Respiratory medicine Flashcards
What is pleuritis
How is it commonly diagnosed
Main symptom
Inflammation of pleura
Pleural rub can be hears
Chest pain whenever you breath or cough
Role of central chemoreceptors
Detect changes in pCO2 via changes in [H+] from carbonic acid
Role of peripheral chemoreceptors ; where are they found?
In the aortic arch and carotid arteries
Involved mainly in detecting changes in pO2 ; cause hyperventilation when pO2 falls
The medulla comprise of two groups of nerves ; name them
Describe Cheyne-stokes breathing
Type of abnormal breathing
Characterised by crescendo-decrescendo pattern of tidal volume followed by a period of apnea
often seen in patients with congestive heart failure
Role of the DRG
Innervate the diaphragm and external ICM
Switches them on and off to cause a rhythmic breathing pattern
diaphragm contraction causes inspiration
Role of VRG
Involved in forced expiration
Innervate abdominal muscles and internal ICM
therefore involved during forced expiration
Describe the role of the pneumotaxic centre, state its location
Location is pons
Fine tunes breathing by sending inhibitory impulses to the DRG
Limits inspiration to prevent over inflation
Role of vagus nerve in respiration
Sends afferent information from there lungs to the DRG
Role is to prevent over inflation by switching off inspiration
Sputum colours and what they indicate
Grey/green indicates elevated WBC but not always
Causes of cough
Common cold
Tracheitis - painful cough due to viral infection
COPD
Pneumonia
Bronchitis
Bronchiectasis - enlarged air ways and excess mucus (can be due to CF)
TB
Congestive heart failure - plus breathlessness and oedema of ankles
Cancer
Anxiety (Nervous cough )
How do you differentiate between smokers cough and COPD cough ?
Smokers with persistent cough (>3 weeks)
History of smoking associated with haemoptysis (coughing up of blood)
Change in cough
Auscultation of lungs in COPD sufferer
Compare healthy and abnormal breathing
What is a polyphonic wheeze
Small pause between insipiration and expiration in healthy breathing
Patients with COPD have prolonged expiration (2-3 times as long than inspiration)
Polyphonic wheeze - varied freq common in COPD
What is a monophonic wheeze
Monophonic wheeze may indicate tumour in one lung
Use of spirometer in COPD
Confirm diagnosis - not used as first step
Tells us severity of airways obstruction
Identify those most at risk
How to diagnose between COPD or ephysema
COPD - chronic bronchitis and some emphysema
Emphysema - some chronic bronchitis
How to diagnose between COPD or ephysema
COPD - chronic bronchitis and some emphysema
Emphysema - some chronic bronchitis
Difference between obstructive and restrictive lung diseases
In obstructive low FEV1:FVC
In restrictive , both FEV1 and FVC are low so ratio unaffected
Low FEV1 in both
Why might Hb increase in COPD sufferers
Due to polycythaemia due to adaptation of body to prolonged hypoxia (bc impaired lung function )
Can beta blockers be prescribed to patients with COPD and hypertension
Yes as long as spirometer test rules out asthma
Location of central chemoreceptors
Medulla
explain respiratory acidosis
impaired lung function due to COPD/pneumonia/asthma/MG/muscle dystrophy can lead to CO2 accumulation and respiratory acidosis - kidneys respond by excreting [H+] and reabsorbing [HCO3-]
characterised by increased PaCO2 (arterial partial pressure of CO2)
pCO2, pO2 and pH are all ventilation stimuli
place them in order of importance
pCO2
pH
pO2
fucntion of neural regulation of ventilation
Sets the rhythm and pattern of ventilation
controls respiratory muscles
What is respiratory depression ?
how is it reversed ?
Occurs when the rate and/or depth of respiration is insufficient to maintain adequate gas exchange in the lungs
reverse by analeptics
Describe the role of the apneustic centre
Responsible for prolonged insipiratory gasps via prolonged DRG stimulation (apneusis) this is observed during severe brain injUrey
what is a sign an asthma attack is severe when you listen to the chest
Silent chest
How does pO2 and pCO2 change during an asthma attack
pO2 increase and pCO2 decreases at first due to hyperventilation
but as airways continue constricting, pCO2 increases and pO2 decreases as gas exchange does not work anymore
Should you give oxygen to a patient with long term chronic lung disease
No because their body has adapted to hypoxia
they will stop breathing if you give them oxygen
Healthy pO2 and pCO2
Healthy pCO2 4.5–6.0 kPa
healthy pO2 >10 kPa
Clinical presentation of COPD
Exercise tolerance reduced
hyper expanded chest
expiratory wheeze bilaterally
COPD spirometry
FEV1/FVC ratio reduced
little/no reversibility post inhaler
low FEV1
Type 1 and type 2 respiratory failure
type 1 - lungs unable to cope because of disease ; pCO2 goes down later
type 2 - chronically low pO2, dependent on hypoxic conditions,
Case 5: A 65 year old man presents with gradual onset breathlessness and dry cough which has worsened over 9 months. He previously smoked 10/day. On examination he is short of breath on mild exertion, clubbed and mildly cyanosed, with fine inspiratory crackles at both bases.
A)COPD
B)Left ventricular failure
C)Bronchiectasis
D)Pulmonary fibrosis
E)Lung cancer
D
what is pulmonary consolidation
presence of exudate in alveoli due to inflammation (seen as white on x-ray)
Most common pathogens causing CAP (COMMUNITY ACQUIRED PNEUMONIA)
S.pneumoniae
H.influenzae
both bacteria
what are the atypical bacteria causing CAP (COMMUNITY ACQUIRED PNEUMONIA)
M.pneumoniae (has no cell wall) ; extra-pulmonary features
L.pneumophila - accompanied by diarrhoea
both cause severe cases of CAP
Microbiological investigations for CAP
Sputum analysis / culture
immunofluorescence on sputum samples
blood cultures
urine sample - test for pneumococcal and legionella antigen
What factors indicate a high risk CAP patient
Confusion
Urea >7mmol/l
Respiratory rate >30 per min
Blood pressure : systolic BP >90mmHg
65 or older
S.pneumoniae typically infect 2 lobes
true or false
False ; typically infects 1 lobe only
what is bronchial breathing
it is abnormal if hear in the parts of the lung that are far from main airways
loud and tubular quality
high pitched
inspiration and expiration last the same amount of time (insipiration normally lasts longer)
definited gap between both phases; caused by asthma, bronchitis, bronchiectasis
What is asthma
Reversible increase in airway constriction
Bronchoconstriction and inflammation are the main features
Reversible decrease in FEV1:FVC
Describe COPD - symptoms , causes, clinical features
involves chronic bronchitis and emphysema (Destroyed alveoli )
can cause coughing up mucus, wheezing, shortness of breath, chest tightness
Clinical features : FEV1 reduced and little variation in PEF
caused by long-term exposure to lung irritants
parasympathetic and sympathetic control of bronchial calibre
In parasympathetic control, ACh actors on muscarinic M3 receptors = bronchoconstriction and increased mucus
In sympathetic control, adrenaline acts of B2-adrenoreceptors = relaxation
What provokes asthmatic attacks
Allergens
Cold air
Viral infections (colds)
Smoking
Exercise
Characteristic features of asthma attacks
Wheezing
Breathlessness
Tight chest
Cough (worse at night in children/exercise)
Decreases in FEV1 that can be reversed by a β2-agonist
acute phase(caused by spasmogens) followed by late phase (caused by chemotaxins) ; late phase is more severe
Spasmogens and chemotaxins released by mast cells and mononuclear cells
What are spasmogens
They cause bronchoconstriction - acute phase of asthma attack
derivants of arachidonic acid formed from membrane lipids
Main examples :
histamine, prostaglandin D2
leukotrienes (C4 & D4)
platelet activating factor (PAF)
What are chemotaxins
Chemicals involved in late phase of asthma attack
Leukotriene B4, PAF(also a spasmogen)
attract leukocytes (eosinophils and mononuclear cells)
Cause inflammation and airway hyper-reactivity
Describe the uses of short term and long-term β2-agonists and the problems with them
Short term: reverses asthma attack immediately by causing bronchodilation
long-acting beta agonists (LABA) given for long term prevention and overnight control
problems : receptor down-regulation (reduced expression of receptors and therefore less sensitivity to drug)
What are xanthines
Bronchodilators but not as effective as beta2-adrenoceptors agonists
used in emergency
Have other effects :
adenosine receptor antagonist (increase HR/BP)
phosphodiesterase inhibitors
Describe the use of muscarinic M-receptor antagonists *
Block parasympathetic bronchoconstriction
used to treat COPD , little value in asthma
Anti-inflammatory agents used for asthma - describe their use and mode of action
Used as preventation , not reversal of an attack
corticosteroids
They work by activating intracellular receptors = altered gene transcription = decrease cytokine production = anti-inflammatory
Describe action of corticosteroids
takes days for action
lipocortin/annexin A1 (secondary messenger) inhibits PLA2 enzyme = less leukotriene/prostaglandin
given with β2-agonists
Describe action of leukotriene receptor antagonist *
Preventative and bronchodilator
antagonise action of leukotrienes (inflammatory mediators)
Asthma treatment guidelines
If salbutamol used >2 times :
increase dose or check if technique is correct, give spacer device to help with delivery of drug, ensure bronchodilator is given before steroid
How is COPD treated ?
stop smoking
vaccinations
β2agonists and long acting anti muscarinic
antibiotics for intercurrent infections
NSAIDs and asthma
NSAIDs may provoke asthma in 15% of sufferers by increasing leukotriene production
Describe the use of steroids as an asthma treatment
Given with beta2 agonists to reduce receptor down-regulation (long term effect of beta2 agonists)
side effects - throat infections and hoarsenses
Type 1 hypersensitivity
What are the clinical effects
Characterised by damage to self material in response to recognition of foreign material
Mainly involves :
IgE mediated activation of mast cells - smooth muscle contraction and leaky capillaries
Clinical effects : hay fever, asthma, eczema, anaphylaxis
Describe type II hypersensitivity
And give examples
IgG and IgM bind to antigen on body cells
Body cells directly attacked by antibodies via action of complement system , NK cells and macrophages
Examples :
Haemolytic disease of the newborne ( due to difference in blood type)
Allergic haemolytic anaemia
Describe type III allergy /autoimmunity
Give 3 examples
Antigen form a complex with IgG which accumulate in joints, glomeruli and blood vessels
Results in activation of complement system
Tissue inflammation and destruction
Examples : rheumatoid arthritis, poststreptococcal glomerulonephritis
Describe type IV allergy Give examples
Caused by cell mediated immunity
Involves TH1 cells
late response (takes days )
Examples : transplant rejection and contact dermatitis
What is vital capacity
Max lung capacity (forced inhale/exhale)
What is the functional residual capacity
Amount of air that remains in the lungs at the end of normal expiration
Compare restrictive and obstructive deficits
Restrictive - reduced capacity of lungs ; lowered FVC but normal FEV1 ; increased/normal FEV1:FVC
examples : scoliosis and pulmonary fibrosis
obstructive - restriction in airways ; FVC Normal but reduced FEV1 ; low FEV1:FVC
examples : COPD
What is FVC and FEV1?
Forced vital capacity (FVC) is the amount of air that can be forcibly exhaled from your lungs
The amount of air exhaled may be measured during the first (FEV1), second (FEV2), and/or third seconds (FEV3) of the forced breath
Predict the approximate effect (if any) that restrictive/obstructive deficits would have on:
- Total lung capacity (TLC)
- Functional residual capacity (FRC)
- Residual volume (RV)
In restrictive ventilatory deficit (e.g. pulmonary fibrosis), TLC will decrease FRC will decrease and RV will remain unchanged.
In obstructive ventilatory deficit (e.g. severe asthma), TLC will remain unchanged FRC will decrease RV will decrease.
List three factors that would decrease gas transfer
low Hb (anaemia)
Thickening of alveolar epithelium due to scarring of lung tissue
Decreased pulmonary capillary blood volume
What is atelectasis
Collapse of lungs
Name the examples vascular pulmonary disease
- Pulmonary Hypertension
- Pulmonary Embolism, Haemorrhage and Infarction
Name examples of pleural disease
Pleurisy
Fluid/air in pleural cavity
Cancer
Describe pneumonia
Inflammatory reaction of the alveoli and interstium (CT) of lung due to infectious pathogen
Symptoms : pus in alveolar space , inflammation of alveolar septa
Explain the difference between bronchitis and pneumonia
Bronchitis is an invasive infection of the bronchi (chronic bronchitis due to prolonged exposure to irritants)
Pneumonia is due to an infection in the alveoli
Causative organisms of pneumonia
Gram +ve and -ve bacteria
Virusus
Mycoplasma
Fungi
Inorganic agents (inhaled dust or gases)
Causative organisms of pneumonia
Gram +ve and -ve bacteria
Virusus
Mycoplasma
Fungi
Inorganic agents (inhaled dust or gases)
Describe the anatomical classification of pneumonia
Lobar pneumonia (organisms spread between alveoli)
Bronchopneumonia : spread from bronchi to alveoli ; starts off in one lobe and eventually spreads to whole lobe
Describe the different types of pneumonia and their typical causative agent
Community acquired:
(Acute) Typical: S pneumoniae is most common cause.
Hospital acquired called Nosocomial
Immuno-compromised patient: S pneumoniae is responsible again
Aspiration pneumonia - occurs when gastric contents/saliva is breathed into the lungs
Chronic pneumonia - common in patients with COPD/lung cancer/immunocompromised/bronchiectasis
Necrotizing pneumonia and lung abscess - uncommon, severe complication of pneumonia ; occurs when infected lung commpresses alveolar capillaries - lung ischaemia
Aspiration pneumonia
occurs when the gastric contents inter the trachea due to abnormal gag reflex e.g stroke/excessive drinking/brain injury/general anaesthesia
pneumonia follows due to irritation from acidic gastric contents and bacteria
symptoms : unconsciousness, repeated vomiting or underlying brain disease (typically MS), coughing up green/bloody phlegm
often necrotising/results in abcess formation
Symptoms and treatment of acute bacterial pneumonia
Symptoms : fever, chill, dyspnoea (shortness of breath) , cough with pus-phlegm , crackles on ausculatiation, confirmation With x-ray
antibitoitic treatment
Possible outcomes of pneumonia
Resolution (recovery)
organization (scarr tissue formation)
abscess formation
empyema (pockets of pus that have collected inside a body cavity)
TB is a form of …
Chronic pneumonia
Describe TB - symptoms and treatment
Localised lesion of granulomatous inflammation (called a Ghon focus)
symptoms : gradual decrease in appetite, weight loss, fever, night sweats, chest pain, prolonged cough with sputum production
slender robes under sputum analysis, identifiied by acid fast stain
Describe the pathogenesis of TB
In first 3 weeks:
Inhaled mycobacteria engulfed by macrophages
Defective phagolysosome formation
Mycobacterial proliferation in macrophages
Mild flu symptoms/ asymptomatic
Cell mediated immune response
Macrophages drain to lymph nodes
Antigens presented to T cells
T cells converted to Th1 cells
Th1 cells activate macrophages (gamma IFN)
Monocytes recruited
Hypersensitivity of host
What is miliary TB
Occurs upon rexposure of the mycobacterium tuberculosis
Cavitation - TB erodes into lung vasculature and then can spread to any organ via the pulmonary vein (most commonly liver,kidney and spleen)
What is metastatic TB
Invasion of brain, kidneys, adrenal glands by mycobacterium tuberculosis
Often latent infection
Describe the course of infection in primary and secondary TB
Primary TB :
- Primary lesion is subpleural caseous granuloma: Ghon focus
- When ghon focus spreads to lymph nodes on hilum and ghon focus begins being broken down via caseating necrosis: Ghon complex
- Heals by fibrous encapsulation.
- Latent TB in tubercle
- Resistance of organism and hypersensitivity of host. Few symptoms
Secondary TB :
- due to reactivation of old lesions/gradual progression of primary TB/reinfection
- extensive tissue damage due to inflammatory response
- caseation erodes into bronchial wall or vessel – live microbes in sputum
- Tuberculous bronchopneumonia
- Vessel: miliary or isolated organ
- immunocompromised patients can go straight to secondary TB
Compare restrictive and obstructive pulmonary diseases
Obstructive disease
Limitation of airflow due to obstruction
Airway narrowing (asthma), loss of elasticity (emphysema) or increased secretions (bronchitis/asthma)
Restrictive disease
Restrict normal lung movement during respiration
Reduced expansion of lung tissue due to fibrosis/chest wall disorders
damage to lungs impairs gaseous exchange leading to hypoxia
Decreased total lung capacity
Describe chronic bronchitis
Hyper-secretion of mucus in large airways or small airways
defined clinically (persistent cough at least 3 consecutive months )
t cells macropahges and neutrophils present
remodelling of airway wall narrows lumen : increased mucus secreting glands/goblet cells/oedematous mucosa and bronchial wall fibrosis
Describe the types of emphysema
Centriacinar (CA) or centrilobular
Dilated respiratory bronchioles
Most common
More common in upper lobes
Smoking related
Panacinar (PA) or panlobular
Dilated alveoli
More common in lower lobes
Hereditary
Features of emphysema of a histological slide
Enlarged alveolar spaces
Presentation and causes of emphysema
Caused by:
Smoking (99%)
Inherited emphysema - α1 anti-trypsin deficiency (protease inhibitor) (1%)
Presentation:
Shortness of breath and prolonged expiration
barrel chest due to use of accessory muscles
Prolonged onset >40 years
Congenital α1 anti-trypsin deficiency will present earlier
Often co-presents with chronic bronchitis - cough and excess mucus production
pursed lips breathing to maintain airway
Mechanism of smoking related emphysema
Lung protected against protealytic enzymes (from inflammatoray cells) by anti-protease enzyme
anti-protease production affected by :
inherited deficiency
smoking stimulates realease of proteases = uncontrolled proteolysis of elastic tisssue
smoking also causes oxidative injury - tissue damage and inactivation of antiproteases
Pneumoconioses
group of fibrosing diseases caused by silica and asbestos
develops over decades even after exposure is stopped
characterised by lesions of particulate laden macrophages and dense collagen (fibrosis)
silicosis and asbestosis associated with increased risk of cancer
causes/symptoms of pleural efffusion
exudate (pus) from pneumonia and cancer
congestive heart failure, kidney disease (fluid overload)/liver disease
symptoms: dyspnea , sharp chest pain when breathing deeply, fever, cough
Bronchiectasis - what is it, causes/symptoms
Permanent dilation of main bronchi and bronchioles from contraction of scar tissue = build up of excess fluid = lungs more vulnerable to infection (as music more likely to stagnate)
damage to epithelium causes bleeding (heamoptysis)
causes: recurrent infection, bronchial obstruction(due to CF/immunodeficiency/immotile cilia syndrome) or lung fibrosis
symptoms : persistent cough, dyspnoea, foul-smelling sputum, digital clubbing
give examples of restrictive disorders if airway and gaseous exchange
Acute ARDS
pulmonary fibroses - scarring of airways due to pollutanuts, medicine or CT disease
pneumoconioses such as asbestosis and silicosis
granulomatous disease - genetic condition where phagocytes malfunction
What is a tubercule ?
enlarged clump of macrophages and lymphocytes
fibroblasts on the outside
central region undergoes caseous necrosis to form a soft tubercule
may later calcify (shows up on x-ray)
Describe emphysema
Irreversible obstructive disease
occurs in terminal bronchioles
dilation of bronchioles and alveoli / destruction of elastic tissue
decreased SA for gaseous exchange
Describe lung fibrosis
Inflammation of alveolar walls - activation of macrophages stimulate fibroblasts
Damaged to pneumocytes = proliferation of type II pneumocytes
fibroblasts lay down collagen - decrease lung expansion
pleural pathologies - describe characteristics and clinical signs
Infection - sharp pain on breathing deeply, dry coughing/sneezing sound
effusion - transudate(excess normal fluid) / exudate (pus)
tumour - pleural effusion can be due to local tumour/metastasis via lymphatics
Infections of the kidneys result in progressive damage ti. The kidneys and impaired renal functions ; this results in
Metabolic acidosis
Equation for alveolar ventilation rate (L/min)
Alveolar ventilation rate = (tidal volume - dead space) x respiratory rate
What is consolidation caused by
fluid accumulation in the alveolar airspaces
pus, blood, malignant cells, lymphatic fluid
Identify the conditions and suggest the possible causes
Right pleural effusion
infection , trauma, malignancy, CHF
Identify the condition
left tension pneumothorax
left side of thorax is more visible compared to the right
lack of lung marking extending to the periphery
trachea and heart borders also shifted to the right
Identify the condition
rounded area of increased density behind the heart = lung mass on the left side behind the heart
density of heart should be the same throughout but it is more dense on the left than right
describe metabolic acidosis
due to decreased HCO3- (shift eqm to the right); characterised by low blood pH and hyperventilation ; causes - diabetes, lactic acid production during shock, renal impairment, severe diarrhoea, acid ingestion
