Respiratory Infections Flashcards

(122 cards)

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
why is pneumonia caused by legionella tricky to diagnose?
chest symptoms may be absent but GI disturbance is common
26
who gets both influenza and pneumococcal vaccines?
people over 65 patients with chronic chest/cardiac disease patients with diabetes immunocompromised patients
27
what are the benefits of oseltamivir?
reduced duration of symptoms by one day reduced use of antibiotics might reduce infectivity no data on mortality
28
how long is the first wave of an influenza pandemic?
3-5 months
29
when does the second wave of an influenza pandemic occur?
months after the first
30
explain CURB65
``` C = new onset of confusion U = urea >7 R = resp rate > 30/min B = BP, systolic 65 = age 65+ ```
31
why does infection cause consolidation of an area of the lungs?
infection causes an inflammatory exudate (localised oedema) due to the inflammatory-induce leaky blood capillaries. the fluid filled spaces lead to consolidaiton
32
what is lobar pneumonia?
confluent consolidation involving a complete lung lobe
33
what are the 7 major complications of pneumonia?
``` respiratory failure pleural effusion empyema abscess fibrous scarring bronchiectasis death ```
34
what is bronchopneumonia?
infection starting in airways and spreading to adjacent alveolar lung
35
what can be an underlying cause of bronchopneumonia?
COPD cardiac failure complication of viral infection aspiration of gastric contents
36
what is a lung abscess?
localised collection of pus
37
what symptoms does a lung abscess cause?
chronic malaise and fever
38
what type of pneumonia is more likely to cause a lung abscess?
aspiration pneumonia
39
what is bronchiectasis?
abnormal fixed dilation of the bronchi
40
what is bronchiectasis usually the result of?
fibrous scarring followng infection (pneumona, TB, cystic fibrosis) or chornic obstruction (tumour)
41
what is the main consequence of bronchiectasis?
dilated airways accumulate purulent secretions (due to decreased secretion clearance) predisposing to infection
42
how can the pathology of TB be described?
type IV hypersensitivity (granuloma formation + necrosis)
43
apart from mycobacteria tuberculosis/bovis/africanum, what type of patients do other mycobacterias usually infect?
immunocompromised host
44
in TB what is the cause of the granulomatous inflammation, tissue necrosis and scarring?
T cell response to the organism
45
describe primary TB? (1st exposure)
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
46
describe secondary TB?
reinfection/reactivation of TB disease
47
where does secondary TB tend to remain?
localised in the apices of the lung
48
what are the ways secondary TB infection can spread to other parts of the body?
airways and/or bloodstream
49
in primary TB where does there tend to be tissue changes?
Ghon focus- in periphery of mid xone of lung | granulomatous large hilar nodes
50
in secondary TB where does there tend to be tissue changes?
fibrosing and cavitating apical lesion
51
In TB what type of granulomatous tissue is formed?
``` caseating granuloma (necrotic) ```
52
why can TB reactivate?
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
what can happen if you are infected with a virulent common organism? (eg TB)
opportunistic pathogen infection
54
why can TB cause stooping?
if it gets into the bones of the spine
55
why does subsaharan africa have a high TB rate?
due to HIV prevelance
56
what are the 6 factors contributing to the global rise of TB?
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
what infections are part of the M. tuberculosis complex? (ie cause TB)
M. tuberulosis M. bovis M. africanum
58
what are the 2 groups of mycobacteria?
M tuberculosis complex and non tuberculosis mycobacteria
59
what is a mycoplasmic bacteria?
a typical bacteria which has no cell wall | eg mycoplasma pneumoniae DIFFERENT TO MYCOBACTERIA
60
what type of patients get non-tuberculosis mycobacteria?
immunsuppressed
61
what are the 5 main risk factors for TB?
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
what is the primary test for TB?
PCR for mycobacteria tuberculosis
63
How does Interferon Gamma Release Testing (IGRT) work?
quantifies hoe much gamma-inerfoeron is released from circulating T-lymphocytes in response to specific stimuli (IL12-gIFN pathway)
64
what is the pro about IGRT?
no cross reaction with BCG or NTMs- specifically for mycobacterial tuberculosis
65
what is the con about IGRT?
doesnt differentiate between latent, active TB, or previous treated TB
66
who do we treat for TB? | latent, active TB, previously treated TB
only currently active TB is treated
67
who must be informed of any cases of highly suspected TB/confirmed cases of TB?
public health
68
what test shows if a patient has 'open TB'? (ie and therefore are contagious)
positive smear test
69
if a patient has 'open TB' (and therefore are contagious) what can be done to reduce spread?
patient can be detained in hospital until they no longer have 'open TB' BUT patients cannot be forced to take treatment
70
why do you start with empircal treatment for TB before having the bacteria's sensitivities?
cultures take 8 weeks, so treatment has to start before the results have come back
71
what are the 4 empircal anti-tuberculosis drugs? | antibiotics
``` (R) rifampicin (H) isoniazide (Z) pyrazinamide (E) ethambutol all are in tablet form ```
72
if patient has HIV and gets TB or NTBM how long must he/she take the 4 antibiotics for?
life long
73
for children and adults with respiratory and non-respiratory TB what is the drug course?
``` Initial phase: HRZ(E) 2 months isoniazide, rifampicin, pyrazinamide (ethambutol) Continuation phase: HR 4 months isoniazide, rifampicin ``` (total = 6 months)
74
for children and adults with meningitis and CNS TB what is the drug course?
``` Initial phase: HRZ(E) 2 months isoniazide, rifampicin, pyrazinamide, (ethambutol) Continuation phase: HR 10 months isoniazide, rifampicin ``` (total = 12 months)
75
what is the result of the smear test in the intial phase of TB treatment?
positive | person is infectious and can be detained in hospital
76
what is the result of the smear test in the continuation phase of TB treatment?
negative | person is no longer infectious and can't be detained in hospital
77
what is done in all TB isolates to test if the bacteria susceptibilities?
in vitro drug susceptibility testing
78
why does initial TB treatment use 4 anti-tuberculosis drugs?
to cover unsuspected resistance
79
in underdeveloped countries/if compliance is an issue, what is an effective way of management?
Directly Observed Therapy Short-course | DOTS
80
what is a Directly Observed Therapy Short-course?
a course of treatment where a responsible observer administers the drugs and observes ingestion of the drugs ensuring compliance
81
what are the adverse drug reactions of isoniazid (H)?
hepatitis cutaneous hypersensitivity (pins and needles) peripheral neuropathy
82
what causes peripheral neuropathy?
deficiency/or excess of a cofactor of vitB6 | can be caused by isoniazid
83
what are the adverse drug reactions of rifampicin (R)?
``` hepatitis cutaneous reactions GI Upset Febrile reactions/flu syndrome Tears and urine become orange ```
84
what are the adverse drug reactions of pyrazinamide?
``` hepatitis anorexia (loss of appetite) vomiting flushing hyperuricaemia (high uric acid conc) arthlagia ```
85
what are the adverse drug reactions of ethambutol?
``` arthralgia retrobular neuritis (Colour blind then fully blind) ```
86
why do liver function tests need to be regularly measured?
because isoniazide (H), rifampicin (R) and pyrazinamide (Z) can cause hepatitis
87
when is latent TB treated?
it isn't | there are certain circumstances- ie if patient is about to undergo immunsuppressive therapy (anti-TNF)
88
what drugs are used to treat latent TB prior to immunosuppressive therapy?
3 months of Isoniazide (H) and Rifampicin (R) before starting immunosuppressive drugs
89
what drugs are MDR-TB types resistant to? | multi-drug resistant
isoniazide (H) and rifampicin (R)
90
what drugs are XDR-TB types resistant to? | extra-drug resistant
isoniazide (H) rifampicin (R) fluoroquinolones injectables
91
what are the groups of patients you should suspect TB in?
return travellers immunocompromised patients non-resolving pneumonia
92
what are the 3 classes of risk factors for developing chronic pulmonary infections?
1. abnormal host response 2. abnormal innate host defence 3. repeated insult
93
what type of abnormal host response are risk factors for developing chronic pulmonary infection?
immunodeficiency (congenital or acquired) | immunosuppression (drugs or malignancy)
94
what type of abnormal innate host defence are risk factors for developing chronic pulmonary infection?
damaged bronchial mucosa abnormal cilia abnormal secretions
95
what are the 2 major causes of repeated insult that can be risk factors for developing chronic pulmonary infection?
aspiration | indwelling material
96
what 3 things can cause damaged bronchial mucosa and therefore can be risk factors for developing chronic pulmonary infection
smoking recent pneumonia/viral infection malignancy
97
what 2 things can cause abnormal cilia and therefore can be risk factors for developing chronic pulmonary infection ?
kartenagers syndrome | youngs syndrome
98
what 2 things can cause abnormal secretions and therefore can be risk factors for developing chronic pulmonary infection?
cystic fibrosis | channelopathies
99
what are the 5 forms of chronic pulmonary infection?
1. intrapulmonary abscess 2. empyema 3. chronic bronchial seps 4. bronchiectasis 5. CF and others
100
on a CXR of an abescess what will usually be apparent?
air/fluid level
101
what is the sequence of events from a viral infection to an abscess?
viral infection staph aureus pneumonia cavitating pneumonia abscess
102
what 3 forms of emboli can cause pulmonary abscesses?
right sided endocarditis infected DVT septicaemia
103
what is empyema?
pus in the pleural space
104
what is primary empyema?
empyema not caused by pneumonia
105
what is the progression from effusion to empyema?
simple parapneumonic effusion complicated paraneumonic effusion empyema
106
when are anaerobes likely to be the causative pathogen in lung infection?
severe pneumonia | poor dental hygiene
107
what is the sign for empyema on an x ray?
D-sign
108
what is used to differentiate between empyema and pleural effusion?
CT scan
109
why do exudates occur?
due to increase in permeability of local circulation | ie inflammatory causes- infection, cancer, PE
110
why do transudates occur?
due to increased hydrostatic pressure within the local circulation (eg cardiac failure)
111
what type of chest drain do you used to drain complicated parapneumonic effusion?
small bore seldinger type drain
112
as well as increase disposition to infection, why does bronchiectasis also cause airflow obstruction?
bronchi are dilated, inflamed and easily collapsible | similar collapsing to emphysema
113
how does a patient with bronchiectasis present?
recurrent lower resp tract infections, short lived/no response to antibiotics, persistent sputum production
114
what is chronic bronchial sepsis?
presents as bronchial sepsis but no bronchiectasis on the HRCT confirmed with sputum resulrs
115
what type of patients get chronic bronchial sepsis?
younger patients, mainly women, often involved in childcare | olders patients with COPD/airway disease
116
what is the treatment options of bronchiectasis and chronic bronchial sepsis?
stop smoking flu and pneumococcal vaccine reactive antibodies appropriate to most recent positive culture
117
when a patient with bronchiectasis or chronic bronchial sepsis is actually colonised with persistent bacteria what drug treatment should you give?
prophylactic antibiotic nebulised gentamicin pulsed IV antibiotics alternating oral antibiotics
118
what antibiotic has been shown to reduce exacerbation rates in bronchiectasis?
low dose macrolide antibiotics
119
what is a congenital cause of bronchiectasis?
CF
120
what are the 6 major complications of CF?
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
what does endocrine pancreatic dysfunction in CF cause?
CFRDM | cystic fibrosis related diabetes mellitus
122
what does exocrine pancreatic dysfunction in CF cause?
steatorrhoea