Respiratory Block Flashcards

1
Q

Define community acquired pneumonia.

A

Pneumonia occurring in individuals who have been in hospital for <48 hours and are NOT significantly immunocompromised (e.g. CF, bronchiectasis, high level residential care).

Streptococcus pneumoniae, Haemophilus influenzae.

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2
Q

Describe risk factors for Community Acquired Pneumonia.

A

> 50 years, ETOH, smoking, IV drug use, asthmatics, CKD, COPD, dementia, heart failure, immunosuppression, Indigenous, seizure disorders, stroke, recent viral respiratory infection.

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3
Q

Describe some of the most common pathogens responsible for pneumonia.

A

Streptococcus pneumoniae, Klebsiella pneumoniae, Haemophilus influenzae.
Atypicals include:
Mycoplasma pneumoniae, Chlamydia pneumoniae, Legionella species, Staphylococcus aureus.

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4
Q

Which pneumonia causing pathogen is common in the elderly?

A

Mycobacterium tuberculosis.

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5
Q

Which pneumonia causing pathogen is common in the immunocompromised, particularly HIV?

A

Pneumocystis jirovecii or carinii.

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6
Q

Which melioidosis causing pathogen is common in the north of Western Australia?

A

Burkholderia pseudomalleii.

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7
Q

What is a PICO question?

A

Population/Patient
Intervention
Comparison
Outcome

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8
Q

What immunisation regime prevents pneumonia infection?

A

Pneumococcal vaccination, starting at 2 mths of age.
Increased freq. for ATSI individuals and immunocompromise e.g. CSF leak, asplenia, HIV.
Non-ATSI > 70 years, ATSI >50 years.

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9
Q

Name the clinical features of pneumonia.

A
SIGNS:
Fever, sweats, rigors. 
Cough, sputum, haemoptysis. 
Lethargy, anorexia. 
Pleuritic chest pain.
SYMPTOMS:
Febrile
Decreased cap refill. 
Crackles on chest auscultation. 
Consolidation, dull percussion, increased vocal resonance, bronchial breathing.
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10
Q

Which pneumoniae pathogen commonly occurs after influenzae?

A

Staphylococcus aureus.

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11
Q

Which pneumonia pathogen commonly occurs in conjunction with aspiration or alcoholism?

A

Streptococcus pneumoniae, Klebsiella pneumoniae, Acinetobacter and the anaerobes.

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12
Q

Which pneumonia pathogen commonly occurs in close proximity to birds?

A

Chlamydia psittaci.

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13
Q

Which pneumonia pathogen commonly occurs in conjunction with gingivitis?

A

Streptococcus viridans.

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14
Q

Which antibiotics are used to cover pneumococcus?

A

Beta-lactams e.g. penicillins and 3rd generation cephalosporins.

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15
Q

Which antibiotics are used to cover the ‘atypicals’?

A

Macrolides or doxycycline.

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16
Q

Which antibiotics is used in patients with a macrolide or penicillin allergy?

A

Mocifloxacin i.e. a QUINOLONE.

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17
Q

What is the moderate-severity drug regimen for pneumonia?

A

Benzyl-penicillin 1.2g IV, 6 hourly;
PLUS either:
Doxycycline 100mg orally 12 hourly,
OR
Clarithromycin 500mg orally 12 hourly.
Oral amoxicillin can be given instead of BenPen in patients who can tolerate orals.
If oral not available, then IV azithromycin.

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18
Q

Which investigations are appropriate for a ? pneumonia patient?

A

Sputum sample for a PCR and MC+S, as well as gram stain and cultures.
Bloods for cultures, if poss.
Serology:
- mycoplasma, legionella, chlamydia, influenzae, parainfluenzae, RSV.
(before ABx administration).
Viral PCR for extended respiratory screen.
COVID RAT and PCR.
Urinary pneumococcal (+/- legionella) antigen.

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19
Q

What secondary investigations are necessary for a ?pneumonia patient?

A

CXR
ABG/VBG
FBC, UandE’s, LFT’s, CRP (also procalcitonin, ESR)

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20
Q

Name 3 methods of grading pneumonia severity and their acronyms.

A

CURB-65 - Confusion, Urea, Respiratory Rate above 35, Blood pressure below 90, aged over 65 (Community Acquired).
SMART-COP - Systolic below 90mmHg, Multilobar Involvement, Albumin <3.5, RR >30, Tachycardia, Confusion, 02 Sats <90, pH <7.35 (Community-Acquired).
PSI Pneumonia Severity Index - lots.

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21
Q

Describe other considerations when providing supportive therapies for pneumonia patients?

A

Manage cardiac dysfunction, prevent sepsis, DVT prophylaxis, corticosteroids, correct neutropenia.

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22
Q

Define nosocomial pneumonia.

A

Pneumonia acquired after >72 hours in hospital care.

Pseudomonas aeruginosa, Staph. aureus, Klebsiella pneumonia, Enterobacter.

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23
Q

What is the most common cause of nosocomial pneumonia?

A

Most commonly the GRAM NEGATIVES;

Pseudomonas aeruginosa, Escherichia coli, Klebsiella pneumoniae and Acinetobacter.

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24
Q

What are the most common NOSOCOMIAL pathogens in immunocompromised patients?

A

Streptococcus pneumoniae, Mycobacterium pneumoniae, Legionella.
LYMPHOCYTIC ORIGIN:
Pneumocystis jirovecii, TB, viral pneumonia.
NEUTROPHILIC ORIGIN:
Pseudomonas aeruginosa, Staph aureus, aspergillus.

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25
Q

How do bronchioles differentiate from bronchi?

A

Bronchi have cartilage and submucosal glands within their walls.
Bronchi are pseudostratified columnar, bronchioles are CILIATED simple cuboidal. Bronchioles include CLUB CELLS.

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26
Q

Define the elements of the respiratory acinus.

A

Respiratory bronchioles, alveolar ducts, alveolar sacs, and alveoli.

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27
Q

What is the definition of pneumonia?

A

Infection of the lung parenchyma, distal to the terminal bronchiole.
Bronchopneumonia is infection of the airways including the bronchioles.

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28
Q

Describe some situations in which the host defence mechanisms for pneumonia may be impaired.

A

Immunosuppression, intubation, coma, general anaesthetic, anything reducing the respiratory drive or cough reflex, intubation, neuromuscular disease.

Injury to the mucociliary escalator e.g. smoking, gas inhalation, CF, obstruction.

Decreased macrophage function e.g. smoking, alcohol.

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29
Q

Describe the 3 main classifications of pneumonia by anatomical location.

A

Lobar, bronchopneumonia, interstitial pneumonia.

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30
Q

When might you be able to see an air bronchogram?

A

When the parenchymal tissue is opacified by fluid/exudate etc so that the air-filled spaces of the bronchioles and bronchi are more clearly visible.

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31
Q

What are the pores of Kohn?

A

Small communicating channels between adjacent alveoli, providing a collateral pathway for aeration.

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32
Q

Describe the process of congestion in pneumonia.

A

1-2 days in which lungs become heavy, red and boggy;
++intra-alveolar exudate,
not many neutrophils,
++bacteria present,
vascular congestion is evident.
Watery sputum and fine crackles on auscultation.

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33
Q

Describe the process of red hepatisation in pneumonia.

A

2-4 days.
Lung becomes red, airless.
Fibrinopurulent pleuritis.
Erythrocytes, neutrophils and fibrin in the intra-alveolar exudate.
Bronchial breathing and rust coloured sputum.

34
Q

Describe the process of grey hepatisation.

A
4-8 days. 
Dry, grey brown cut surface. 
\++intra-alveolar fibrin and macrophages,
Degradation of erythrocytes and polymorphic cells = less red, more pale. 
Moist ronchi.
35
Q

Describe the process of resolution in pneumonia.

A

8-9 days.
Enzymes begin to degrade and digest the exudate, resorption through phagocytosis and expectoration of sputum through coughing.

36
Q

What are some of the possible complications of pneumonia?

A

Pleural effusion, empyema, carnification of exudate, abscess formation, and bacteraemia including endocarditis, meningitis and arthritis.

37
Q

How does bronchopneumonia differ from lobar pneumonia?

A

No air bronchograms, diffuse inflammation centred around bronchioles, no segmental distribution.
Patchy, multilobar, bilateral and/or bi-basal. Can become suppurative, is generally more destructive than lobar pneumonia.
Can lead to abscesses, empyema, suppurative pericarditis.

38
Q

How is atypical pneumonia defined/classified?

A

Based on both atypical clinical presentation AND the variety of causative pathogen.

Children and young adults, immunocompromised.

Mycoplasma pneumoniae, chlamydia pneumoniae, RSV, CMV, influenza, Coxiella burnetii.

39
Q

What is the most common atypical pneumonia pathogen?

Other examples?

A

Mycoplasma pneumoniae
Chlamydia pneumoniae
Legionella species.

40
Q

What are the most common causes of viral pneumonia?

A

Influenza A and B
RSV
Rhinovirus
Also;
CMV, varicella zoster, adenovirus, measles, para-influenza.
Predisposing factors include alcohol. malnutrition and immunosuppression.

41
Q

Describe the pattern of disease characterised by Klebsiella pneumoniae?

A

Male, ETOH consumption, diabetes mellitus, COPD.
Middle-aged to elderly.
Predominantly lobar pattern.

Often is cavitating/necrotic/empyema.

42
Q

Describe the pattern of disease caused by STAPHyloccus pneumoniae (not streptococcus).

A

<5% of pneumonias, previous influenza virus, CF, causes necrosis and abscess formation +/- empyema and pneumothorax.

43
Q

What is diffuse alveolar damage? (DAD)

A

Elevated levels of pro-inflammatory mediators combined with decreased expression of anti-inflamm molecules = damage to lung tissue.
Often a pre-cursor to/the histological manifestation of ARDS (Acute Respiratory Distress Syndrome) in which fluid fills the alveolar sacs due to global inflammatory cytokines increasing permeability of membranes.

44
Q

Describe the evolution of the Penicillins in order, and what they cover.

A

Benzylpenicillin - staphs and streps.
Flucloxacillin - staphs, streps, MSSA.
Amoxicillin - staphs, streps, more gram negative cover e.g. Haemophilus influenzae, Neisseria meningitidis, E. coli
Augmentin (Amoxicillin + clavulonic acid)
Ticarcillin/Piperacillin - Pseudomonas cover and GRAM NEGATIVE RODS. Need clavulonic acid to cover the anaerobes e.g. Tazocin (Piperacillin + Tazobactam) or Timentin (Ticarcillin + Clavulonic acid).

45
Q

Describe the cephalosporins and what they cover.

A

1st Gen: Gram positives, less Gram negatives. No anaerobe cover. CEPHALEXIN.
2nd Gen:
3rd Gen: CEFTRIAXONE
4th Gen: Pseudomonas cover, no MRSA. CEFIPIME.
5th Gen: MRSA cover, no Pseudomonas. CEFTAROLINE. Used if allergies or renal failure to VANC.
There is now anaerobe cover via CEFTOLOZANE and TAZOBACTAM.

46
Q

Describe the monobactams and their cover.

A

AZTREONAM is the only one available. Only consists of a beta lactam ring. It only kills gram negatives.

47
Q

Describe the carbapenems and their cover.

A

MEROPENEM, ERTAPENEM.
Very broad gram negative and positive cover, and anaerobes. NO MRSA or pseudomonas cover. Used for gram negatives with inducible beta-lactamase (EBL’s) and the ESCAPPM group. e.g. acinetobacter.

48
Q

Describe the glycopeptides and their cover.

A

VANCOMYCIN, TEICOPLANIN.
MRSA. Gram positive cover only. Kills C. difficile.
BEWARE: Nephrotoxicity.

49
Q

What are the 4 main categories of antibiotic?

A

CELL WALL DISRUPTORS
- transpeptidase inhibitors (e.g. penicillins)
- peptidoglycan inhibitors (e.g. vancomycin)
RIBOSOMAL INHIBITORS
- transpeptidase inhibitors between peptides
- codon:anticodon disruptors
- either on the 50S, 30S or 70S elements of the ribosome.
DNA DISRUPTORS
- folic acid synthesis inhibitors (co-trimoxazole)
- DNA gyrase inhibitors (quinolones)
- rifampicin (turns everything orange)
OTHER
- cell membrane disruptors e.g. polymixins
- daptomycin

50
Q

Name the categories of cell wall disruptors.

A

Penicillins, cephalosporins, carbapenems, glycopeptides, monobactams.

51
Q

Name the categories of DNA inhibitors.

A

Quinolones, metronidazole, rifampicin, cotrimoxazole (including trimpethoprim), fusidic acid.

52
Q

Name the categories of ribosomal inhibitors.

A

Aminoglycosides, tetracyclines, lincosamides, macrolides, linezolid, streptogramins, chloramphenicol.

53
Q

Name the categories of antibiotics: other.

A

Cell membrane disruptors, including polymixins and daptomycin.

54
Q

Name as many macrolides as you can remember, and any salient information about them.

A

GENTAMICIN, CLARITHROMYCIN.
Metabolised via the CP450 pathway in the liver; will compete with others in this pathway e.g. WARFARIN.
Good for atypicals and gram positives, e.g. respiratory tract and UTI’s.
BEWARE: Prolonged QT interval and interaction with CP450 drugs e.g. WARFARIN

55
Q

Name as many lincosamides as you can remember, and any salient information about them.

A

CLINDAMYCIN, LINCOMYCIN.
Only gram positives and anaerobes.
Stops toxin production so good for gangrene, necrotising fasciitis. Good for C. difficile.

56
Q

Name as many aminoglycosides as you can remember, and any salient information about them.

A

GENTAMICIN, STREPTOMICIN, TOBRAMYCIN.
Gram negative rods including PSEUDOMONAS.
Levels are required 30 mins and then 6-12 hourly. (bacteriostatic, concentration dependent). Good for UTI’s.
BEWARE: Nephrotoxicity and ototoxicity.

57
Q

Name as many tetracyclines as you can remember, and any salient information about them.

A

DOXYCYCLINE, METHACYCLINE.
Gram positive cover.
Good for skin conditions, UTIs, malaria and acne.
BEWARE: photosensitivity, gastritis, not for pregnant women or children under 12.

58
Q

Name as many quinolones as you can remember, and any salient information about them.

A

MOXIFLOXACIN, NORFLOXACIN.
Inhibits DNA gyrase. Good for gram negative rods, pseudomonas, but mostly limited to the urinary system.
BEWARE: tendon rupture.

59
Q

Describe METRONIDAZOLE, and any salient information about it.

A

Anaerobe cover. Good for C. difficile. Hepatic metabolism.

BEWARE: Do not combine with ETOH.

60
Q

Describe COTRIMOXAZOLE, and any salient information about it.

A

Combination of SULPHAMETHOXAZOLE and TRIMPETHOPRIM.
Good for negative and positive gram stain. Inhibits folic acid synthesis.
Used for respiratory tract, UTI’s and pneumonias.
BEWARE: Bone marrow suppression in long term cover. Contraindicated in sulphur allergies.

61
Q

Describe RIFAMPICIN, and any salient information about it.

A

Not to be used in isolation, just creates resistance.
Turns bodily fluids orange.
Only gram positive cover, usually in combination with a beta-lactam. e.g. VANCOMYCIN and RIFAMPICIN.
Makes up part of the treatment for Tuberculosis.
(RIFAMPICIN, ETHAMBUTOL, PYRAZINAMIDE + ISONIAZID).

62
Q

Which kind of bacteria has a many-layered peptidoglycan wall?

A

Gram positive bacteria.

63
Q

Describe the slime that some bacteria produce.

A

LIPO-POLYSACCHARIDE layer.

Not to be confused with the Peptidoglycan wall

64
Q

Name as many gram-negative bacteria as you can remember.

A

E. coli, Neisseria meningitidis, Haemophilus influenzae, Klebsiella, Acinetobacter, Pseudomonas aeruginosa.

65
Q

Name as many gram positive bacteria as you can remember.

A

Streptococcus, staphylococcus, enterococcus.

66
Q

Name as many anaerobes as you can remember.

A

Lactobacillus, Clostridium difficile, Staph aureus can survive anaerobically.

67
Q

Name as many antibiotics as you can which are effective against anaerobes.

A

METRONIDAZOLE, AUGMENTIN, TAZOCIN, TIMENTIN, CARBAPENEMS, LINCOSAMIDES.

68
Q

Name as many antibiotics as you can which are effective against gram positives.

A

Earlier penicillins e.g. benzylpenicillin, flucloxacillin, the earlier CEPHALOSPORINS, GLYCOPEPTIDES (vanc and teico), COTRIMOXAZOLE, MACROLIDES, LINEZOLID, MOXIFLOXACIN STREPTOGRAMINS, DAPTOMYCIN (MRSA not VRE).

69
Q

Name as many antibiotics as you can which are effective against gram negatives.

A

AMOXICILLIN, CARBAPENEMS, AMINOGLYCOSIDES, 3,4,5TH GEN CEPHALOSPORINS, MONOBACTAMS, QUINOLONES and POLYMIXINS.

70
Q

Name as many antibiotics as you can remember, which are effective against MRSA.

A

VANCOMYCIN, TEICOPLANIN, DAPTOMYCIN, CEFTAROLINE, RIFAMPICIN.

71
Q

Name as many antibiotics as you can which are effective against ESCAPPM.

A

CARBEPENEMS, QUINOLONES, POLYMIXINS, AMINOGLYCOSIDES, CEFTOLOZANE+ TAZOBACTAM.

72
Q

Name as many antibiotics as you can which are effective against VRE.

A

LINEZOLID, STREPTOGRAMINS, DAPTOMYCIN, TIGECYCLINE.

73
Q

Name as many antibiotics as you can which are effective against pseudomonas.

A

4TH GEN CEPHALOSPORINS, TAZOCIN/TIMENTIN/AUGMENTIN, AMINOGLYCOSIDES, MONOBACTAMS, POLYMIXINS.

74
Q

Name as many antibiotics as you can which are effective against atypicals.

A

MACROLIDES, TETRACYCLINES, QUINOLONES, COTRIMOXAZOLE.
Remember that atypicals don’t have a cell wall, so they need to exist inside the cell e.g. malaria parasites inside erythrocytes. So it needs to penetrate the cell e.g. that’s why we use DOXYCYCLINE.

75
Q

Describe 4 ways in which a bacteria might resist antibiotics.

A
  1. Prevent entry e.g. porin downregulation, thicker membrane (lipopolysaccharide slime), efflux pumps.
  2. Upregulate targets e.g. folA gene overproducing DHFR and DHPS to overwhelm cotrimoxazole.
  3. enzymatic inhibiton e.g. betalactamase on beta lactam rings.
  4. change structure e.g. VANA or VANB gene in VRE/VRSA enterococcus mutates its peptide chains so that vancomycin can’t inhibit the transpeptidases.
76
Q

How might a bacteria change its DNA?

A

Point mutations
Plasmids
Bacteriophagy

77
Q

Describe the characteristics of bronchopneumonia.

A

Patchy, not limited to one segmental area.
No air bronchograms due to lack of alveolar consolidation.
Can be multifocal.
Haemophilus influenzae, pseudomonas aeruginosa, Moraxella catarrhalis and Legionella pneumonia.
Inflammation of the TERMINAL BRONCHIOLES (conducting airways).

78
Q

Describe the characteristics of atypical (INTERSTITIAL) pneumonia.

A

Diffuse interstitial infiltrates.
Comparatively mild URTI symptoms.
Atypical bacteria (Mycoplasma pneumoniae, chlamydia pneumoniae, RSV, CMV, Influenza and Coxiella burnetti ANAEROBES).
Moderate sputum production, no consolidation, moderate WCC elevation.

PATHOLOGY: Type II pneumocyte hyperplasia, hyaline alveolar membranes, increased mononucleated cells within the alveolar septa.
CXR: Predominantly lower lung fields or perihilar pattern, less “impressive”.

79
Q

Name some of the common anaerobes.

A

Bacteroides, Fusobacterium, Peptococcus.

80
Q

What is laryngotracheobronchitis? Describe presentation.

A
"Croup". 
Barking cough with inspiratory stridor. 
Sounds like a dog or seal barking. 
Predominantly children aged 9 months to 3 years of age. 
Worse at night. 
Inspiratory stridor on auscultation.
81
Q

Define acute bronchitis and discuss presentation.

A

Acute inflammation of the tracheobronchial tree. Usually comes after an URTI.
Cough and sputum.
Wheeze and dyspnoea.
Usually caused by viral pathogen.
Scattered wheeze on auscultation.
Occasionally fever and haemoptysis.
Usually spontaneously improves in 4-8 days.

Can be complicated with Haemophilus influenzae or Strep. pneumoniae in compromised patients/chronic bronchitis.

82
Q

Define bronchiolitis and describe presentation.

A

Inflammation of the bronchioles due to acute viral infection (usually RSV).
Extremely common in infants.
2 weeks to 9 months of age usually.
Prodrome of 48 hours with cough, coryza, then worsens.
Squeaks, worsening on inspiration.
Wheezy breathing.
Tachypnoea.
Hyperinflated chest; barrel chest, subcostal recessions.
Widespread fine inspiratory crackles.
Dehydration is a complication (decreased feeding due to resp. distress and exhaustion).