?

A

Muscular arteries have vein on either side so artery compression slightly compresses veins, driving blood to heart

107
Q

What is a portal system?

A

Connects two capillary beds (i.e. portal vein)

108
Q

What is an anastomosis?

A

Direct link between an artery or vein, without capillary bed inbetween

Arterial-arterial (arteries around knee)

Arterial-venous (skin circulation)

Venous-venous (superficial hand veins)

109
Q

What is the funciton of the lymphatic system?

A

Brings fluid from leaky capillaries back into blood circulation

Have no erythrocytes

110
Q

Which antibiotic types inhibit cell wall synthesis?

A

Beta lactams

Glycopeptides

111
Q

Which antibiotics inhibit protein synthesis?

A

Macrolides

Aminoglycosides

Tetracylines

112
Q

Which antibiotics interfere with DNA synthesis and replication?

A

Sulphonamides

Quinolones

Diaminopyridamines

Medicine 1 (28 decks)

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