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Respiratory medicine > Pneumonia > Flashcards

Pneumonia Flashcards

1
Q

is community acquired pneumonia normally bacterial or viral and what is the pathophysiology behind it?

A

often bacterial infection which follows an upper respiraotry tract infection
bacterial invasion of the lung parenchyma causes the alveoli to fill with inflammatory exudate causing consolidation of the pulmonary tissue

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2
Q

what are some predisposing factors for CAP

A
  • age: 65 years
  • co-morbidities: HIV infection, diabetes mellitus, chronic kidney disease, malnutrition, recent iral respiraory infection
  • other respiratory conditions: CF, bronchiectasis, COP, obstructing lesion
  • iatrogenic: immunosuppressant therapy
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3
Q

list some common bacteria which cause CAP and some of their virulence factors

A
  • Streptococcus pneumonae: virulence factors - contain polysaccaride capsule, lack catalase, IgA protease, autolysis, pilli that mediate adherence to eopithelium, gram positive, lancet shaped diplococci, neutrophils, penicillin
  • Haemophilus influenxae: encapsulated or unencapsualted (95%), virulence factors- pili, factor that disorganised ciliary beating, protease that degrades IgA, capsule, gram negative
  • Moraxella - increasing cause
  • Staphylococcus aureus: secodnary following viral respiraotry illness, associated with high incidence of complications (lung abscess, empyema)
  • Klebseilla Pneumoniae: gram negative, affects delibiated and malnourished esp alcoholics, thick gelatinous sputum due to abundant viscid capsular polysaccharide
  • Pseudomonas aeruginosa: nosocomial infections
  • Leginella Pneumophilia: rapid diagnosis via antigens in urine or positive fluorescent antibody test
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4
Q

list some organisms that cause community acquired pneumonia and some that cause hospital acquired pneumonia

A

CAP: streptococcus pneumoniae, H influenzae, moraxella catarrhalis, staph aureus, legionalle pneuophilia

Atypical CAP: mycoplasma pneumoniae, chlamydia, coxiella burnetti, viruses (RSV, parainfluenza, influenza A and B)

Nosocomial pneumonia: gram negative rods belonging to enterobacteriaeceae (klebsiella, serratia marcescens, E coli) and pseudomonas spp, staph aureus

Aspiration pneumonia: anaerobic oral flow (bacteriocides, prevotella, fusobacterium), aerobic bacteria (strep pneumoniae, staph aureus)

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5
Q

list some organisms that cause pneumonia in an immunocompromised host

A

Pneumonia in an immunocompromised host: CMV, pneumocystic carinii, mycobacterium avium, invasive candidiasis, invasive aspergillosis

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6
Q

what is the mechanism of action of a penicillin

A

target the penicillin binding proteins (PBO) in bacterial wall including transpeptidases. this results in irreversible inactivation of transpeptidase via blocking cross-linking peptide chains attached to peptidoglycan backbone - bacteriocidal to growing cells (autolysis) and bacteriostatic to entire populations

include: benzylpenicillin, amoxicillin, phenoxymethylpenicillin, flucolaxicillin

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7
Q

what is the mechanism of action of cephalosporins

A

bacteriocidal drugs containing a beta lactam that inhibit bacterial wall synthesis similar to penicillins - generations (I-V) are defined on spectrum of activity, with later generations having expended activity against gram negative bacteria (but decreasing against gram positive)
list: cefadroxil, cefuroxime and ceftriaxone)

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8
Q

what is the mechanism of action of glycopeptides

A

bacteriocidal drugs that inhibit peptidoglycan synthesis with possible effects on RNS synthesis
list: vancomycin

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9
Q

what is the mechanism of action of carbapenems

A

binds to penicillin binding proteins, preventing bacterial wall synthesis.
able to circumvent beta-lactamases by binding with high affinity and acylating the enzyme, rendering it inactive - broadest antibacterial spectrum compared with other beta-lactam drugs
list: ertapenem, imipenem

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10
Q

what is the mechanism of action of monobactams

A

bind to penicilling binding proteins, inhibiting synthesis of bacterial cell wall, thereby blocking peptidogylcan crosslinking
list: aztreonam

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11
Q

what is the mechanism of action of metronidazole

A

bactericidal drugs that is metabolised to an intermediate that inhibits bacterial DNA synthesis and degrades existing DNA. it is selective as it is intermediate is not produced in mammalian cells - should not be given to pregnant women
list: tinidazole

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12
Q

what is the mechanism of action of quinolones

A

DNA gyrase inhibitors
inhibit bacterial nucleic acids - affect DNA replications and packaging
bactericidal drugs that inhibit prokaryotic DNA gyrase, preventing packaging DNA into supercoils that is essential for DNA replication and repair - cannot give quinolones with theophylline this will prevent toxicity

List: nalidix acid, ciprofloxacin

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13
Q

what is the mechanism of action of Rifampicin

A

Rifampicin
affect transcription
bactericidal drug that inhibits DNA dependent RNA polymerase

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14
Q

what is the mechanism of action of macrolides and lincosamides

A

bacteriostatic/bacteriocidal drugs that reversibly bind to the 50S subunit of the bacterial ribosome, preventin translocation movement of ribosome alone mRNA
list: erythromycin, clarithromycin, azithromycin
list (lincosamide): clindamycin

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15
Q

what is the mechanism of action of aminoglycosides

A

MOA: bacteriocidal drug that bind irreversibly to the 30S portion of the bacterial ribosome. this inhibits the translation of mRNA to protein and causes more frequent misreading of the prokaryotic genetic code
list: gentamycin, streptomycin, netilimycin, amikacin

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16
Q

what is the mechanism of action of tetracyclines

A

MOA: bacteriostatic drugs that work by selective uptake into bacterial cells due to bactive bacterial transport system not possessed by mamalian cells - binds reversibly to the 30S subunit of the bacterial ribosome, interfering with the attachment of tRNA to the mRNA ribosome complex
list: tetracyclin, minocycline, doxycycline

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17
Q

what is the mechanism of folic acid inhibitors

A

Trimethroprim
Sulphonamids
MOA
- folate is an essential co-factor in the sunthesis of purines and DNA. bacteria unlike mammals synthesie their own folic acid from para-aminobenzoic acid. this pathway can be inihibited at two points - sulfonamides (inhibit dihydrofolate synthetase) and trimethoprim (inhibits dihydrofolate reductase)
- both drugs are bacteriostatic. sulfonamides are used for simple UTIs whereas trimethoprim and co-trimoxizole are used for UTIs and respiratory tract infection

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18
Q

list the broad categories of how antibiotics work

A
  • DNA gyrase
  • DNA-dpt RNA polymerase
  • 50S inhibitors
  • 30S inhibitors
  • tRNA inhibitors
    CM structure disruption
    inhibit folic acid metabolism
    inhibit cell wall synthesis
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19
Q

list the normal defenses of the lung

A

physical defenses

  • humidification
  • filtering of large particles (by nose hairs)
  • turbulent air flow - particles are removed in the nostrils and nasopharynx by adhering to mucosa
  • mucociliary escalator - betwene the nose and terminal bronchioles - mucus coating is secreted by goblet cells in epithelium - traps small particles in inspired air and ciliated epithelium beats continually towards the pharynx and removes particles
  • particle expulsion - sensory nerves receive irritating signals and respond - gag, cough, sneezing reflex
  • barrier function

respiratory tract secretions

  • mucus (secreted by goblet cells) contains acidic and neutral polysaccharides
  • alveolar lining fluid contains surfactant, phospholipids, neutral lipids, IgG, IgE, ansd IgA

innate immunity

  • pulmonary alveolar macrophages - phagocytose particles and are removed by the mucociliary escalator
  • cytokines - alpha-1-antitrypsin, interferons
  • complement
  • granulocytes
  • nautral killer cells

Adaptive immunity

  • B cells/plasma cells
  • T cells
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20
Q

what is the role of IgA

A

a benign immunoglobulin that binds to mucus and optimises viscocity, neutralises foreign antigens, does not active the complement cascade, may also block IgG induced complement activation (hence anti-inflammatory) and can induce apthogen killing when required

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21
Q

impairment of host defense mechanisms

A
  • loss/suppression of cough reflex –> coma, general anaesthetics, pain, neuromuscular disease, endotracheal tube and drugs
  • injury to mucociliary blanket/escalator - smoke, viral, alcohol
  • descrease in macrophage function - alcohol, anorexia, oxygen toxicity and phagocyte killing defect
  • impairment of immune system
  • unusual virulent microbes
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22
Q

what are some common virulence factors for respiratory pathogens

A

establishment (staying in) - polysaccharide capsule (inhibit phagocytosis and adhere to surfaces), fimbrae (allow attachment), adhesins (glycolipids/lipoproteins allows adherence to tissue), virions

defeating the host defenses
passive defenses - capsule (protects against phagocytosis) and cell walls (defends against host defenses)
active defesnes - enzymes - leukocidins (destroy WBC), hemolysins (membrane damaging toxins that disrupt PM of host cells and cause cells to lyse), coagulase (cause fibrin clots to form the blood of the host), kinsase (breakdown dibrin and dissolve clots), hyaluronidase/collagenase AND penetrating inside host cell - invasion and cadherin (pathogen able to use host cell cadherin to move from cell to cell without exposing itself to the host’s immune defenses

Damaging the host
direct damage -
indirect damage - exotoxins, endotoxins, immune system

23
Q

what is lobar pneumonia

A
  • acute bacterial infection resulting in fibrinosuppruative consolidation of a larger portion of a lobe or an entire lobe. may spread through pores of Kohn (Alveolar connections)
  • common in health young adults and has an acute onset
  • pathogens involved: pneumococci (90%), Klebsiella, staph, strep, H influenzae, proteus and pseudomonas
24
Q

what are the complications of lobar pneumonia

A 
- pleural effusion
empyema
organisation of exudate (calcification)
abscess formation
bacteraemia, endocarditis, meningitis, arthritis
25
Q

what are the stages of the inflammatory responses (pathology)

A

congestion (1-2 days) - lung is heavy, boggy and red - characterised by vascular engorgment, intra-alveolar fluid with few neutrophils, numerous bacteria and vascular congestion, clinically fine crackles and watery sputum

red hepatitisation (2-4 days) - characterised by massive confluent exudation with red cells (congestion), neurophils and fibrin filling with alveolar spaces, on examination - appears distinctly red, firm and airlness with a live like consistency (hence the term hepatitisation), vlinically - bronchial breathing and rusty sputum

gray hepatitisation (4-8 days) - disintegration of red cells and persistence of a fibrinosuppurative exudate give the gross appearance of a grayish brown, dry surface - clinically moist bronchi

resolution (8 days) - consolidation within the alveolar spaces undergoes progressive enzymatic digestion to produce granular, semifluid debris that is resorbed, ingested by macrophages, coughed up or organised by fibroblasts growing into it

26
Q

what is bronchopneumonia?

A

inflammation of conducting airways (Terminal bronchioles)

often the cause of death in the eldery in conjunction with a debilitating illness

27
Q

what pathogens are involved with bronchopneumonia

A

strep, staph, pneumococci, H influenzae, pseudomonas, cloiforms, candida, aspergiullus

28
Q

what is the pathology behind bronchopneumonia

A
  • patchy consolidation of acute suppurative inflammation. may occur in one lobe but is more often multilobar and frequently beilateral and basal because of the tendency of secretions to gravitate into the lower lobes
  • well developed lesions are usually 3-4 cm in diameter, slightly elevated, drug, granular, gray red to yellow and poorly delineated at their margins
  • necrosis centrally, tends to be more destructive than lobar pneumonia

histologically: reaction usually elicits a suppuratives, neutrophil-rich exudate that fills the bronchi, bronchioles and adjacent alveolar spaces

29
Q

what are some complications of bronchopneumonia

A

abscess formation
empyema
suppruative pericarditis
emtastatic abscesses

30
Q

what is the clinical course of bronchopneumonia

A

major symptoms for CAP, abrupt onset of high fever, shaking, chills, productive cough of mucopurulent sputum, haemoptysis, pleuritic pain and pleural friction rub

clinical picture is dramatically modifiable by the administration of antibiotics. treated patients may be relatively afebrile with few clinical signs in 48-72 hours after the initiation of antibiotics

31
Q

what is atypical (interstitial) pneumonia?

A

a combination of atypical presentation and atypical organisms, usually, CAP
clinically defined based on the presence of extrapulmonary manigestations
transmitted via droplet spread (inhalation) in children and young adults and generally is insidious onset gfollowing UTRI

32
Q

what is the clinical presentation of atypical (interstitial) pneumonia

A 
moderate sputum production
no eviedence of consolidation
moderate elevation of WCC
lack of alveolar exudate
CXR: more impressive than expected with lower lung fields, bilateral and perihilar
33
Q

what is the pathology of atypical (interstitial) pneumonia

A

predominant in the interstitial nature of the inflammatory reaction, virtually localised within the walls of the alveoli. alveolar septa are widened and edematous and usually have a mononuclear inflammatory infiltrate of lymphocytes, histiocytes and occasionally plasma cells (neutrophils may be present acutely)

alveoli may be free from exudate but many patients may hav eintra-aveolar proteinaceous material (cellular exudate) and a characteristically pink hyaline member lining the alveolar walls. these changes reflext alveolar similar (similar to ARDS). Eradication of infection is followed by reconstruction of normal lung architecture

34
Q

what is the clinical course of atypical (interstitial) pneumonia

A
  • clinical course extremely varies and even patients with well established pneumonnias may have few localisation symptoms
  • cough may be absent and the major manigestations may consist only of fever, headaches, muscle aches and pains in legs
  • oedema and exudation are both strategically located to cause mismatching of ventilation and blood flow and thus evoke symptoms out of proportion to the scanty physical findings
35
Q

discuss the principles of choosing empirical antibiotic therapy

A

empirical antibiotic therapy is employed on the basis of choosing an antibiotic that will treat the most probable organism based on the patients clinical signs, history and radiological investigations
it is employed as it is important to begin therapy early to avoid the patients deteriorating

36
Q

recognise the importance of microbiological diagnosis in management

A

microbiological diagnosis is important to the narrow the antibiotic treatment

Microbiology
Indication
Narrowest spectrum possible
Doseage needs to be adequate to achieve MIC
Minimise duration of treatment
Ensure monotherapy where possible
37
Q

explain the pathophysiology of acute respiratory failure in severe pneumonia

A

respiratory failure is inadequate gas exchange by the respiraotry system, with the result that levels of arterial oxygen, carbon dioxide or both cannot be maintained within their normal ranges

during an infection such as pneumonia the acut einflammatory response will result in an increas ein cytokine production –> vasodilation of pulmonary arterioles –> increased blood flow to fight infection –> poorly ventilated areas receive a large blood flow –> V/Q mismatch –> blood in corresponding pulmonary venules low in oxygen
in healthy lung - vasodilation of arterioles in well-ventilated areas increases gas transport. poorly ventilated lung areas result in vasoconstriction, decrese blood flow to the aras

38
Q

what are some types of respiratory distress

A
  • hypoxaemia

- hypercapnoea

39
Q

what is the treatment of respiratory failure

A

specific, treat the underlying cause/diserase process
general supportive management:- correct hypoxaemia (oxygen therapy), deal with hypercapnoea (HIV), nutrition, prevent DVT, monitor patient

40
Q

explain type 1 respiratory failure

A

failure of lung parenchyma/perfusion
hypoxia without hypercapnia (CO2 must be normal or low) that is caused by V/Q mismatch
classification: PaO2 low (>55-60mmHg) and PaCO2 normal or low ((

41
Q

explain type 2 respiratory failure

A

failure of pump/ventilation
hypoxia with hypercapnea and is caused by inadequate alveolar ventilation
classification: PaO2 decreases (55-60mmHg), PaCO2 increase (>50mmHg)
caused by conditions that build up CO2 but cannot get rid of it. these include: increased airway resistance (eg COPD, pulmonary disease and asthma), reduced breathing effort (eg drug effects, obesity, brainstem lesion), decreased area of lung available for gas exchange (eg chronic bronchitis), neuromuscular conditions (Eg GBS), deformed, rigid or flail chest

42
Q

clinical symptoms of CAP

A
  • acute onset with a cough, purulent sputum, breathless, fever, together with physical and radiologicla signs/changes showing lung consolidation
43
Q

clinical features of CAP

A 
cough
breathlessness
fever
chest pain
extrapulmonary features: haemolysis, thrombocytopenia, myalgia, arthalgia and malaise, myocarditis, pericarditis, headache, skin rashes
44
Q

how to interpret and CXR

A 
airway
bones/soft tissue
cardiac
diaphragm
equal volume
fine detail
gastric bubble
hilum/hardware
45
Q

clinical methods of obtaining samples for microbiological investigations

A 
throat swap
nasopharyngeal swab
sputum
blood
nasal swap
pleural fluid aspirate
percutaneous transtracheal aspiration
46
Q

what is the criteria for refusal for treatment

A
  • valid refusal of treatment requires the satisfaction of the same conditions as consent to treatment
    decisions must be
  • voluntary (not under duress)
  • informed (patient has received sufficient information to make the decision)
  • made by a competent person, who is someone who can - comprehend and retain info, understand nature and effects of decisions, elevate information and predicted consequences in relation to one’s situation, goals and values; offer reasons for one’s decisions (justification); communicate one’s decision to others; ability to follow through with decision
  • for specific procedure
47
Q

what are some values in medical ethics

A
  • autonomy
  • beneficience
  • non-maleficence
  • justice
48
Q

what are some risk factors for pneumonia

A
  • age over 50 years
  • alcoholism
  • asthma
  • COPD
  • dementia
  • heart failure
  • immunosuppression
  • indigenous background
  • location - eg tropical settings
  • insitituationalisation
  • seizure disorders
  • smoking
  • stroke
49
Q

what are the virulence factors of strep pneumoniae

A

capsule
pili
IgA protease

50
Q

what are the microbiological causes of community acquired pneumonia

A

lobar: strep pneumoniae, Klebsiella, burkholderia mallei (meiliodisis) tropical issue
bronchopneumonia: strep, H influenzae, S aureus, moraxella catterhalis
atypical/interstitial: moraxella cattarhalis
aspiration: enterococci (E coli, serratoa), klebsiella

51
Q

what are the microbiological causes of nosocomial pneumonia

A

aspiration as above

polymicrobial
paseudomonas, S aureus

differ as they are harder to treat and bugs have increased exo and endotoxins

52
Q

what are the microbiological causes of immuno compromised pneumonia

A

candida
fungal eg pneumocysitis jiemii
CMV
all of the above

53
Q

how can you prevent (or try to prevent) pneumonia

A

vaccination
dont smoke
compliance
pneumococcal vaccination –> part of routine

Respiratory medicine (3 decks)

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