Respiratory Flashcards
Name the 4 pairs of paranasal sinuses.
Frontal, maxillary, ethmoid and spenoid
What drains into the speno-ethmoidal recess?
Spenoidal sinus
What drains into the superior meatus?
Posterior ethomoidal sinuses
What drains into the middle nasal meatus?
Most paranasal sinuses
What drains into the inferior meatus?
The naso lacrimal duct which drains tears from the eye.
Define URT
The part of the respiratory tract above the lower border of the cricoid cartilage= found at inferior part of larynx, C6 vertebral level, only complete ring of cartilage around trachea.
How do nasal turbinates help with respiratory functions of nasal cavity?
Increase SA for warming + humidification, and cause turbulence so slow air flow, increasing time available for air processes such as filtering to occur.
Name the component parts of the bony thorax and where in the thorax they are located
Anteriorly: sternum and costal cartilages
Laterally: ribs and intercostal spaces
Posteriorly: thoracic vertebrae
Why is rib 2 an atypical rib?
Poorly defined costal groove and presence of tuberosity on upper surface for serratus anterior.
Which ribs only have 1 articular facet in their heads?
ribs 1, 10, 11 and 12
Compare pulmonary circulation with systemic circulation
Pulmonary: much lower resistance, lower pressures. Vascular resistance more evenly distributed and pulmonary capillary flow remains pulsatile. Low oxygen results in hypoxic pulmonary vasoconstriction so blood flow to areas of lung which are well ventilated, improving gas exchange.
Lacks systemic autoregulation, so when CO increases, pulmonary vascular resistance falls, as vessels recruited and distended, and rise in pulmonary arterial pressure is small. In systemic, response to changes in perfusion pressure by constricting or dilating to hold blood flow fairly constant.
What is empyemea?
A collection of pus in the pleural cavity, most commonly due to pneumonia
What are the anatomical hazards of pleurocentesis?
- Damage to intercostal veins, arteries and nerves
- Damage to lung- air may enter pleural space (pneumothorax)
- Liver injury
Why do people with COPD breathe through pursed lips?
This enables the mouth to be the area of highest resistance and extends the time during which airway pressure remains high and the airways patent. This is to partly compensate for mechanical support lost- loss of elastic recoil and airway collapse.
Describe the shape of a patient’s chest if narrowing of small airways increases their functional residual capacity.
Barrel shaped
What is the solubility coefficient of O2?
0.01mmol/L/kPa at 37 degrees C.
At normal partial pressure and temp, how much dissolved O2 does plasma contain?
0.13mmol/L
What is the normal alveolar pO2?
13.3kPa
What is the normal alveolar pCO2?
5.3kPa
What are the partial pressures of O2 and CO2 in mixed venous blood?
O2:5.3kPa
CO2: 6.6kPa
What O2 binding does Hb exhibit and what bidning curve shape does this create?
Cooperative binding
Sigmoidal binding curve
Describe the Bohr shift.
The affinity of Hb for O2 is reduced by lower pH in tissues, as T state of Hb promoted, so O2 is released to the tissues, necessary for highly metabolically active tissues which produce lots of CO2 and H+ which lowers pH. Same also happens with increase in temp.
So dissociation curve shifted to the right.
In the lungs- lots of O2, so binds to Hb- promotes high affinity R state, CO2 expired, so Hb can become saturated with O2 and transport it to the tissues requiring it.
Above what pO2 is Hb saturated?
8.5kPa
When is Hb half saturated with O2?
Between 3.5 and 4 kPa
Why do rises or modest falls in pO2 from 13kPa e.g. in hyperventilation or mild hypoventilation, causes little change in arterial O2 content?
As dissociation curve is flat in this region, so Hb is fully saturated with O2 from around a pO2 of 8.5kPa, so small changes in the pO2 still correspond with around 97% saturation with O2.
Describe effect of 2,3BPG on Hb saturation
By-product of glycolysis that promotes T state of Hb, so shifts dissociation curve to the right, decreasing affinity of Hb for O2 so O2 is more readily released to the tissues. 2,3BPG increased in anaemia and at high altitude.
Describe myoglobin
O2 store in tissues. Composed of a single haem group attached to a single globin chain, no cooperative binding so dissociation curve is hyperbolic and far to the left of HbA. High affinity for O2 means O2 store only released when local pO2 is severely reduced, e.g. in heavy exercise.
What is the Henderson-Hasselbalch equation and what does it represent?
pH=pKa+log([HCO3-]/(pCO2x0.23)) pKa=6.1
That pH of plasma and hence ECF depends on the ratio of pCO2 to [HCO3-].
How is the thoracic cavity separated?
By the mediastinum, extending from the vertebral bodies behind to the sternum in front?
What lies in the posterior mediastinum?
Azygos vein, thoracic aorta, oesophagus, vagus nerve, sympathetic trunks
What lies in the middle mediastinum?
Heart, pericardium, roots of great vessels, main bronchi
Describe obstructive and restrictive defecits, and give examples of each.
Restrictive: problem with inspiration. FEV1.0 proportion doesn’t change, still > or equal to 70% of FVC, but FVC much less as less air inspired in the first place. FEV1.0 less aswell but both affected to same proportion as all of expiration is affected to the same extent.
Obstructive: problem with expiration, e.g. airway narrowing, e.g. in asthma, COPD. FVC relatively normal, but FEV1.0 markedly reduced as increased resistance to air expiration, so air comes out more slowly.
What factors influence diffusion of gases across alveolar membrane?
- diffusion resistance
- SA for diffusion
- Concentration gradient
What is the concentration of dissolved CO2 in the plasma determined by and why?
The pCO2 as the solubility is fixed (solubility constant of 0.23)
What is the pH of plasma determined by?
The ratio of [HCO3-] to pCO2. This is normally about 20:1
What is the O2 content of the blood determined by?
The arterial pO2 and the concentration of Hb.
What determines the supply of O2 to individual tissues?
Appropriate O2 content in arterial blood and an adequate CO and adequate local perfusion of tissues.
What name is given to the aperture between the 2 true vocal cords?
rima glottidis
What is the glottis?
The 2 true vocal cords and the aperture between them
Where is the oblique fissure of the lung?
Runs from spinous process of T2 to costal cartilage of 6th rib. Sepatates upper and lower lobes of lung.
Where is the horizontal fissure of the lung?
Found along the 4th rib, from the mid axillary line, on the right side.
Why is a perforating wound of lower intercostal spaces considered to be an abdominal as well as a thoracic wound?
Dome shape of diaphragm means periphery attached to inferior margin of thoracic cage but dome extends upwards in expiration to level of 5th rib on right side and level of 5th intercostal space on left side so organs in the upper abdomen e.g. liver, spleen, stomach and the kidneys, can be damaged in a perforating thoracic wound.
Define hyperventilation
breathing more than required for your metabolic state.
What does hyperventilation cause?
Hypocapnia- pCO2 decreases. This can cause lethal tetany.
Why can hyperventilation cause lethal tetany?
Expiring more so removing more CO2 from alveloi than produced, so pCO2 decreases, increasing the pH of the blood- respiratory alkalosis, and calcium is relatively insoluble in alkaline conditions so as calcium unable to dissolve in blood, it us uptaken by bone and binds to proteins, so its free ionised concentration is reduced to life-threateningly low levels. Muscles go into involuntary spasms, may cause airway obstruction.
Why can pO2 fall quite significantly before hypoxia?
As on flat part of dissociation curve, Hb remains 100% saturated with O2 from around 8 kPa so decreases in pO2 from 13.3kPa can be as much as 4-5kPa and Hb will still be 100% saturated.
What is compensation by the kidneys?
pH of blood is returned to normal by altering the other variable ( the concentration of HCO3-),rather than the variable which was disturbed (the pCO2), because pH depends on the ratio between the concentration of HCO3- and the pCO2. Important as ventilation can’t really change in certain problems e.g. respiratory infection.
Define metabolic acidosis
A fall in [HCO3-] in the blood
How are metabolic changes in pH of blood compensated for?
By breathing
What is arterial pO2 monitored by?
peripheral chemoreceptors
What do large falls in pO2 stimulate?
- increase in breathing
- changes in HR
- diversion of b.flow to brain via changes in resistance vessels.
What do central chemoreceptors actually respond to?
Changes in pH of CSF.
What controls the CSF [HCO3-]?
Choroid plexus cells, so [HCO3-] is fixed in the short term, but in persisting changes in pH, choroid plexus cells correct this by changing [HCO3-].
What might happen if O2 is administered to a COPD patient?
They might stop breathing as they have type 2 respiratory failure, so their pCO2 is persistently highm meaning CSF acidity is corrected by choroid plexus cells increasing [HCO3-] to maintain normal pH, and so the central chemoreceptors ‘reset’ to higher CO2 level as they lose their stimulation due to pH correction, so reduced resp drive, and this is now driven by hypoxia so if O2 given, they’ll be no resp drive!
What is polycythaemia?
increase in haemoglobin in blood
Where are peripheral chemoreceptors located?
Carotid and aortic bodies
Where are central chemoreceptors located?
In the medulla
Why would the pCO2 be normal in a patient with pneumonia, but their pO2 would be reduced?
Type 1 respiratory failure: ventilation/perfusion mis-match: O2 poorly soluble in liquid in inflammatory exudate, hyperventilation will try and increase O2 but affected alveoil consolidated, and those unaffected by pneumonia won’t be able to increase O2 in blood as Hb already 100% saturated. But CO2 diffusion isn’t limited in those alveoli unaffected by consolidation, so it is able to diffuse easily from the blood into the alveoli unaffected by consolidation when hyperventilating.
Describe how Boyle’s law is associated with our ability to fill our lungs on inspiration.
Boyles law states that pressure is inversely proportional to volume. When we inspire, our diaphragm flattens, our ribs are pulled upwards and ourwards, so the vertical, transverse and AP diameters of our thoracic cavity are increased, hence volume is increased, so pressure is markedly reduced, allowing air to flow into the lungs down a pressure gradient.
Why is the partial pressure of gases inspired different to the alveolar partial pressures.
Mixing of inspired and expired air in trachea.
Describe the pleural cavity
a potential space between the parietal pleura adhering to the thoracic wall and the visceral pleura covering the lungs. The cavity is lined by a single layer of flat cells-mesothelium-simple squamous epithelium, and associated supporting CT, which together form the pleura. Cavity normally contains a thin film of serous fluid. Visceral pleura continuous with parietal at lung hilum.
What names are given to the different parts of the parietal pleura?
Cervical, costal, diaphragmatic and mediastinal
Describe parietal pleura innervation
Somatic afferent fibres. Costal part innervated by IC nerves, and diaphragmatic and mediastinal innervated by phrenic nerves- pain in these areas would be referred to C3, C4 and C5 dermatomes, so lateral neck and supraclavicular region of shoulder.
Describe the costodiaphragmatic recess
region between inferior part of lung and inferior part of pleural cavity. Occurs between costal and diaphragmatic pleura. Deepest after forced expiration and shallowest after forced inspiration.
What is the innervation of visceral pleura?
Autonomic innervation- visceral sensory afferents.
How does inflammation cause airway narrowing in asthma?
- mucosal oedema
- bronchial wall thickening as inflammatory cell infiltration
- mucus over prod. and abnorma
- smooth muscle contraction
- shed epithelium- incorporated into thick mucus
What pharmacologic therapies are available for asthma?
Relievers and preventers.
- Short and long-acting Beta 2 agonists
- Inhaled corticosteroids
- Oral steroids
- Leukotriene receptor antagonsits
- Xanthines
- Muscarinic antagonists
List signs of acute severe asthma
pulse>110 RR>25 Can't complete sentences No wheeze PEFR 35-50% predicted
Main causative virus of pneumonia
Influenza
Describe microscopic evaluation of COPD
Bronchial inflammation, fibrosis, and mucus hypersecretion characteristic of obstructive bronchitis, and destruction of alveoli seen in emphysema.
Both implicated in progressive airflow obstruction.
Why is smoking cessation so important in COPD?
Cigarette smoke= primary RF for COPD related mortality. Among those with COPD, those who continue to smoke have more symptoms, a faster decline in lung function and a higher death rate than those who stop smoking.
What genetic disease can predispose to COPD?
Alpha 1 antitrypsin deficiency
Why is FEV1.0 not particularly useful in assessing patient important outcomes in COPD?
This tells you the max volume of air exhaled in first s of a forced expiration from a position from a full inspiration, but only weak correlation exists between objective measures of airflow obstruction and patient important outcomes such as mortality and risk of future exacerbations. Some patients are better able to cope with same degree of airway obstruction, so their QOL will be better, and they may be better able to carry out exercise and live for longer.
Describe flow volume loop of airway obstruction
Reduced PEFR with scooped-out (sharply concave) appearance of expiratory limb.
When should COPD diagnosis be considered?
Current or former smokers over age of 35 who have history of progressive and persistent exertional dyspnoea with or without chronic cough and sputum production. History of frequent episodes of winter bronchitis, wheezem and fatigue common.
How is airflow obstruction severity classified?
According to FEV1.0 as a percentage of the predicted normal value as adjusted for sex, age, height, and race.
How is airflow obstruction defined using spirometry?
post-bronchodilator FEV1.0/FVC ratio of less than 70%
List signs of life-threatening asthma
sat. O2 less than 92% pCO2 rising or normal Exhaustion Altered state of consciousness Silent chest PEFR less than 33% predicted
What options are available for asthma management?
- pharmacologic therapy
- education of patient and their family
- avoidance of triggers
- dealing with environmental factors
How can COPD be differentiated from asthma?
- pre- and post- bronchodilator spirometry, large response to bronchodilators suggestive of asthma e.g. >15% increase in FEV1.0.
- serial peak flow measurements using a peak flow meter- asthma suggested when diurnal or day to day variability exceeds 20%.
Describe pulmonary rehabilitation
Programme normally lasting 6 wks involving exercise training, disease education, psychiatric counselling, and behavioural/nutritional instruction. It improves exercise capacity, reduced admissions to hospital, improves health-related QOL and symptomatic breathlessness.
What is the mainstay drug treatment for COPD?
Bronchodilators. Inhaled corticosteroids not given alone and should be used only in combination with ling acting bronchodilators in those with a FEV1.0 less than 60% predicted. Potential risk of pneumonia with use of inhaled corticosteroids- anti-inflammatory.
Why is a patient with COPD susceptible to R sided HF?
Airflow obstruction causes hypoxia, which leads to pulmonary hypertension as a result of hypoxic pulmonary vasoconstriction, AND pulmonary capillary destruction occurs with emphysema, so R heart must work harder to pump blood through a higher pressure pulmonary circulation as increased resistance, so impaired R heart function as filling pressure increased, which can then back up into the systemic circulation, with a raised CVP and *peripheral oedema, subsequently leading to cor pulmonale- fluid retention/HF secondary to lung disease.
How is chronic bronchitis defined?
A daily morning cough and excessive mucus production most days for 3 mnths in 2 successive yrs, in absence of airway tumour, acute/chronic infection or uncontrolled cardiac disease.
So based on clinical history
Describe how alpha 1 antitrypsin deficiency can lead to emphysema.
Alpha 1 antitrypsin is an anti-protease which inhibits the action of proteases released from bacteria and neutrophils which degrade proteins e.g. elastin, so if deficiency, there is a predisposition to elastin disruption in airways.
What is COPD?
A chronic, slowly progressive disorder characterised by airflow obstruction which does not change markedly over several months. Encompasses chronic bronchitis and emphysema.
How do xanthines e.g. theophylline work in the treatment of asthma?
Bronchodilators as inhibit breakdown of cAMP so more around, and also anti-inflammatory.
Describe effects of acute hypoxia
-cardiac arrythmias
-CNS function impaired
-hypoxic pulmonary vasoconstriction
-central cyanosis
Peripheral chemoreceptors will increase ventilation.
Describe effects of chronic hypoxia
- cor pulmonale
- polycythaemia
- increase 2,3-BPG
- renal correction and increased ventilation
Describe effects of acute hypercapnia
- breathlessness
- impaired CNS function
- cardiac arrythmias
- cerebral vasodilatation
- peripheral vasodilatation
Describe effects of chronic hypercapnia
- CSF compensation, central chemoreceptors reset to higher pCO2, problem with administering O2 and may reduce patient’s breathing
- renal compensation
What is tachypnoea
increased resp. rate e.g. where increased central drive in resp.failure
Describer resp. failure in acute asthma attack
Excessive bronchoconstriction reduces ventilation to particular alveoli, resulting in ventilation/perfusion mismatch and hypoxia. PaCO2 falls as attack worsens as peripheral chemoreceptor and pulmonary receptor stimualtion produce reflex increase in ventilation despite increased work of breathing.
How can arterial pH indicate proportions of acute and chronic hypercapnia?
Chronic- near-normal pH as compensation by choroid plexus cells of brain.
Acute- arterial pH decrease as renal adjustments slow
Other than reduced CO2 sensitivity, why might a COPD patient’s PaCO2 rise when given O2?
Lose hypoxic pulmonary vasoconstriction, increasing ventilation perfusion mismatch
How are patients with resp. failure managed?
All need arterial blood gas analysis as severity difficult to assess clinically.
Chest X-ray
Lung function tests
Airway maintenance, O2 therapy, mechanical ventilation, clearance of secretions
bronchodilators and antibiotics
Treat problems with CO, Hb conc and fluid balance
Why is chronic type 2 respiratory failure tolerated better than type 1?
Chronic develops gradually so time for compensatory mechanisms to occur- hypoxia and hypercapnia tolerated better
What is the primary complex in TB?
the primary (Ghon’s focus)- sub-pleural focus of tubercles, and the draining lymph (hilar) nodes together.
Would you want to carry out lung function tests on a patient with pneumonia?
Probably not as patient usually quite sick and information not particularly useful
Why is inspiration more painful in pneumonia?
During inspiration, inflamed pleura moves against the thoracic wall, causing pain.
How would you describe chest X-rays of pneumonia patients?
Opacities visible, may be one opacity-lobar pneumonia, or more patchy opacification-bronchopneumonia
Define pneumonia
infection of lung parenchyma with consoldation, involving distal airways and with resultant inflammatory exudation
Treatment for acute bacterial pneumonias
mild to moderate= amoxicillin
severe= co-amoxiclav
How is a wheeze caused?
Vibration of intra-thoracic airway wall at site of flow limitation. More pronounced in expiration as intrathoracic airways narrower than in inspiration, with increased pressure on very small airways, so become compressed, and narrowing worsened.
Give 3 non-specific triggers of asthma
smoke, cold air, exercise
Give 2 specific triggers of asthma in sensitised patients
pollen, HDM faeces
How can hyperresponsiveness of airways be determined in asthma?
Bronchial provocation tests- inhale increasing dosages of histmaine or methacholine until FEV1.0 reduces by 20%.
Why might asthma treatment with a Beta 2 agonist result in hypokalaemia?
Beta 2 adrenergic agonists acitvate Beta 2 receptors, resulting in stimulation of Na+ pump, increasing K+ uptake into cells.
Name 2 common bacterial causes of pneumonia assoicated with COPD exacerbations
H.influenzae
Moraxella catarralis
Why might a patient who has recently had a BM transplant be at a greater risk of pulmonary TB?
Patient will be on immunosuppressive medication to prevent rejection of transplant by her IS.
Describe mycobacterium TB
An acid-fast bacillus-requires ziehl neelsen staining e.g. of sputum sample- 3 samples taken. Bacilli slow-growing- 4 to 6 wks. BM or CSF culture may confirm diagnosis of miliary TB
Describe the Mantoux test
Diagnostic test of TB which is strongly +ve in post-primary TB and often -ve in military TB (reduced host response) and HIV- reduced cellular immunity.
Injection of tuberculin into skin, inflammatory reaction development
What is the concern with a patient with suspected TB if complaining of a headache?
May have been haematogenous spread of M.TB to the meninges, resulting in bacterial meninigits.
What are the clinical features of primary pulmonary TB?
often asymptomatic mild fever erythema nodosum small pleural effusions wheeze may result from bronchial compression by lymphadenopathy
What is drug regime for uncomplicated pulmonary TB?
Rifampicin, isoniazid, pyrazinamide and ethambutol for 2 mnths, followed by rifampicin and isoniazid for 4 mnths. ethambutol given if drug resistance suspected. Corticosteroids occasionally improve results in severe pulmonary TB.
Drug reaction of isoniazid
Peripheral neuropathy
Prevention of TB?
BCG vaccination of non-immune subjects
Adequate living space
RFs for lung cancer?
Cigarette smoking
Asbestos-mesothelioma*
Radon gas
What are the 2 pathological divisions of lung cancer?
Small cell and non-small cell- majority
Why might squamous cell carcinomas-arise from bronchial epithelium?, cause hypercalcaemia?
Release of PTH-related peptide- increases release of calcium from bone, reduces renal Ca2+ excretion and reduces renal phosphate reabsorption, BUT doesn’t increase renal 1 alpha-hydroxylase activity, so doesn’t increase calcitriol, unlike PTH.
How is non small cell cancer staged?
TNM staging
Treatments for lung cancer?
Surgical resection
Chemotherapy
Radiotherapy
Only palliative care suitable for stage 4 disease-incurable.
Why might a patient being treated for TB develop orange urine?
Side effect of rifampicin drug
When should ITU be informed in pneumonia?
- Resp failure
- rising pCO2
- worsening metabolic acidosis
- hypotension despite fluid resucitation
Early and later infections CF patient prone to
Early -staph. aureus, H.influenzae
Later- pseudomonas aeruginosa
Process of diagnosis and treatment of pneumocystis pneumonia
Opportunistic.
Pneumocystis jirovecii- fungus, produces spores which enter lungs and cause acute alveolitis. May not detect on specimens. Induced sputum, bronchoalveolar lavage, lung biopsy- silver stain?, PCR to detect fungus, DNA.
High dose cotrimoxazole
Describe features of chronic type 2 resp failure
polycythaemia
pulmomary hypertension with RHF (cor pulmonale)
CO2 retention- flapping tremors, warm hands, bounding pulse
If patient with COPD in chronic type 2 resp. failure and is given O2, and aBG check shows their hypercapnia is worsening, what should be done?
Give non-invasive ventilator support as well as O2.
Describe chronic bronchitis pathology
- goblet cell hyperplasia in epithelium, so increased mucus prod.
- reduced cilia as ciliated cells lost, preventing mucus sweep up
- mucous gland hypertrophy in SM, resulting in mucus hypresecretion and bronchial wall swelling.
How does chronic bronchitis cause airway obstruction
Increased mucus and bronchial wall swelling narrow airways by reducing lumen calibre, causing airway obstruction.
Describe emphysema pathology
Progressive alveolar wall destruction with air space enlargement and reduction in capillary bed as pulmonary capillaries lost.
Define emphysema
Permanent destructive enlargement of airspaces distal to terminal bronchiole
What cell type produces proteases which may cause emphysema if alpha 1 antitrypsin deficiency?
Neutrophil
LFTs for COPD?
Spirometry- VC, TV, FEV1.0 and FVC, and ratio, and flow volume loops.
Body plethysmography and/or helium dilution for lung vol measurements e.g. TLC, RV and FRC
TLCO- transfer factor of lung, to measure diffusion
CXR findings for COPD
Hyperinflated lungs- large, blunting of costophrenic angles and flattened hemidiaphragms
Elevated ribs and loss of rib curvature, >6 ribs seen anteriorly
Narrowed and elongated heart shadow
Low, flat diaphragm
Narrow mediastinum
Main factors involved in causing COPD
cigarette smoke environmental pollutants smoke from cooking fires where poor ventilation and no chimneys coal mining alpha 1 antitrypsin deficiency
Cause of airway obstruction emphysema
loss of radial traction of lung so pressure collapsing airways greater than lung elastic recoil, airways can’t be held open on expiration
loss of lung elastic recoil
reduced SA for GE
Why might it be difficult to breath in if asthmatic?
Residual vol. of lung increased as air trapping, and FRC increased, so will be breathing close to total lung volume, and lung hyperinflated, so reduced compliance of lung as breathing in from a more expanded position, so larger change in intrathoracic pressure necessary to produce lung volume change.
Why might an asthmatic who is breathing faster than normal experience paraesthesia?
Low pCO2 results in vasoconstriction, which can cause blackouts, paraesthesia and chest pain.
What effects can LT steroid use have on an adult patient?
Oral candidiasis- immunosuppressive Hypertension Central obesity Bruising Skin thinning Osteoporosis Adrenal suppression
Why is M.TB an acid fast bacterium?
Requires Ziehl-Neelsen staining as lipid-rich cell wall retains some dyes, resisting decolourisation with acid.
Also resistant to gastric acid in stomach.
What viruses are resistant to gastric acid in stomach?
Coxsackie, polio, hepatits A
What happens when M.TB enters alveoli, typically those well ventilated and poorly perfused upper lung lobes subpleurally?
Phagocytosed by alveolar macrophages but resulting phagosome prevented from fusing with lysosome by cell wall lipids of bacterium, so MTB excapes into cytoplasm and multiplies.
Clinical features of primary pulmonary TB
Often asymtomatic, may cause mild febrile illness, erythema nodosum, small pleural effusions.
Who is at high risk of TB in the UK?
Immunocompromised people: DM, HIV, corticosteroid therapy, Vit D deficiency, chronic kidney disease
Lifestyle: alcohol/drug- IV-HIV abuse, homelessness
Contact: travelling to high incidence areas
Why is TB incidence highest in Sub-Saharan Africa?
Because of HIV prevalence
Why would alternate birth-control methods be used rather than OCP in people being treated for TB?
Rifampicin drug used in treatment induces liver enzymes, so oral contraception will not be effective
Frequent sites of spread of lung cancer?
Mediastinal, cervical, axillary and intra-abdominal nodes.
Metastases to liver, bone, adrenal glands and brain.
Most common symptom of lung cancer?
Cough
Why does LC cause breathlessness?
Central tumours occlude large airways resulting in lung collapse and breathlessness on exertion. Many patients have co-existent COPD-obstructive-airways resistance
Phrenic nerve involvement- diaphragm paralysis
pleural effusions
Breathlessness in COPD, why?
Airway occlusion- bronchial wall hypertrophy and excess mucus secretion.
Reduced SA for gas exchange
Small airway collapse as loss of elastic tissue in alveolar walls
Why might a LC patient present with a hoarse voice?
L recurrent laryngeal nerve compression by invading tumour into mediastinal lymph nodes or direct mediastinal invasion. Nerve innervates intrinsic laryngeal muscles controlling vocal cord movement?
Characterisitc feature of sarcoidosis?
Non-caseating granulomata
How can sarcoidosis be suppressed in stages I to III of the disease?
Steroids
Why poor prognosis in lung cancer- typically around 5% 5 yr survival?
Late stage presentation so few are operable, age of patient presenting and their co-morbidities e.g. IHD and COPD
What is a chylothorax?
Accumulation of triglyceride-rich lymph in pleural space, generally as result of damage to thoracic duct, causing leakage into pleural space e.g. as result of trauma or carcinoma.
What is a heamothorax?
Blood within pleural cavity
What may cause haemoptysis?
Infective- pneumonia, TB Lunc cancer Lung infarction-PE Pulmonary hypertension- pulmonary oedema Colagulopathies- thrombocytopenia Trauma/foreign body
Transudative effusions?
imbalance in Starling’s forces, protein-poor fluid (<30g/L), often bilateral, not assoc. with fever, pleuritic pain or tenderness to palpation. Most common cause= congestive HF. May also be result of cirrhosis with ascites, hypoalbuminaemia, nephrotic syndrome, pericardial disease or peritoneal dialysis, sepsis increasing capillary permeability.
Exudative effusions?
imply disease of pleura or adjacent lung, protein-rich fluid (more than 30g per litre). May be result of infection e.g. TB, pneumonia, maliganancy e.g. of pleura, or secondary e.g. breast cancer, lung, AI disease- RA, SLE, maybe abdominal disease e.g. pancreatitis causing an inflamed diaphragm
How are pulmonary crackles or crepitations caused?
By re-opening of small airways , during inspiration, which have become occluded during expiration
Nuclei appearance in malignant cells?
High nuclear to cytoplasmic ratio Hyperchromatic Prominent nucleoli Pleomorphic- irregular in shape Frequent/abnormal mitoses
Architectural abnormalities of malignant cells?
Ulceration Necrosis Infiltrative margins Vascular invasion Poorly circumscribed Reaction in surrounding tissue/stroma Little resemblance to normal tissue= anaplastic
You know the FRC. How would you work out the ERV, if you know the RV?
ERV=FRC-RV
What is IC the sum of?
TV+IRV
How do you work out VC-vital capacity?
IC+ERV
What is your TLC?
FRC + IC
Where is the serous fluid lining the pleura produced?
By parietal pleura, and is absorbed from parietal lymphatic vessels
Why is intra pleural pressure increased during a forced expiration?
elastic recoil of lungs
What is the lingula?
A projection of superior lobe of left lung
What do the lung hila consist of?
Bronchi, pulmonary vessels and LNs
How is genuine widening on mediastinum caused on an X-ray?
Vascular abnormality or mediastinal mass
If a patient is unable to stand, and anterior-posterior CXR might be taken, what is the problem of this?
Heart magnification as heart located anteriorly, so if heart larger than normal, would be unable to say whether the heart was actually enlarged
Most important virulence factor of streptococcus pneumoniae?
polysaccharide capsule- anti-phagocytic
Problem with creating vaccine against streptococcus pneumoniae based on its capsule?
Many different capsule serotypes- different antigens
Why is infection with streptococcus pneumoniae more severe in a patient with sickle-cell disease compared to a patient without this autosomal recessive condition?
Sickle-cell disease patient will have functional asplenia as a result of multiple small infarcts, causing the spleen to function less efficiently, and the spleen is necessary for the removal of encapsulated bacteria e.g. S.pneumonia. RBC become sickled when low pO2 causes them to become insoluble and polymerise, and their shape is unable to be accomodated in small blood vessels, so they obstruct splenic vessels, resulting in tissue infarction.
How can bacterial pneumonia be prevented in patients who have sickle cell disease?
Prophylactic antibiotics- penicillin or erythromycin
Vaccination- pneumococcal 13 valent conjugate vaccine
Define cyanosis
A bluish discolouration seen when there is more than 5g/dl of desaturated Hb (which has a darker colour) in the capillary blood
What does the presence of cyanosis depend on?
The total amount of Hb in the blood, the extent of desaturation of Hb and state of capillary circulation
Difference between central and peripheral cyanosis
Central: discolouration of tongue or oral mucosa. Result of arterial hypoxia, detected when O2 sat. below 90% and hence pO2 of 8 kPa. May result from poor oxygenation in lungs or cyanotic heart disease
Peripheral: cyanosis is limited to the extremities (eg hands, feet,). It is usually due to poor peripheral circulation, as may happen in cold weather due to vasoconstriction of skin vessels; or poor arterial circulation (eg due to peripheral vascular disease or heart failure). In these circumstances the increase in tissue oxygen extraction → increased deoxygenated Hb in the capillaries→ cyanosis.
All patients with central will have peripheral
A patient is hypoxic because he is unable to ventilate his lungs efficiently. His pCO2 is increased as CO2 is retained causing a resp. acidosis, but why might he also have a met. acidosis?
Hypoxia resulting in lactic acidosis as tissues have insufficient O2 for aerobic respiration- pyruvate converted to lactate via lactate dehydrogenase
Important signs of lung cancer?
Clubbing of fingers weight loss anaemia wheeze/stridor pleural effusion pneumonia neurological ACTH/ADH/PTH
Where does a lung cancer normally spread to locally?
Hilar LNs
Mediastinal LNs- occasionally causes oesophageal obstruction
Pericardium- causing effusion
Pleura- causing effusion
RLN- hoarseness of voice, doesn’t improve as with laryngitis
Phrenic nerve- diaphragm paralysed on affected side, sudden breathlessness as reduced capacity of lung to fully expand on inspiration
Bronchus- causing obstruction and lung collapse distal to obstruction
Why might a patient with small cell lung cancer have hyponatremia?
Paraneoplastic syndrome- syndrome of inappropriate ADH secretion- stimulating AQP-2 insertion in apical membrane of CD cells, so increasing water reabsorption, reducing concentration of Na+ in blood
Key description of small cell carcinoma of lung?
Central, highly invasive and rapidly metastasises.
Very cellular, apoptotic bodies, nuclear moulding, often necrosis and lots of mitoses
Why might cavities appear on a CXR of TB patient?
Caseous necrosis occurs with granuloma formation. Inflammatory material may leak out into vessels, leaving a space behind where the material was- cavity.
What factors determine whether a patient with a non-small cell carcinoma of the lung is suitable for surgery?
o Is patient’ general health good?
o Is pulmonary function adequate to cope with major surgery and pulmonary resection?
o Is surgery technically feasible (depends on exact site of tumour)?
o Is there evidence of local spread?
o Is there evidence of distant metastases?
Why might a tyrosine kinase inhibitor be used in treatment of a patient with a non small cell lung carcinoma?
Some adenocarcinomas of lung show EGFR mutations- receptors work via tyrosine kinase
Difference in clinical signs between fibrosing alveolitis and extrinsic allergic alveolitis?
Finger clubbing in fibrosing alveolitis, never present in extrinsic allergic alveolitis
How could asthma in a farmer be distinguished from extrinsic allergic alveolitis?
LFTs- spirometry- restrictive pattern for alveolitis with small lung volumes, and obstructive for asthma with possible lung hyperinflation
Other than sarcoidosis, name another interstitial lung disease where a non-caseating granuloma is present?
Extrinsic allergic alveolitis
In what way might sarcoidosis present extra-pulmonarily in the same way as primary TB infection?
Erythema nodosum
What lies in the superior mediastinum?
Trachea, oesophagus, SVC, aortic arch, thymus, phrenic nerve, L recurrent laryngeal nerve, thoracic duct
What lies in the anterior mediastinum?
Fat, lymph vessels and nodes
3 structural components of gas exchange?
Lungs, pleura and chest wall
3 processes affecting oxygenation of our blood in inspiration?
Ventilation, diffusion and perfusion
