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Respiratory RT > Respiratory Infections > Flashcards

Respiratory Infections Flashcards

1
Q

where does corzya, pharyngitis, sinusitis and epiglottitis effect?

A

upper respiratory tract

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2
Q

where does acute bronchitis, pneumonia and influenzae effect?

A

lower respiratory tract

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3
Q

where is the cut off between upper and lower respiratory tract?

A 
vocal cord
(vocal cords and above = upper
below vocal cords = lower)
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4
Q

what is corzya?

A

acute viral infection of the nasal passages

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5
Q

what is acute sinusitis usually preceded by?

A

corzya

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6
Q

what type of discharge is associated with acute sinusitis?

A

purulent nasal discharge

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7
Q

what is the reason diptheria is so life-threatening?

A

the toxin produced

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8
Q

why is diptheria not seen in the UK anymore?

A

vaccination

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9
Q

what is the reason epiglottits (in children) is so life-threatening?

A

risk of respiratory obstruction

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10
Q

what is acute bronchitis usually preceded by?

A

corzya

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11
Q

what are the clinical features of acute bronchitis?

A 
productive cough (rememeber bronchitis is an over production of mucus)
sometimes a fever
possibly a transient wheeze
normal chest examin
normal CXR
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12
Q

what is the treatment for acute bronchitis?

A

supportive

antibiotics are not indicated unless patient has underlying chronic lung disease

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13
Q

what is an acute exacerbation of chronic bronchitis?

A

worsening of sputum production (now purulent) of a patient with pre-existing lung disease

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14
Q

what usually precedes an acute exacerbation of chronic bronchitis?

A

upper respiratroy tract infection

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15
Q

what are the clinical features of acute exacerbation of chronic bronchitis?

A 
breathlessness
wheeze
crackles
cyanosed
ankle oedema (in advanced disease- cor pulmonale)
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16
Q

what is the management of an acute exacerbation of chronic bronchitis? (patient has purulent sputum)

A

primary care:
amoxicillin or doxycycline
bronchodilator inhalers
short steroid course in some cases

hospital:
(refer if evidence of resp failure or not coping at home)
measure ABGs
give oxygen if resp failure
CXR
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17
Q

what are the main investigations for a patient who has suspected pneumonia? (7)

A 
blood culture
serology
ABGs
FBC
Urea
LFTs
CXR
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18
Q

why can herpes simplex be reactivated in patients with pneumonia?

A

opportunistic infection

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19
Q

why is CRB65 more useful in primary care than CURB 65?

A

don’t need to do a blood test

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20
Q

who tends to get severe chicken pox pneumonia?

A

adult smokers

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21
Q

what is the management of CAP?

A 
antibiotics
oxygen (maintain SaO2 94-98%)
fluids
bed rest
no smoking
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22
Q

what can radiological technique can you use to help guide a chest drain?

A

ultrasound

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23
Q

what type of antibiotic cover is generally needed for hospital acquired pneumonia?

A

gram negative cover

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24
Q

what type of antibiotic cover is generally needed for aspiration pnumonia?

A

anaerobic cover

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25
Q

why is pneumonia caused by legionella tricky to diagnose?

A

chest symptoms may be absent but GI disturbance is common

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26
Q

who gets both influenza and pneumococcal vaccines?

A

people over 65
patients with chronic chest/cardiac disease
patients with diabetes
immunocompromised patients

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27
Q

what are the benefits of oseltamivir?

A

reduced duration of symptoms by one day
reduced use of antibiotics
might reduce infectivity
no data on mortality

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28
Q

how long is the first wave of an influenza pandemic?

A

3-5 months

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29
Q

when does the second wave of an influenza pandemic occur?

A

months after the first

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30
Q

explain CURB65

A 
C = new onset of confusion
U = urea >7
R = resp rate > 30/min
B = BP, systolic 
65 = age 65+
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31
Q

why does infection cause consolidation of an area of the lungs?

A

infection causes an inflammatory exudate (localised oedema) due to the inflammatory-induce leaky blood capillaries.
the fluid filled spaces lead to consolidaiton

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32
Q

what is lobar pneumonia?

A

confluent consolidation involving a complete lung lobe

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33
Q

what are the 7 major complications of pneumonia?

A 
respiratory failure
pleural effusion
empyema
abscess
fibrous scarring
bronchiectasis
death
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34
Q

what is bronchopneumonia?

A

infection starting in airways and spreading to adjacent alveolar lung

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35
Q

what can be an underlying cause of bronchopneumonia?

A

COPD
cardiac failure
complication of viral infection
aspiration of gastric contents

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36
Q

what is a lung abscess?

A

localised collection of pus

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37
Q

what symptoms does a lung abscess cause?

A

chronic malaise and fever

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38
Q

what type of pneumonia is more likely to cause a lung abscess?

A

aspiration pneumonia

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39
Q

what is bronchiectasis?

A

abnormal fixed dilation of the bronchi

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40
Q

what is bronchiectasis usually the result of?

A

fibrous scarring followng infection (pneumona, TB, cystic fibrosis) or chornic obstruction (tumour)

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41
Q

what is the main consequence of bronchiectasis?

A

dilated airways accumulate purulent secretions (due to decreased secretion clearance) predisposing to infection

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42
Q

how can the pathology of TB be described?

A

type IV hypersensitivity (granuloma formation + necrosis)

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43
Q

apart from mycobacteria tuberculosis/bovis/africanum, what type of patients do other mycobacterias usually infect?

A

immunocompromised host

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44
Q

in TB what is the cause of the granulomatous inflammation, tissue necrosis and scarring?

A

T cell response to the organism

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45
Q

describe primary TB? (1st exposure)

A

inhaled organisms phagocytosed and carried to hilar lymph nodes. immune activation leads to a granulomatous response in the nodes and lung and usually results in killing of the organism

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46
Q

describe secondary TB?

A

reinfection/reactivation of TB disease

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47
Q

where does secondary TB tend to remain?

A

localised in the apices of the lung

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48
Q

what are the ways secondary TB infection can spread to other parts of the body?

A

airways and/or bloodstream

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49
Q

in primary TB where does there tend to be tissue changes?

A

Ghon focus- in periphery of mid xone of lung

granulomatous large hilar nodes

50
Q

in secondary TB where does there tend to be tissue changes?

A

fibrosing and cavitating apical lesion

51
Q

In TB what type of granulomatous tissue is formed?

A 
caseating granuloma
(necrotic)
52
Q

why can TB reactivate?

A

decreased T cell function (ie age, coincident disease- HIV, immunosuppressive therapy- steroids, chemotherapy, immunosuppressants)
or reinfection at high dose or with more virulent organism

53
Q

what can happen if you are infected with a virulent common organism? (eg TB)

A

opportunistic pathogen infection

54
Q

why can TB cause stooping?

A

if it gets into the bones of the spine

55
Q

why does subsaharan africa have a high TB rate?

A

due to HIV prevelance

56
Q

what are the 6 factors contributing to the global rise of TB?

A
  1. HIV pandemic
  2. displacement and migration
  3. poverty
  4. disruption to health infrastructure arising from political changes and conflict
  5. poorly managed TB programmes
  6. anti TB drug resistance (MDR)
57
Q

what infections are part of the M. tuberculosis complex? (ie cause TB)

A

M. tuberulosis
M. bovis
M. africanum

58
Q

what are the 2 groups of mycobacteria?

A

M tuberculosis complex and non tuberculosis mycobacteria

59
Q

what is a mycoplasmic bacteria?

A

a typical bacteria which has no cell wall

eg mycoplasma pneumoniae DIFFERENT TO MYCOBACTERIA

60
Q

what type of patients get non-tuberculosis mycobacteria?

A

immunsuppressed

61
Q

what are the 5 main risk factors for TB?

A
  1. contact of patients with tuberculosis (smear positive)
  2. children with a positive skin test for tuberculosis
  3. immigrants from African and the Indian Subcontinent
  4. poverty and homelessness
  5. HIV infection
62
Q

what is the primary test for TB?

A

PCR for mycobacteria tuberculosis

63
Q

How does Interferon Gamma Release Testing (IGRT) work?

A

quantifies hoe much gamma-inerfoeron is released from circulating T-lymphocytes in response to specific stimuli
(IL12-gIFN pathway)

64
Q

what is the pro about IGRT?

A

no cross reaction with BCG or NTMs- specifically for mycobacterial tuberculosis

65
Q

what is the con about IGRT?

A

doesnt differentiate between latent, active TB, or previous treated TB

66
Q

who do we treat for TB?

latent, active TB, previously treated TB

A

only currently active TB is treated

67
Q

who must be informed of any cases of highly suspected TB/confirmed cases of TB?

A

public health

68
Q

what test shows if a patient has ‘open TB’? (ie and therefore are contagious)

A

positive smear test

69
Q

if a patient has ‘open TB’ (and therefore are contagious) what can be done to reduce spread?

A

patient can be detained in hospital until they no longer have ‘open TB’
BUT patients cannot be forced to take treatment

70
Q

why do you start with empircal treatment for TB before having the bacteria’s sensitivities?

A

cultures take 8 weeks, so treatment has to start before the results have come back

71
Q

what are the 4 empircal anti-tuberculosis drugs?

antibiotics

A 
(R) rifampicin
(H) isoniazide
(Z) pyrazinamide
(E) ethambutol
all are in tablet form
72
Q

if patient has HIV and gets TB or NTBM how long must he/she take the 4 antibiotics for?

A

life long

73
Q

for children and adults with respiratory and non-respiratory TB what is the drug course?

A 
Initial phase:
HRZ(E) 2 months
isoniazide, rifampicin, pyrazinamide (ethambutol)
Continuation phase:
HR 4 months
isoniazide, rifampicin

(total = 6 months)

74
Q

for children and adults with meningitis and CNS TB what is the drug course?

A 
Initial phase:
HRZ(E) 2 months
isoniazide, rifampicin, pyrazinamide, (ethambutol)
Continuation phase:
HR 10 months
isoniazide, rifampicin

(total = 12 months)

75
Q

what is the result of the smear test in the intial phase of TB treatment?

A

positive

person is infectious and can be detained in hospital

76
Q

what is the result of the smear test in the continuation phase of TB treatment?

A

negative

person is no longer infectious and can’t be detained in hospital

77
Q

what is done in all TB isolates to test if the bacteria susceptibilities?

A

in vitro drug susceptibility testing

78
Q

why does initial TB treatment use 4 anti-tuberculosis drugs?

A

to cover unsuspected resistance

79
Q

in underdeveloped countries/if compliance is an issue, what is an effective way of management?

A

Directly Observed Therapy Short-course

DOTS

80
Q

what is a Directly Observed Therapy Short-course?

A

a course of treatment where a responsible observer administers the drugs and observes ingestion of the drugs ensuring compliance

81
Q

what are the adverse drug reactions of isoniazid (H)?

A

hepatitis
cutaneous hypersensitivity (pins and needles)
peripheral neuropathy

82
Q

what causes peripheral neuropathy?

A

deficiency/or excess of a cofactor of vitB6

can be caused by isoniazid

83
Q

what are the adverse drug reactions of rifampicin (R)?

A 
hepatitis
cutaneous reactions
GI Upset
Febrile reactions/flu syndrome
Tears and urine become orange
84
Q

what are the adverse drug reactions of pyrazinamide(Z)?

A 
hepatitis
anorexia (loss of appetite)
vomiting
flushing
hyperuricaemia (high uric acid conc)
arthlagia
85
Q

what are the adverse drug reactions of ethambutol?

A 
arthralgia
retrobular neuritis (Colour blind then fully blind)
86
Q

why do liver function tests need to be regularly measured?

A

because isoniazide (H), rifampicin (R) and pyrazinamide (Z) can cause hepatitis

87
Q

when is latent TB treated?

A

it isn’t

there are certain circumstances- ie if patient is about to undergo immunsuppressive therapy (anti-TNF)

88
Q

what drugs are used to treat latent TB prior to immunosuppressive therapy?

A

3 months of Isoniazide (H) and Rifampicin (R) before starting immunosuppressive drugs

89
Q

what drugs are MDR-TB types resistant to?

multi-drug resistant

A

isoniazide (H) and rifampicin (R)

90
Q

what drugs are XDR-TB types resistant to?

extra-drug resistant

A

isoniazide (H)
rifampicin (R)
fluoroquinolones
injectables

91
Q

what are the groups of patients you should suspect TB in?

A

return travellers
immunocompromised patients
non-resolving pneumonia

92
Q

what are the 3 classes of risk factors for developing chronic pulmonary infections?

A
  1. abnormal host response
  2. abnormal innate host defence
  3. repeated insult
93
Q

what type of abnormal host response are risk factors for developing chronic pulmonary infection?

A

immunodeficiency (congenital or acquired)

immunosuppression (drugs or malignancy)

94
Q

what type of abnormal innate host defence are risk factors for developing chronic pulmonary infection?

A

damaged bronchial mucosa
abnormal cilia
abnormal secretions

95
Q

what are the 2 major causes of repeated insult that can be risk factors for developing chronic pulmonary infection?

A

aspiration

indwelling material

96
Q

what 3 things can cause damaged bronchial mucosa and therefore can be risk factors for developing chronic pulmonary infection

A

smoking
recent pneumonia/viral infection
malignancy

97
Q

what 2 things can cause abnormal cilia and therefore can be risk factors for developing chronic pulmonary infection ?

A

kartenagers syndrome

youngs syndrome

98
Q

what 2 things can cause abnormal secretions and therefore can be risk factors for developing chronic pulmonary infection?

A

cystic fibrosis

channelopathies

99
Q

what are the 5 forms of chronic pulmonary infection?

A
  1. intrapulmonary abscess
  2. empyema
  3. chronic bronchial seps
  4. bronchiectasis
  5. CF and others
100
Q

on a CXR of an abescess what will usually be apparent?

A

air/fluid level

101
Q

what is the sequence of events from a viral infection to an abscess?

A

viral infection
staph aureus pneumonia
cavitating pneumonia
abscess

102
Q

what 3 forms of emboli can cause pulmonary abscesses?

A

right sided endocarditis
infected DVT
septicaemia

103
Q

what is empyema?

A

pus in the pleural space

104
Q

what is primary empyema?

A

empyema not caused by pneumonia

105
Q

what is the progression from effusion to empyema?

A

simple parapneumonic effusion
complicated paraneumonic effusion
empyema

106
Q

when are anaerobes likely to be the causative pathogen in lung infection?

A

severe pneumonia

poor dental hygiene

107
Q

what is the sign for empyema on an x ray?

A

D-sign

108
Q

what is used to differentiate between empyema and pleural effusion?

A

CT scan

109
Q

why do exudates occur?

A

due to increase in permeability of local circulation

ie inflammatory causes- infection, cancer, PE

110
Q

why do transudates occur?

A

due to increased hydrostatic pressure within the local circulation (eg cardiac failure)

111
Q

what type of chest drain do you used to drain complicated parapneumonic effusion?

A

small bore seldinger type drain

112
Q

as well as increase disposition to infection, why does bronchiectasis also cause airflow obstruction?

A

bronchi are dilated, inflamed and easily collapsible

similar collapsing to emphysema

113
Q

how does a patient with bronchiectasis present?

A

recurrent lower resp tract infections,
short lived/no response to antibiotics,
persistent sputum production

114
Q

what is chronic bronchial sepsis?

A

presents as bronchial sepsis but no bronchiectasis on the HRCT
confirmed with sputum resulrs

115
Q

what type of patients get chronic bronchial sepsis?

A

younger patients, mainly women, often involved in childcare

olders patients with COPD/airway disease

116
Q

what is the treatment options of bronchiectasis and chronic bronchial sepsis?

A

stop smoking
flu and pneumococcal vaccine
reactive antibodies appropriate to most recent positive culture

117
Q

when a patient with bronchiectasis or chronic bronchial sepsis is actually colonised with persistent bacteria what drug treatment should you give?

A

prophylactic antibiotic
nebulised gentamicin
pulsed IV antibiotics
alternating oral antibiotics

118
Q

what antibiotic has been shown to reduce exacerbation rates in bronchiectasis?

A

low dose macrolide antibiotics

119
Q

what is a congenital cause of bronchiectasis?

A

CF

120
Q

what are the 6 major complications of CF?

A
  1. bronchiectasis
  2. tenacious sputum
  3. biliary obstruction and obstructive hepatitis
  4. pancreatic dysfunction (endocrine and exocrine)
  5. infertility for males
  6. psychological issues for all
121
Q

what does endocrine pancreatic dysfunction in CF cause?

A

CFRDM

cystic fibrosis related diabetes mellitus

122
Q

what does exocrine pancreatic dysfunction in CF cause?

A

steatorrhoea

Respiratory RT (10 decks)

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