Flashcards in Respiratory Infections Deck (122):
where does corzya, pharyngitis, sinusitis and epiglottitis effect?
upper respiratory tract
where does acute bronchitis, pneumonia and influenzae effect?
lower respiratory tract
where is the cut off between upper and lower respiratory tract?
(vocal cords and above = upper
below vocal cords = lower)
what is corzya?
acute viral infection of the nasal passages
what is acute sinusitis usually preceded by?
what type of discharge is associated with acute sinusitis?
purulent nasal discharge
what is the reason diptheria is so life-threatening?
the toxin produced
why is diptheria not seen in the UK anymore?
what is the reason epiglottits (in children) is so life-threatening?
risk of respiratory obstruction
what is acute bronchitis usually preceded by?
what are the clinical features of acute bronchitis?
productive cough (rememeber bronchitis is an over production of mucus)
sometimes a fever
possibly a transient wheeze
normal chest examin
what is the treatment for acute bronchitis?
antibiotics are not indicated unless patient has underlying chronic lung disease
what is an acute exacerbation of chronic bronchitis?
worsening of sputum production (now purulent) of a patient with pre-existing lung disease
what usually precedes an acute exacerbation of chronic bronchitis?
upper respiratroy tract infection
what are the clinical features of acute exacerbation of chronic bronchitis?
ankle oedema (in advanced disease- cor pulmonale)
what is the management of an acute exacerbation of chronic bronchitis? (patient has purulent sputum)
amoxicillin or doxycycline
short steroid course in some cases
(refer if evidence of resp failure or not coping at home)
give oxygen if resp failure
what are the main investigations for a patient who has suspected pneumonia? (7)
why can herpes simplex be reactivated in patients with pneumonia?
why is CRB65 more useful in primary care than CURB 65?
don't need to do a blood test
who tends to get severe chicken pox pneumonia?
what is the management of CAP?
oxygen (maintain SaO2 94-98%)
what can radiological technique can you use to help guide a chest drain?
what type of antibiotic cover is generally needed for hospital acquired pneumonia?
gram negative cover
what type of antibiotic cover is generally needed for aspiration pnumonia?
why is pneumonia caused by legionella tricky to diagnose?
chest symptoms may be absent but GI disturbance is common
who gets both influenza and pneumococcal vaccines?
people over 65
patients with chronic chest/cardiac disease
patients with diabetes
what are the benefits of oseltamivir?
reduced duration of symptoms by one day
reduced use of antibiotics
might reduce infectivity
no data on mortality
how long is the first wave of an influenza pandemic?
when does the second wave of an influenza pandemic occur?
months after the first
C = new onset of confusion
U = urea >7
R = resp rate > 30/min
B = BP, systolic
65 = age 65+
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
what is lobar pneumonia?
confluent consolidation involving a complete lung lobe
what are the 7 major complications of pneumonia?
what is bronchopneumonia?
infection starting in airways and spreading to adjacent alveolar lung
what can be an underlying cause of bronchopneumonia?
complication of viral infection
aspiration of gastric contents
what is a lung abscess?
localised collection of pus
what symptoms does a lung abscess cause?
chronic malaise and fever
what type of pneumonia is more likely to cause a lung abscess?
what is bronchiectasis?
abnormal fixed dilation of the bronchi
what is bronchiectasis usually the result of?
fibrous scarring followng infection (pneumona, TB, cystic fibrosis) or chornic obstruction (tumour)
what is the main consequence of bronchiectasis?
dilated airways accumulate purulent secretions (due to decreased secretion clearance) predisposing to infection
how can the pathology of TB be described?
type IV hypersensitivity (granuloma formation + necrosis)
apart from mycobacteria tuberculosis/bovis/africanum, what type of patients do other mycobacterias usually infect?
in TB what is the cause of the granulomatous inflammation, tissue necrosis and scarring?
T cell response to the organism
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
describe secondary TB?
reinfection/reactivation of TB disease
where does secondary TB tend to remain?
localised in the apices of the lung
what are the ways secondary TB infection can spread to other parts of the body?
airways and/or bloodstream
in primary TB where does there tend to be tissue changes?
Ghon focus- in periphery of mid xone of lung
granulomatous large hilar nodes
in secondary TB where does there tend to be tissue changes?
fibrosing and cavitating apical lesion
In TB what type of granulomatous tissue is formed?
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
what can happen if you are infected with a virulent common organism? (eg TB)
opportunistic pathogen infection
why can TB cause stooping?
if it gets into the bones of the spine
why does subsaharan africa have a high TB rate?
due to HIV prevelance
what are the 6 factors contributing to the global rise of TB?
1. HIV pandemic
2. displacement and migration
4. disruption to health infrastructure arising from political changes and conflict
5. poorly managed TB programmes
6. anti TB drug resistance (MDR)
what infections are part of the M. tuberculosis complex? (ie cause TB)
what are the 2 groups of mycobacteria?
M tuberculosis complex and non tuberculosis mycobacteria
what is a mycoplasmic bacteria?
a typical bacteria which has no cell wall
(eg mycoplasma pneumoniae DIFFERENT TO MYCOBACTERIA)
what type of patients get non-tuberculosis mycobacteria?
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
what is the primary test for TB?
PCR for mycobacteria tuberculosis
How does Interferon Gamma Release Testing (IGRT) work?
quantifies hoe much gamma-inerfoeron is released from circulating T-lymphocytes in response to specific stimuli
what is the pro about IGRT?
no cross reaction with BCG or NTMs- specifically for mycobacterial tuberculosis
what is the con about IGRT?
doesnt differentiate between latent, active TB, or previous treated TB
who do we treat for TB?
(latent, active TB, previously treated TB)
only currently active TB is treated
who must be informed of any cases of highly suspected TB/confirmed cases of TB?
what test shows if a patient has 'open TB'? (ie and therefore are contagious)
positive smear test
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
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
what are the 4 empircal anti-tuberculosis drugs?
all are in tablet form
if patient has HIV and gets TB or NTBM how long must he/she take the 4 antibiotics for?
for children and adults with respiratory and non-respiratory TB what is the drug course?
HRZ(E) 2 months
isoniazide, rifampicin, pyrazinamide (ethambutol)
HR 4 months
(total = 6 months)
for children and adults with meningitis and CNS TB what is the drug course?
HRZ(E) 2 months
isoniazide, rifampicin, pyrazinamide, (ethambutol)
HR 10 months
(total = 12 months)
what is the result of the smear test in the intial phase of TB treatment?
(person is infectious and can be detained in hospital)
what is the result of the smear test in the continuation phase of TB treatment?
(person is no longer infectious and can't be detained in hospital)
what is done in all TB isolates to test if the bacteria susceptibilities?
in vitro drug susceptibility testing
why does initial TB treatment use 4 anti-tuberculosis drugs?
to cover unsuspected resistance
in underdeveloped countries/if compliance is an issue, what is an effective way of management?
Directly Observed Therapy Short-course
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
what are the adverse drug reactions of isoniazid (H)?
cutaneous hypersensitivity (pins and needles)
what causes peripheral neuropathy?
deficiency/or excess of a cofactor of vitB6
(can be caused by isoniazid)
what are the adverse drug reactions of rifampicin (R)?
Febrile reactions/flu syndrome
Tears and urine become orange
what are the adverse drug reactions of pyrazinamide?
anorexia (loss of appetite)
hyperuricaemia (high uric acid conc)
what are the adverse drug reactions of ethambutol?
retrobular neuritis (Colour blind then fully blind)
why do liver function tests need to be regularly measured?
because isoniazide (H), rifampicin (R) and pyrazinamide (Z) can cause hepatitis
when is latent TB treated?
there are certain circumstances- ie if patient is about to undergo immunsuppressive therapy (anti-TNF)
what drugs are used to treat latent TB prior to immunosuppressive therapy?
3 months of Isoniazide (H) and Rifampicin (R) before starting immunosuppressive drugs
what drugs are MDR-TB types resistant to?
isoniazide (H) and rifampicin (R)
what drugs are XDR-TB types resistant to?
what are the groups of patients you should suspect TB in?
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
what type of abnormal host response are risk factors for developing chronic pulmonary infection?
immunodeficiency (congenital or acquired)
immunosuppression (drugs or malignancy)
what type of abnormal innate host defence are risk factors for developing chronic pulmonary infection?
damaged bronchial mucosa
what are the 2 major causes of repeated insult that can be risk factors for developing chronic pulmonary infection?
what 3 things can cause damaged bronchial mucosa and therefore can be risk factors for developing chronic pulmonary infection
recent pneumonia/viral infection
what 2 things can cause abnormal cilia and therefore can be risk factors for developing chronic pulmonary infection ?
what 2 things can cause abnormal secretions and therefore can be risk factors for developing chronic pulmonary infection?
what are the 5 forms of chronic pulmonary infection?
1. intrapulmonary abscess
3. chronic bronchial seps
5. CF and others
on a CXR of an abescess what will usually be apparent?
what is the sequence of events from a viral infection to an abscess?
staph aureus pneumonia
what 3 forms of emboli can cause pulmonary abscesses?
right sided endocarditis
what is empyema?
pus in the pleural space
what is primary empyema?
empyema not caused by pneumonia
what is the progression from effusion to empyema?
simple parapneumonic effusion
complicated paraneumonic effusion
when are anaerobes likely to be the causative pathogen in lung infection?
poor dental hygiene
what is the sign for empyema on an x ray?
what is used to differentiate between empyema and pleural effusion?
why do exudates occur?
due to increase in permeability of local circulation
(ie inflammatory causes- infection, cancer, PE)
why do transudates occur?
due to increased hydrostatic pressure within the local circulation (eg cardiac failure)
what type of chest drain do you used to drain complicated parapneumonic effusion?
small bore seldinger type drain
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)
how does a patient with bronchiectasis present?
recurrent lower resp tract infections,
short lived/no response to antibiotics,
persistent sputum production
what is chronic bronchial sepsis?
presents as bronchial sepsis but no bronchiectasis on the HRCT
confirmed with sputum resulrs
what type of patients get chronic bronchial sepsis?
younger patients, mainly women, often involved in childcare
olders patients with COPD/airway disease
what is the treatment options of bronchiectasis and chronic bronchial sepsis?
flu and pneumococcal vaccine
reactive antibodies appropriate to most recent positive culture
when a patient with bronchiectasis or chronic bronchial sepsis is actually colonised with persistent bacteria what drug treatment should you give?
pulsed IV antibiotics
alternating oral antibiotics
what antibiotic has been shown to reduce exacerbation rates in bronchiectasis?
low dose macrolide antibiotics
what is a congenital cause of bronchiectasis?
what are the 6 major complications of CF?
2. tenacious sputum
3. biliary obstruction and obstructive hepatitis
4. pancreatic dysfunction (endocrine and exocrine)
5. infertility for males
6. psychological issues for all
what does endocrine pancreatic dysfunction in CF cause?
cystic fibrosis related diabetes mellitus