Respiratory Flashcards
What is Boyles Law?
Pressure of a gas is inversely proportional to its volume
As long as temperature and number of gas molecule remains constant
How does Boyles law explain inspiration and expiration?
Inspiration: diaphragm moves down, volume increases, alveolar pressure drops below atmospheric pressure, air moves in
Expiration: volume decreases, air above atmospheric pressure, air flows out of the lungs
The airway has 23 divisions, which are the conducting zone and the respiratory zone?
1-16: conducting zone, no gas exchange, anatomical dead space
17-23: respiratory zone, gas exchange
What is the pO2 in alveolar air and venous blood?
Alveolar air: 13.3 kPa
Venous blood: 6.6 kPa
(Hence moves down its conc gradient from alveoli in pulmonary veins)
What is the atmospheric partial pressure in air?
101 kPa
Hence partial pressure of a gas is directly proportional to its %,
so pO2 = 101 x 20.9% = 21.1kPa
pCO2 = 101 x 0.03 = 0.03kPa
At body temperature, what is the saturated vapour pressure?
6.28 kPa
When water enters inspired air, water molecules enter gas phase until gas phase is saturated with water
How does atmospheric pressure change at altitude?
Atmospheric pressure is lower so gas molecules disperse (hence less air molecules available when you breathe).
What is the anatomy within the nasal cavity?
Turbinates/ conchae are bony projections (superior, middle, inferior)
Meatuses are in between, and increase SA
Floor of nasa cavity = roof of mouth = hard and soft palates
What are the 4 paranasal sinuses?
Frontal (above eyes) maxillary (below eyes), ethmoidal (between eyes), sphenoidal (behind eyes)
Air filled spaces that drain into nail cavity to humidify and warm inspired air
What are the functions of the nasal cavity?
- warm and humidify air
- drain paranasal sinuses and lacrimal ducts
- traps pathogens from the air
- sense of smell
What is the ‘glottis’?
The vocal cords and the aperture between them
Are the vocal cords adducted or abducted during respiration, phonation and swallowing?
Adducted during swallowing
Partially abducted in phonation
Abducted for respiration
Vocal cord movements are due to which muscles?
Intrinsic laryngeal muscles
What is the costodiaphragmic recess?
The inferior part of the pleural cavity not occupied by lung
How do the surface markings of the pleural cavity compare the the surface markings of the lungs?
Pleura both pass vertically down the sternum to 4th sternal angle, where left pleura deviates laterally (due to heart) to 6th cc, right continues vertically to 6th. Both go lateral and cross mid clavicular line at 8th rib, then mid Axillary at 10th rib and 12th rib at scapular line.
Lungs are 2 ribs higher than pleural cavity so cross mid clavicular at6th, mid Axillary at 8th then cross the 10th rib at the scapular line.
How many lobes do the lungs have and what are the lobes separated by?
Left has 2 lobes, separated by oblique fissure
Right has three lobes; upper and middle separated by horizontal fissure, middle and lower separated by oblique fissure
What will be the pO2 in blood exposed to gas with 14% O2 at a total pressure of 101.1kPa, saturated with water vapour at Boyd temperature?
(101.1-6.28) x 0.14 = 13.27 kPa
How does the epithelium change along the respiratory tract?
URT is pseudostratified with goblet cells and cilia.
Bronchioles is simple columnar will Clara cells but no goblet cells.
Respiratory bronchioles are simple cuboidal with Clara cells.
Alveoli are simple squamous.
How is the arrangement of cartilage different in primary bronchi compared the secondary & tertiary bronchi?
In primary bronchi it’s in rings
In secondary bronchi it’s in irregular islands
How do bronchi and bronchioles differ histologically?
Bronchioles have no cartilage or glands, unlike bronchi
Surrounding alveoli keep the lumen of bronchioles open
What are alveoli surrounded by?
A network of capillaries and elastic fibres. Lot of type 1 pneumocytes and some type 2 pneumocytes.
Lots of macrophages also line alveolar surface.
What is the difference between type 1 and 2 alveolar cells in terms of function and abundance?
Type 1 cover 90% of surface area and permit gas exchange with capillaries.
Type 2 cover 10% of surface area and secrete surfactant.
Emphysema destroys alveolar walls. How does this affect bronchioles?
Alveoli hold bronchioles open so that air can leave on exhalation.
Emphysema will cause bronchial collapse, and hence make it difficult for the lungs to empty (hence the hallmark sign of pursed lip breathing).
How does the diaphragm move in inspiration?
Moves down
What are the muscles between the ribs?
External intercostal muscles
Internal intercostal muscles
Innermost intercostal muscles
At what spinal level does the vena cava pass through the diaphragm?
T8
8 letters!
At what spinal level does the oesophagus pass through the diaphragm?
T10
10 letters
At what spinal level is the aortic hiatus in the diaphragm?
T12
12 letters!
When performing a chest drain, should the needle be inserted at the upper or lower border of the rib and why?
Insert needle at the upper border, to avoid injury to the neurovascular bundle (intercostal nerve, artery and vein) which lies below each rib?
The azygos venous system collects blood from between the intercostal veins and drains it into where?
SVC
Why do foreign bodies usually go to the right lung and not the left?
Right main bronchus has a less acute angle (is more vertical) than the left, and is also slightly larger
Is inspiration and expiration active or passive?
Inspiration is active
Expiration to resting expiratory level is passive,
But forced expiration is active
How does volume and pressure change during inspiration and expiration?
Inspiration: volume increases, pressures decreases, air moves in
Expiration: volume decreases, pressure increases, air moves out
Forced expiration requires which muscles?
Abdominal muscles (& internal intercostal muscles)
Is the pressure in the intrapleural space negative or positive?
Negative
Forced inspiration uses which muscles?
External intercostal muscles, sternocleidomastoid, scalene, serratus anterior and pectoralis major
What is the compliance of the lungs?
Aka the stretchiness of the lungs
(Volume change per unit pressure change)
Higher compliance = easier to stretch
How would emphysema affect a patients compliance?
More compliance due to a loss of elasticity
- elastic recoil is inversely proportional to compliance *
How would lung fibrosis affect a patients compliance?
Less compliance due to stiffening and hardening of the lungs
Does a higher surface tension make it harder or easier to stretch the lungs?
Higher surface tension makes it harder to stretch the lungs, as more force is needed to exceed the elastic recoil
What substance reduces surface tension in the lungs?
Surfactant, breaks up H-bonds to disrupt interactions between surface molecules so they’re easier to inflate.
What is surfactant composed of?
Mainly phospholipids, specifically surfactant protein A.
What is surfactant produced by?
Type 2 alveolar cells (pneumocytes)
Does surfactant reduce surface tension more when lungs are deflated or inflated?
Reduces surface tension more when lungs are deflated, so little breaths are easy but big breaths (forced inspiration) is difficult.
If a big bubble is connected to a small bubble, what will happen to the air flow inside them?
Smaller bubbles have higher pressure inside than big bubbles.
So, the air would move from the higher pressure in the smaller bubble, to the lower pressure in the larger bubble and the smaller bubbles would collapse. Surfactant is needed to equalise the pressure between different sized alveoli so they do not collapse into each other.
Hence “big bubbles eat smaller bubbles”
What are the roles of surfactant?
- reduce surface tension
- increase compliance
- prevent alveoli collapsing into each other
- prevent atelectasis (parts of the lung collapsing) at the end of expiration
What is acute respiratory distress syndrome?
Infants born with too little surfactant, lungs are very stiff with few and large alveoli hence breathing and gas exchange is compromised.
- different to adult respiratory distress syndrome which is not due to loss of surfactant *
What are the divisions of the mediastinum?
?
What is the innervation of the diaphragm?
Phrenic nerve: c3,4,5
How does the blood supply to the visceral and parietal pleura differ?
Visceral pleura supplied by bronchial arteries
Parietal pleura supplied by intercostal arteries and internal thoracic arteries
How does the nerve supply of the parietal and visceral pleura differ?
Visceral pleura has no somatic innervation, only autonomic
Parietal pleura has somatic innervation including pain fibres from intercostal and phrenic nerves, as well as autonomic innervation
Why does CO2 diffuse much faster then O2?
As CO2 is 20 times more soluble than O2.
Although this is usually compensated for because O2 has a larger partial pressure than CO2
What factors affect diffusion rate of a gas in fluid?
- solubility of the gas
- pressure difference
- molecular weight of gas
- surface area
- disunion distance
- temperature
What are the layers of the diffusion barrier from the alveolus to the blood?
Alveolus membrane, tissue fluid, capillary endothelium, plasma, red cell membrane
What happens to carbon dioxide when it enters RBCs as a waste product from cells?
Reacts with water to form carbonic acid, which breaks down to bicarbonate and H+.
Bicarbonate enters plasma and H+ is buffered by Hb in RBCs.
In normal lungs what is the PO2 and PCO2 of alveolar air?
PO2 = 13.3 kPa PCO2 = 5.3 kPa
How would fibrotic lung disease, emphysema and pulmonary oedema each affect diffusion of gases in the lungs?
Fibrosis: increases diffusion distance due to thickened alveolar wall
Oedema: increases fluid in interstitial space increases diffusion distance
Emphysema: reduces SA
- all cause low arterial pO2
What is the difference between the anatomical, distributive and physiological dead space?
Anatomical is conducting zone of the airways not involved in gas exchange.
Distributive is portion of airways eg damaged alveoli that aren’t involved in gas exchange.
Physiological is combined anatomical + distributive dead space.
How do we account for dead space when calculating alveolar ventilation rate?
Subtract resp rate x dead space volume from pulmonary ventilation rate = AVR
What is the ideal V/Q ratio?
1
What is tidal volume?
Volume breathed in and our with each breath
What is inspiratory reserve volume?
Extra volume that can be breathed in over that at rest
What is expiratory reserve volume?
Extra volume that can be breathed out over that at rest
What is residual volume?
Volume remaining in the lungs after maximum expiration
So CANNOT BE MEASURED BY SPIROMETRY
What is a lung capacity?
Two or more volumes added together
Capacities are fixed but volumes can change over the cycle
What is vital capacity?
Biggest breath that can be taken, measured from maximum inspiration to maximum expiration (usually about 5L)
= IRV + TV + ERV
What is inspiratory capacity?
Biggest breath that can be taken from resting expiratory level, usually about 3L
What is functional residual capacity?
The volume of air in the lungs at resting expiratory level, usually about 2L
= ERV + RV
What is total lung capacity?
Volume of air in the lungs at the end of maximum inspiration, usually about 5.8L
What is a vitalograph trace?
Plots volume expired against time, measureS FVC
What is FEV1?
Volume expired in the first second, will decrease if airway is narrowed
What should the FEV1 to FVC ratio be?
> 70% in healthy patients
How will an obstructive deficit affect FEV1 and FVC?
Lungs narrowed so increased resistance in airways when breathing out, although they can still full normally.
So reduced FEV1 but normal FVC
How will a restrictive deficit affect FEV1 and FVC?
Lungs cannot fill as well so start less full but air comes out normally
So, both FEV1 and FVC reduced although FEV1:FVC still >70%
How would obstructive and restrictive deficits present differently on a flow volume loop?
Obstructive would show as more scooped out upon expiration due to the increased resistance.
Restrictive would generally show the same shape but a narrowed curve (less volume expired as lungs less full to start)
How can the anatomical dead space be measured?
Nitrogen washout test
- subject takes breath of pure O2
- breathes out via meter measuring nitrogen %
- initially only O2 expired (as last air in is first air out)
- then air mixed with nitrogen will be breathed out
- volume of air that was pure O2 is the anatomical dead space
How can we measure the residual volume?
Via the helium dilution test and calculation
Helium is not metabolised by the body
Patient breathes in a known volume of gas with a known volume of helium
Starts at FRC
Can measure the change in helium concentration as it becomes diluted in a larger volume of air in the lungs
How many oxygen molecules can haemoglobin transport compared to myoglobin?
Hb can bind 4 molecules as its a tetramer
Myoglobin can bind 1 as it is only a monomer
What factors shift the Hb dissociation curve to the right (Bohr shift)?
Acid
Increased temperature
Increased 2,3-DPG (anaemia or altitude)
What is pulse oximetry?
An easy and non-invasive method to measure saturated Hb levels in pulsation arterial blood
but doesn’t say how much Hb is present (Ie wouldn’t detect anaemia) and ignores levels in tissues and venous blood
What is the Henderson Hasselbalch equation?
pH = 6.1 + log[HCO3-]/(pCO2 x 0.23)
Must be 20 x as much bicarbonate as CO2 for pH to be in range
How is high HCO3- established in red blood cells?
CO2 reacts with water to produce bicarbonate and H+ (catalysed by carbonic anhydrase)
Bicarbonate enters plasma and H+ are mopped up by Hb, so reaction proceeds in forwards direction
Via which channel does bicarbonate leave RBCs to enter plasma?
Chloride bicarbonate exchanger
Do H+ bind more easily to Hb in the T or R state?
In the T state (as at tissues, so then more H+ mopped up so more bicarbonate can be produced which means more CO2 is present in plasma as the bicarbonate pushes the plasma reaction to the left)
By what methods can CO2 be transported?
- dissolve in plasma
- as hydrogen bicarbonate
- as carbamino compounds
If hypoxia is corrected by ventilation, what can this lead to?
Could lead to hypocapnia
(But the plateau at the end of the Hb dissociation curve shows that a considerable drop in O2 can be tolerated before having an affect)
What can a low and a high pH outside the normal range cause?
Low pH can denature enzymes
High pH causes a drop in free Ca levels and can lead to tetany
Which are more sensitive to changes in pCO2: peripheral or central chemoceptors?
Central chemoceptors
Can then increase or decrease ventilation by negative feedback based on pCO2
Central chemoceptors respond to changes in the pH of which fluid?
CSF
Which cells control the CSF concentration of HCO3-?
Choroid plexus cells
So can correct pH
What is type 1 respiratory failure?
Type 1 affects only 1 (oxygen)
So low O2 and normal/ low CO2
What is type 2 respiratory failure?
Type 2 affects 2.
So, low O2 AND high CO2
How can oxygen levels in the blood be measured?
- pulse oximetry (measures saturated Hb in arterial blood)
- arterial blood gas (can measure pCO2, pO2 and pH of arterial blood)
What can cause type 2 respiratory failure?
Ventilatory (pump) failure unable to move sufficient air into and out of lungs
Eg: kyphoscoliosis, flail segments, COPD, myopathy of resp muscles, head injury (affect resp centre), severe obesity, lung fibrosis, pneumothorax, Guillain Barre syndrome
What can cause type 1 respiratory failure?
- diffusion defects across the alveolar membrane
(Eg fibrosis causing membrane thickening, or emphysema reducing SA) - v/q mismatch
(V/q <1 causes O2 to fall and CO2 to rise.)
Due to problems with ventilation of part of lungs eg pneumonia, COPD, asthma, RDS of newborn.
Or, due to reduced perfusion of part of lungs eg pulmonary embolism, which diverts blood to other parts of the lungs so they’re more perfused
Which receptors does hypoxia stimulate?
Peripheral chemoreceptors (stimulates hyperventilation)
How can respiratory failure be managed?
In type 1 oxygen therapy can treat hypoxia
In type 2 may require assisted ventilation for the hypercapnia
What are some clinical features of hypoxia?
- exercise intolerance
- central cyanosis
- tachypnoea
- confusion (cerebral hypoxia as brain very sensitive to low O2)
What is cyanosis?
Purple discolouration of skin and mucous membranes due to the colour of desaturated Hb
What is the difference between peripheral and central cyanosis?
Central seen in tongue and oral mucosa, these areas are very well perfused so not usually affected by perfusion problems, is due to low arterial pO2
Peripheral is seen in the extremities and can occur without central cyanosis due to poor perfusion eg peripheral vascular disease
What is the effects of chronic hypercapnia?
- warm hands flapping tremors
- CSF acidity corrected by choroid plexus cells so central chemoceptors reset to the new higher pCO2 but peripheral chemoceptors do not adapt and remain sensitive to hypoxia, hence respiration is driven by hypoxia
What is the effects of chronic hypoxia?
- increased oxygen delivery by increased Hb levels due to increase erythropoietin production
- increased 2,3-DPG in RBCs
- pulmonary vasoconstriction of pulmonary arterioles can lead to right sided heart failure, pulmonary hypertension, cor pulmonale
Why may oxygen administration worsen hypercapnia? (So cannot give oxygen to COPD patient)
As the central chemoceptors reset to the higher pCO2. If oxygen is administered, the respiratory drive to the peripheral chemoceptors is lost and so they reduce ventilation which will cause CO2 to rise even more
What is bronchitis?
Inflammation of medium sized airways
What are some causative organisms of ACUTE bronchitis?
Chronic bronchitis is not primarily infective
Streptococcus pneumoniae
Haemophilius influenzae
How would acute bronchitis present?
Cough, increased sputum production, breathlessness, fever, normal CXR
How could acute bronchitis be treated?
Physiotherapy/ antibiotics/ bronchodilators
What is pneumonia and how does it present?
Inflammation of the lung alveoli
Presents as fever, cough, shortness of breath and pleuritic chest pain with an ABnormal CXR (unlike bronchitis)
What are some typical and some atypical causative organisms of community acquired pneumonia?
Typical:
Streptococcus pneumonia, Haemophilius influenzae, staphlococcus pneumoniae
Atypical:
Legionella, mycoplasma, coxiella
How would a patient with pneumonia show on examination?
Tachycardia Tachypnoea Dullness on percussion Pyrexia Cyanosis Bronchial breathing Crackles
What is the CURB-65 score?
Basis of where to manage a patient C: confusion U: urea > 7mmol/L R: resp rate > 30 B: blood pressure (<90 systolic or <60 diastolic) 65 years or older
Why do penicillins not work for atypical pneumonias?
Atypical pneumonia is caused by organisms without a cell wall (eg chlamydia, legionella), so cell wall active antibiotics like penicillins will be ineffective.
Need antibiotics that will work on protein synthesis eg macrolides (erythromycin, clarithromycin) or tetracyclines (doxycycline).
What antibiotics can be used for atypical pneumonias?
Need antibiotics that will work on protein synthesis eg macrolides (erythromycin, clarithromycin) or tetracyclines (doxycycline).
What are some preventative measures for lower respiratory tract infections?
- stop smoking
- flu vaccine for at risk patients
- chemoprophylaxis for at risk patients ie asplenia, immunodeficiency (give penicillin/ erythromycin)
What is an example of an obligate anaerobe?
Clostrodia
Cannot survive in presence of oxygen unless spores have formed
If hypoxia is corrected by ventilation, what can this lead to?
Could lead to hypocapnia
(But the plateau at the end of the Hb dissociation curve shows that a considerable drop in O2 can be tolerated before having an affect)
What can a low and a high pH outside the normal range cause?
Low pH can denature enzymes
High pH causes a drop in free Ca levels and can lead to tetany
Which are more sensitive to changes in pCO2: peripheral or central chemoceptors?
Central chemoceptors
Can then increase or decrease ventilation by negative feedback based on pCO2
Central chemoceptors respond to changes in the pH of which fluid?
CSF
Which cells control the CSF concentration of HCO3-?
Choroid plexus cells
So can correct pH
What is type 1 respiratory failure?
Type 1 affects only 1 (oxygen)
So low O2 and normal/ low CO2
What is type 2 respiratory failure?
Type 2 affects 2.
So, low O2 AND high CO2
How can oxygen levels in the blood be measured?
- pulse oximetry (measures saturated Hb in arterial blood)
- arterial blood gas (can measure pCO2, pO2 and pH of arterial blood)
What can cause type 2 respiratory failure?
Ventilatory (pump) failure unable to move sufficient air into and out of lungs
Eg: kyphoscoliosis, flail segments, COPD, myopathy of resp muscles, head injury (affect resp centre), severe obesity, lung fibrosis, pneumothorax
What can cause type 1 respiratory failure?
- diffusion defects across the alveolar membrane
(Eg fibrosis causing membrane thickening, or emphysema reducing SA) - v/q mismatch
(V/q <1 causes O2 to fall and CO2 to rise.)
Due to problems with ventilation of part of lungs eg pneumonia, COPD, asthma, RDS of newborn.
Or, due to reduced perfusion of part of lungs eg pulmonary embolism, which diverts blood to other parts of the lungs so they’re more perfused
Which receptors does hypoxia stimulate?
Peripheral chemoreceptors (stimulates hyperventilation)
How can respiratory failure be managed?
In type 1 oxygen therapy can treat hypoxia
In type 2 may require assisted ventilation for the hypercapnia
What are some clinical features of hypoxia?
- exercise intolerance
- central cyanosis
- tachypnoea
- confusion (cerebral hypoxia as brain very sensitive to low O2)
What is cyanosis?
Purple discolouration of skin and mucous membranes due to the colour of desaturated Hb
What is the difference between peripheral and central cyanosis?
Central seen in tongue and oral mucosa, these areas are very well perfused so not usually affected by perfusion problems)
Peripheral is seen in the extremities and can occur without central cyanosis due to poor perfusion
What is the effects of chronic hypercapnia?
- warm hands flapping tremors
- CSF acidity corrected by choroid plexus cells so central chemoceptors reset to the new higher pCO2 but peripheral chemoceptors do not adapt and remain sensitive to hypoxia, hence respiration is driven by hypoxia
What is the effects of chronic hypoxia?
- increased oxygen delivery by increased Hb levels due to increase erythropoietin production
- increased 2,3-DPG in RBCs
- pulmonary vasoconstriction of pulmonary arterioles can lead to right sided heart failure, pulmonary hypertension, cor pulmonale
Why may oxygen administration worsen hypercapnia? (So cannot give oxygen to COPD patient)
As the central chemoceptors reset to the higher pCO2. If oxygen is administered, the respiratory drive to the peripheral chemoceptors is lost and so they reduce ventilation which will cause CO2 to rise even more
What is bronchitis?
Inflammation of medium sized airways
What are some causative organisms of ACUTE bronchitis?
Chronic bronchitis is not primarily infective
Streptococcus pneumoniae
Haemophilius influenzae
How would acute bronchitis present?
Cough, increased sputum production, breathlessness, fever, normal CXR
How could acute bronchitis be treated?
Physiotherapy/ antibiotics/ bronchodilators
What is pneumonia and how does it present?
Inflammation of the lung alveoli
Presents as fever, cough, shortness of breath and pleuritic chest pain with an ABnormal CXR (unlike bronchitis)
What are some typical and some atypical causative organisms of community acquired pneumonia?
Typical:
Streptococcus pneumonia, Haemophilius influenzae, staphlococcus pneumoniae
Atypical:
Legionella, mycoplasma, coxiella
How would a patient with pneumonia show on examination?
Tachycardia Tachypnoea Dullness on percussion Pyrexia Cyanosis Bronchial breathing Crackles
What is the CURB-65 score?
Basis of where to manage a patient C: confusion U: urea > 7mmol/L R: resp rate > 30 B: blood pressure (<90 systolic or <60 diastolic) 65 years or older
Why do penicillins not work for atypical pneumonias?
Atypical pneumonia is caused by organisms without a cell wall (eg chlamydia, legionella), so cell wall active antibiotics like penicillins will be ineffective.
Need antibiotics that will work on protein synthesis eg macrolides (erythromycin, clarithromycin) or tetracyclines (doxycycline).
What antibiotics can be used for atypical pneumonias?
Need antibiotics that will work on protein synthesis eg macrolides (erythromycin, clarithromycin) or tetracyclines (doxycycline).
What are some preventative measures for lower respiratory tract infections?
- stop smoking
- flu vaccine for at risk patients
- chemoprophylaxis for at risk patients ie asplenia, immunodeficiency (give penicillin/ erythromycin)
What is an example of an obligate anaerobe?
Clostrodia
Cannot survive in presence of oxygen unless spores have formed
What are some facts about mycobacterium tuberculosis?
Obligate aerobe Non-motile bacilli Long chain fatty acids in cell wall (hence cannot use gram staining) Relatively slow growing Spread via droplet
What is the pathogenesis of tuberculosis?
Bacteria inhaled and engulfed by leveller macrophages
Can form a primary infection, or often lies dormant as a latent infection for many years. Latent TB can then self-cure or reactivate to post-primary TB.
What are some differences between latent TB infection and TB disease?
Latent TB is inactive, has no symptoms, will show positive on TST and IFN gamma, normal CXR, negative sputum smears, not infectious, not a case of TB
TB disease is active, will show positive on TST and bloods, positive sputum smears, has symptoms, is active, CXR abnormal, infectious, case of TB
What are some risk factors for reactivation of TB?
HIV, low body weight, substance abuse, immunosuppression, organ transplant, malignancy, diabetes Mellitus
How would TB appear histologically?
Caseating granulomas with Langhans giant cells
Where can TB occur?
Most cases are pulmonary
Can become extra pulmonary at kidneys, brain, lymph nodes, bones and joint, pleura, larynx
Military TB when spread throughout the body via the bloodstream
What are some risk factors for catching TB?
Non-UK born, HIV positive, homeless, drug users, Immunocompromised
What are some signs and symptoms of pulmonary TB?
Fever, malaise, abnormal CXR, weight loss, night sweats, anorexia, tiredness, cough, haemoptysis
What is the TST?
Tuberculin sensitivity test Tuberculin injected intradermally and measure 3 days later Subjective!! Easy and cheap Positive in latent and active
How can TB be investigated?
CXR
Sputum smears -> analyse in lab or culture (gold standard)
Detect antigen specific IFN-gamma production (but cannot distinguish latent and active)
What drugs are used in TB?
RIPE
Rifampicin, isoniazid, pyrazinamide, ethambutamol
3/4 drugs for 2/12 then R and I for 4/12
What is a side effect of Rifampicin?
Orange secretions
How can TB be prevented?
PPE, negative pressure isolation BCG vaccine (live M bovis strain)
What are some triggers of asthma?
Indoor allergens (dust mites, mold, pets) Outdoor allergens (pollen, smoke, pollutants) Cold air, exercise, medications (NSAIDs, beta blockers)
Is asthma obstructive or restrictive?
Obstructive
What are some symptoms of asthma?
Wheeze, dry cough, breathlessness, chest tightness
Worse after exposure to triggers, at night or early morning
How can asthma be diagnosed?
Examination (assess RR, tracheal tug, accessory muscle use)
History (aggregating triggers, family history, medication)
PEFR and spirometry (can do before and after bronchodilators)
How can asthma be managed?
Use inhalers (correct education!)
Change bedding every few years
Stop smoking
Fresh air
What is the difference between a blue, brown and green inhaler?
Blue inhaler: SABA (short acting beta agonist), relaxes smooth muscle for quick relief
Brown: prevention, steroid to reduce inflammation
Green: LABA (long actin beta agonist), used if still have asthma symptoms despite steroid, not for acute attacks due to slow onset
How could a severe asthma attack be treated?
Oxygen Nebulised salbutamol (IV if mucus blocks it getting in)
COPD is an umbrella term for which two conditions?
Emphysema and chronic bronchitis
Both causing airflow obstruction
What is emphysema?
Destruction of terminal bronchioles and alveoli So less SA for gas exchange Develop bullae (large redundant air spaces)
What is chronic bronchitis?
Inflammation of the large airways and mucus hypersecretion
What causes COPD?
- smoking!!!
- also alpha 1 antitrypsin deficiency (1%)
- occupational exposure eg coal dust
- pollution
What are some signs and symptoms of COPD?
Signs: pursed lip breathing, use of accessory muscles, tachypnoea, hyperinflated barrel chest, if serious cyanosis and right sided heart failure, wheeze
Symptoms: progressive breathlessness (graded by MRC dyspnea score 1-5 with 5 being worse), cough and sputum
How would COPD present on spirometry?
FEV1 < 80% predicted
FEV1/FVC <70%
How should COPD be managed?
- smoking cessation
- pulmonary rehabilitation
- bronchodilators
- steroids
- mucolytics
- antimuscarinics
- long term oxygen therapy
- lung volume reduction or lung transplant if young
How does a beta 2 agonist eg salbutamol work?
Salbutamol binds to Gs receptor Activates adenylyl cyclase Activates PKA Phosphorylates MLCK Causes smooth muscle relaxation
How does pulmonary rehabilitation work?
6-12 week exercise and education programme
Aims to break the cycle of deconditioning for patients (ie when symptoms prevent them from doing activities so they do less and in effect worsen their condition)
How can lung cancer be staged?
TNM staging (T= tumour size 1-4, N= node involvement 0-3, M= metastases 0 or 1)
What are the main types of lung cancer?
Non small cell carcinoma
(Squamous cell carcinoma, adenocarcinoma, large cell carcinoma)
Small cell carcinoma
What are some treatments for lung cancer?
Surgery (mostly for non small cell) Chemotherapy Radiotherapy Combination therapy Palliative care
What are some paraneoplastic features that may be associated with lung cancer?
Squamous cell -> PTHrp -> raised plasma calcium
Small cell -> ACTHrp -> occasionally Cushing’s
Small cell -> ADHrp -> occasionally dilutional hyponatraemia (SIADH)
Where in the CNS is a cough coordinated?
Medulla oblongata
Why are patients with sickle cell disease at increased risk of bacterial infections?
Have small splenic infarctions
Spleen is important for removal of encapsulated bacteria (by splenic macrophages) and also produce antibodies IgM and IgG
How would hyperinflation of the chest appear on x Ray?
More than 6 ribs anteriorly
Flattened diaphragm
Ribs may appear more horizontal
Narrow heart
What is the difference between a transudate and exudate?
Exudate has high protein content, often due to infection or malignancy
Transudate has low protein content, may be due to heart failure, nephrotic syndrome, hypoalbuminaemia
How would someone with interstitial lung disease present on a lung function test?
Restrictive pattern
Reduced FEV1 and FVC
But FEV1/FVC ratio often >70% (as airway resistance does NOT increase)
How does ILD affect perfusion of O2 and CO2?
Increases the diffusion pathway between alveolar air and blood so impairs gas exchange
O2 affected before CO2 as its less soluble
Hence T1 resp failure then T2 may follow
What are some causes of interstitial lung disease?
Asbestos Silicosis Rheumatoid arthritis Radiation Methotrexate Chemotherapy Lupus Nitrofurantoin Sarcoidosis
What is primary malignancy of the pleura called?
Mesothelioma
What is pleurisy?
Sharp pain worse with large breathing movements
Involvement of diaphragmatic pleura may cause shoulder pain on the same side
What is a haemothorax?
A pleural effusion of blood
When would pleural fluid volume increase?
- Increase in permeability of pulmonary capillaries (inflammation or malignancy)
- rise in pulmonary intra vascular pressure (heart failure)
- fall in plasma osmotic pressure (eg liver failure)
- obstruction to lymphatic flow in lungs
What is fibrosing alveolitis?
Unknown causes
Progressive inflammatory condition of lungs, possibly triggered by pollutant or infection
This increases number of alveolar macrophages which attract neutrophils and cause local tissue damage and fibrosis due to ROS and proteases
Can be strained by steroids in early stages until fibrosis occurs
If a lung function test showed a reduced TLCO, what would this mean?
Reduced carbon monoxide transfer factor
Means reduced diffusing capacity for gases across the alveolar capillary membrane
Which are the true ribs, false ribs, and floating ribs?
True ribs 1-7 attach to the sternum
False ribs 8-12 don’t attach to sternum
Floating ribs 11 and 12
