week 5: respiratory pathology Flashcards
what is a pulmonary disease
- diseases that cause airflow blockage and breathing related problems
what is the differnce between an obstructive and restrictive disease?
obstructive: can get air in, stuggle to get it out
- air flow limitation
- partial/complete blockage
- abnormal narrowing
- loss of elastic recoil
- decrease of max respiratory airflow (decrease FEV)
- eg. emphysema, chronic brochitis, asthma
restrictive: can’t get air in
- decreased expansion of lung parenchyma
- decreased total lung capacity
-acute and chronic infiltrative diseases: (pulmonary oedma, RA, intertestial lung disease)
- chest wall conditions: neuromuscular diease: polio, kyphoscoliosis, RA
describe emphysema
- abnormal/permenant enlargement of airspaces distal to terminal bronchioles, and destruction of alveolar walls
what is the cause?
- smoking (majority)
- people born with antitryspin deficiency
emphysema develops when there is an imbalance between:
oxidant + protease: anti-oxidants, anti-protease
- destruction of alveolar walls and enlargments of airspaces develops
pathophysiology of emphysema
- tobacco smoke
- inflammatioon fo airway epithelium
- infiltration fo inflammatory cells
- break down of luncg elastic tissue
- emphysema (destruction of alveolar septa and loss of elastic recoil fo bronchial walls)
- resulting in airway obstruction, air tapping, loss of gas exchange, infection
what is air trapping in Emphysema?
when air become trapped in distant airspaces, making it hard to push air out due to:
- inflammation and fibrosis in airways
- loss of elastic recoil
- loss of tethering in airways
- increase of smooth muscle and bronchspasm
- airways becoming floppy and collaspsing
- loss of elastic recoil leading to decreased flow
how do bullae develop with emyphysema?
- they are air filled spaces within the lungs that take up/waste areas of lungs
what do X-RAys look like when people have emphysema?
- less lung tissue: this shows up black
- can see “bubbles” which are enlarged bullae
- larger luncgs with low set diaphragms
emphysema symptoms
- progressive dyspnoea (shortness fo breath)
- hunched over (kyphosis)
- increased work of breathing rate
- pursed lip breathing (prolongs repiritory phase and opens airways)
- barrell chested/hyperinflated
- cough/wheeze
- weight loss and muscle atrophy
- less lung chest tissue at front
how does emphysema lead to death?
symptoms may not manifest until 1/3 of lung parenchyma is damged
death can result from
- respiratory failure
- right sided failure
- pneumothorax (air outside the lung)
describe chronic bronchitis
- persistant cough with sputum production fro at least 3 months in at least 2 consecutive years (in absense of other causes)
- chronic inflammation by inhaled smoke (90% ciggarette)
- when there is a hypersecretion of musus in large airways
- marked increase of goblet cells of small airways
define goblet cell
- modified epithelial cells that secrete mucus on the surface of mucous membranes of organs
- particularly those of the lower digestive tract and airways
functions of ciliated epithelial cells and how does this change with chronic bronchitits
form a mucocilliary escalator:
- layer of fluid and mucins lining the peipthelium function to clean the airways by moving mucous continuously from lower respiritory tract
interferes with cililary actions:
- nicotine induces expression of epidermal growth factors in ciliated cells (metaplasia)
- shortens cilia, and decreases beat frequency
- disruption to genes of epithelium
- less hydration of mucous
- slows cilial regeneration
other morphological changes of chronic bronchitits
hyperplasia of muscous secreting glands and incease of goblet cells in airway epithelium
- more mucous
- thicker mucous
- easier to colonise
bronchial walls inflammed and thickened
inhibited availabiloyt of bronchial and alveolar leukocytes
cilial function impaired
pathophysiology of chronic bronchitis
- tobacco smoke
- inflammation of airway epithelium
- infiltration fo inflammatory cells and release of cytokines
- continuous brachial irritation and inflammation
- chronic bronchitis (bronchial edema, hypersecretion of mucus, bacterial colonisation of airways)
- resulting in airway obstruction, air trapping, loss of gas exchange, infection
describe asthma
- chronic infammation of airways which can increase bronchial hyper-responsiveness
- inflammatiopn can cause episodes of wheezing, brethlessness, chest tightness, and coughing (night and morning)
- the intensity vaires, and can be treated spontaneously or with medicine
pathophysiology of asthma
causes:
- allergen or irratant exposure
mediators:
1. immune activation
2. mast cell degranulation
3. release of chemical mediators/vasoactive mediatiors/ chemotaxic mediators
response
5. chemical mediators stimmulate nerve endings, releasing nuerotransmitters causing brachial hyper-responsivness/airway obstuction
6. vasoactive mediators increase vasodilation and capilliary permeability, causing branchospasms, vascular congestion, mucus secretion, impaired cilliary action, increased hyperesponsivness/airway obstruction
7. chemotaxic mediators: cause cellular infiltration (can directly casue asthma), cause autonomic disregulation (direct cause of asthma), releases nueropeptides, leading to epithelial lining removal and fibrosis (excessive connective tissue), leading to airway obstuction/asthma
how does asthma obstruct airflow
- smooth muscle hypertrophy and hyperplasia
- inflammatory cell infiltration
- edma
- goblet cell and mucous gland hyperplasia
- mucpus hypersecretion
- protien deposition, including collagen
- epithelial desquamation (peeling)
how does asthma lead to hyperesponsiveness
- exaggerated bronchoconstricter response (constriction of the airways), to indirect/direct challenge
- bronchoconstriction happens in association with coughing, wheezing, shortness of breath
define COPD
Chronic obstructive pulmonary disease
- such as asthma, chronic bronchitis, and emphysema
charactersitics of COPD
- state is characterised by amount of airflow obstruction that is not fully reversible
- irreversible: effects of inflammation, fibrosis, and remodelling of peripheral airways
- it is a progressive diabiling disease
- has systemic effects
types of COPD
- genetically determined
- related to early life events
- infection related
- related to smoking/vaping
- enviromental exposure
right sided heart failure and COPD
- low oxygen levels due to COPD cause a rise in blood pressure in the arteries of the lungs
- increase in pressure places excess strain on the heart’s right ventricle as it works to pump blood through the lungs.
types of respiritory drugs? can both restrictive and obstructive use drugs for help?
- there is no drugs to help restictive diseases
respiritory drugs:
- bronchidilators
- inhaled corticosteroids
- anitbiotics, antivirals, antifungals
- drugs for cough
- oxygen
what are infectious conditions of lung
- inflamm of lung cuased by infection with bacteria, viruses, and other organisms
- accumulation of inflamm cells in alveolar spaces
- most are in upper respiratory tract-not major threats
- lower respiratory tract infections can develop from a virus or bacteria. eg. pnuemonia
describe pnumonia
- can result when pulmonary defence isnt storng enough
- clearing mechanism may be compromised
- many chronic diseases aquire terminal pnuemonia
pathophysiology of pneumonia
- lower airways are usually sterile
- if person is immunocompromised, a smoker, imparied cough etc. it can establish infection in lower tracts
- alveolar macrophages clear pathogen quickly with out any inflamm infiltration
- however if persistant can tirgger large inflamm response
- therfore: cytokine release, mediators, cellular response, exudate IN THE LUNGS
- not good for gas exchange
what does X-RAYs look like of pnumonia
- the build up of exudate appears white
what is atelectasis
- ioncomplete expansion of lungs, or collapse lung, producing areas of relitivley airless pulmonary parenchyma
types/aquired atelectasis:
- resorbtion (complete obstruction, resorbtion of o2)
- compression (partially/completley filled with fluid)
- contraction (local/general fibrotic changes preventing full expansion)
