Respiratory pathology 2 Flashcards
Total time for the treatment if Tb
6 months if medication and rehabilitation which involves other members of the MDT
Determinants of Tb
Lower income regions
Under nourishment of food
Immunosuppressed people eg HIV
Elderly , neonates and the diabetics
Those with mental health conditions and those in prisons
National epidemiology of Tb
Most prevalent in London
With most people being people who were not vaccinated gainst tb with the BCG vaccine
Summary of epidemiology
TB incidence over time is falling, 2% per year. But, recent rise
TB is still a disease of the poor / social risk factors
TB is the number 1 killer of communicable diseases
TB kills more than HIV and Malaria together
TB is not evenly distributed, globally or nationally
2/3 of all TB cases (prevalence) in 8 countries
An estimated 2 billion people are infected worldwide
Cause TB
mycobacteria species for example tuberculosis , M. africanum and mycobacterium.bovis
PRESENT IN SOIL AND WATER
other species of non-tuberculosis mycobacteria
Non-tuberculous mycobacteria, NTM-infections / ‘Atypical mycobacteria
Leprosy (M.leprae)
characteristics of mycobacteria that cause tuberculosis (AAFBs)
Uniquely has a very thick fatty cell wall
Resistant to acids, alkalis and detergents
Resistant to neutrophil and macrophage destruction
Acid - and alcohol - fast bacilli (AAFB) (Ziehl Neilson stain)
however not all AAFB are mycobacterium
transmission of tuberculosis
airborne only through the laryngeal and pulmonary system
TB in the lymph nodes cannot be spread in other regions in the body
non medicated management of TB
good circulation of air in the house ; TB bacteria will remain suspended in air for many hours
outdoors mycobacteria is eliminated by UV radiation and dilution.
ways in which TB is not spread
Shaking hands
Sharing food
Touching surfaces
Sharing toothbrushes
Kissing
spread of mycobacterium bovis
spread through drinking of unpasteurized milk
cells involved in the defence against TB
as TB is not sensitive to destruction of macrophage and neutrophils , it can only be destroyed by T helper cells that is lymphocytes.
immunopathology of TB
many activated macrophages form epithelioid cells and forms langhan”s giant cells which form granuloma with central necrosis
consequences of the immunological response of t helper cells
Eliminates / Reduces number of invading mycobacteria
Tissue destruction is a consequence of activation of macrophages
history of dvlpmt of tuberculosis
primary infection - helps to build immunity and they are drained on the lymphatic nodes that is the hila lymph nodes , and there are no symptoms , there is development of immunity against tuberculoprotein
primary infection of tuberculosis
progressive disease
contained latent
cleared cured
types of primary TB infection
tuberculosis bronchopneumonia
miliary tuberculosis
tuberculosis bronchopneumonia
there is abnormal enlargement of the hilar node which leads to compression of the bronchi and later on collapse of the lobe has a poor prognosis
milliary tuberculosis
there is spread of the bacteria to multiple organs by blood ; presents with widespread small granulomata
post primary disease
only present in humans the bacteria enters dormant stage with little to no replication over a prolonged period of time
there is a balanced replication and destruction of the immune mechanisms
spread of tuberculosis
primary - progressive primary - milliary , meningeal , pleural TB - post primary pulmonary and skeletal disease - genitourinary and cutaneous TB
clinical presentation of TB
Coughing
fever
sweats at night
weight loss
methods of diagnosing active TB
chest x ray
presentation of mediastinal lymphadenopathy
there is a white patch at the mediastinum just next to the heart
presentation of miliary tuberculosis in an x ray
presents as spots on the lung
tests performed to test for TB
Sputum; 3 samples, 8-24hrs gap, at least 1 early morning sample
Induced sputum
Bronchoscopy with BAL
Endobronchial ultrasound (EBUS) with biopsy
Lumbar puncture in CNS TB / biopsy
Urine in urogenital TB
Aspirate/biopsy from tissue ( lymph-node, bone, joint, brain, abscess …
clinical management of TB
isoniazid
pyrazinamide
rifampicin
ethambutol
rules for prescription of TB
Test for HIV, Hepatitis B and C
Single agent treatment leads to drug resistant organisms within 14 days
Therapy must continue for at least 6 months
Standard treatment of TB
12 tablets a day for 6 moths
2 moths of all the tablets
4 months of rifampicin and isoniazid
pyridoxine with isoniazid which reduces risk of neuropathy
steroids cause side effects of the CNS , milliary TB , pericardial
vitamin D substitution
side effects of ethambutol
Optic neuropathy (check visual acuity)
Pyrazinamide side effects
hepatitis
gout
Isoniazid side effects
Hepatitis
Peripheral neuropathy (pyridoxine B6)
rifampicin side effects
Orange ‘Irn Bru’ urine/tears/lenses
Induces liver enzymes, prednisolone, anticonvulsants
All hormonal contraceptive methods ineffective
Hepatitis
side effects of all drugs
rashes
vaccination against TB
BCG vaccination
screening of latent TB
Contacts of people with active pulmonary or laryngeal TB who are aged ≤65 years As hepatotoxicity risk increases with age those aged 66 years or older: CXR only to rule out active TB only
New entrants to Grampian from high incidence areas
‘Pre-biologics’ (TNF-alpha inhibitors)
screening of latent TB
Mantoux skin test or Interferon Gamma Release Assay (IGRA) blood test
treatment of latent tuberculosis
Rifampicin & Isoniazid for three months, or
Isoniazid or Rifampicin only for six months or
Rifapentine & Isoniazid once weekly for 12 weeks
possible causes of lung infections
microorganism pathogenicity
capacity to resist infection
population at risk that is the removal of the commensal flora
upper respiratory tract infections
common cold
sore throat
acute laryngotracheobronchitis (croup)
laryngitis
sinusitis
acute epiglottitis
acute epiglottitis causative agent
haemophilus influenzae ( Virus)
group A beta haemolytic streptococci ( bacteria )
lower respiratory tract infections
bronchitis
bronchiolitis
pneumonia
mechanisms of defence of the respiratory tract
macrophage engulfs and destroys the bacteria and the foreign particles , production of mucus , the foreign material is wafted away , coughed up through the cough reflex
influenza viral pneumonia
influenza virus during a primary attack causes a destruction of the mucociliary escalator system , because of this the commensal flora staph aureus can thrive and not be removed leading to an acute inflammation
viral infections in the lungs
bronchiolitis
pneumonitis
SARS-CoV-2 (COVID19)
viral infection where there is inflammation of the bronchioles leading to pneumonia of the lungs
classification of pneumonia
part of the lung affected
the circumstances that is hospital acquired or community acquired
the type of causative agent
hospital acquired pneumonia
not sensitive to antibiotics
types of pneumonia based on the cause
Community Acquired Pneumonia
Hospital Acquired (Nosocomial) Pneumonia
Pneumonia in the Immunocompromised
Atypical Pneumonia
Aspiration Pneumonia
Recurrent Pneumonia
anatomical classification of pneumonia
bronchopneumonia
segmental pneumonia
lobar pneumonia
hypostatic pneumonia
fluid retention at the bottom of the lung that causes an optimum environment for the growth of bacteria
aspiration pneumonia
aspiration of contents that lead to movement of fluids into the inner tubes
bronchopneumonia
( exudation ) fluid in the bronchi
seen on the x ray as basal patchy opacification
vasodilation of the bronchioles from the inflammatory response
lobar pneumonia
collapse of an entire lobe caused by an inflammatory response
a whole lobe collapses
exudation of fluid and bleeding
vasodilation of the bronchioles
complications of pneumonia
1.lung abscess form necrosis of the lung tissue
2.pleural effusion caused by infection of the pleura
3.pleurisy which is the inflammation of the pleura
4.bronchiectasis which is the widening of the bronchi such that there is build up of fluid for
bacterial growth .
5.empyema which is collection of pus in the pleural cavity
6.organisation which leads to development of fibrotic tissue such as the case of cryptogenic organising pneumonia
causes of lung abscess
1.aspiration pneumonia
2.tumor
3.organism eg staph
4.metastatic pyaemia that is pus movement
5.necrotic lung
bronchiectasis
Pathological dilatation of Bronchi
causes of bronchiectasis
Severe Infective Episode
Recurrent Infections - many causes
Proximal Bronchial Obstruction
Lung Parenchymal Destruction
most common age group affected by bronchiectasis
most start in childhood
bronchiectasis
COUGH, ABUNDANT PURULENT FOUL SPUTUM, haemoptysis, signs of chronic infection
Coarse crackles, clubbing
Thin section CT
Postural Drainage, Antibiotics, Surgery
diagnostic method of bronchiectasis
a thin CT section
located at the edge of the lung
complications of bronchiectasis
suppuration that is the filling up of the bronchi with pus.
haemorrhage - excessive bleeding from systemic blood supply ( blood supply in the bronchi is from brachial artery and therefore high pressure blood )
aspiration pneumonia
Vomiting
Oesophageal Lesion
Obstetric Anaesthesia
Neuromuscular Disorders
Sedation
opportunistic infections
infections only present in the immunocompromised such as HIV
Low grade bacterial pathogens
CMV
Pneumocystis jirovecii
Other fungi and yeasts
causes of recurrent lung infection
Local Bronchial Obstruction
Local Pulmonary Damage
Generalised Lung Disease COPD?
Non-Respiratory Disease (HIV, other)?, Aspiration?
abnormal gas exchange
type 1 lower partial pressure for oxygen
type 2 lower partial pressure for carbon dioxide
both in the arterial blood
consequences of abnormal pulmonary gas exchange
shunt
ventilation perfusion mismatch
alveolar hypoventilation
diffusion impairement
ventilation perfusion normal values
Normally breathing ~4 l/min. Cardiac Output is ~5 l/min so normal V/Q is 4/5 or 0.8
what is ventilation perfusion mismatch
blood is sent to regions of the lungs where there is less ventilation leading to flow of not fully oxygenated blood back to the lungs
oxygen is given to reverse
shunt
blood passing too the lungs without any oxygenation
right side of the heart has deoxygenated blood
increase in oxygen doesn`t solve this
diseases that display ventilation perfusion abnormality
there is oxygenation although the alveoli is abnormal
Bronchitis / Bronchiolitis
Bronchopneumonia
COPD
diseases that display shunt system
there is no ventilation of the abnormal alveoli
Severe bronchopneumonia
Lobar pattern with large areas of consolidation
alveolar hypoventilation
Hypoventilation increases PACO2, and thus increases PaCO2
Increase in PACO2 decreases PAO2, which causes PaO2 to fall
Fall in PaO2 due to hypoventilation is corrected by raising FIO2
causes of alveolar hypoventilation
1.Upper airway or tracheal obstruction
2.Mechanical problems with breathing mechanism (chest wall damage)
3.Functional problems with breathing mechanism (muscle paralysis, diaphragmatic damage)
4.Neurological problems with breathing mechanism
5.Peripheral nerve damage or loss of function
CNS malfunction – opiate poisoning, COPD
