MAPAS Flashcards
Why would you not give a COPD patient oxygen?
In normal individual respiratory drive is influenced by high CO2 levels (resulting respiratory acidosis detected by central chemoreceptors in ventral medulla which stimulates respiration). In COPD obstructive pathology causes a chronic increase in CO2 levels, the kidneys compensate by producing HCO3- which reduces H+, the hypercapnic drive for respiration is suppressed. Their respitaratory drive is then mediated by low 02 saturations (detected by peripheral chemoreceptors). If high 02 is administered you will suppress this drive causing hypoventilation and resulting hypercapnia.
Describe the mechanism of respiratory drive mediated by CO2 levels and how this is affected in COPD
High CO2 levels in the blood cause acidosis of the blood which is detected by central chemoreceptors near the ventral surface of the medulla. An increase in H+ stimulates respiration whereas a decrease inhibits it.
In COPD the kidneys compensate for the acidosis by producing more HCO3- thus decreasing the H+ concentrations and suppressing the central receptor hypercapniac mediated drive.
What are the effects to the patient of hypercapnia
Headache, confusion, lethargy and death
Where are the peripheral chemoreceptors located and what do they detect? What nerve do they convey their messages via?
Located in the carotid bodies at the bifurcation of the common carotid arteries and at the aortic bodies in the aortic arch. Detect differences in arterial PO2. Vagus nerve.
Where are the central chemoreceptors located, what do they detect and what is their effect
Located in the ventral medulla, detect high levels of H+ (as a proxy for high CO2) in the medullary ISF. High levels of H+ results in stimulation of breathing. Low levels surpasses breathing.
Name the true, false and floating ribs
True ribs first seven (directly attached to sternum)
False ribs ribs 8-10
Floating ribs 11-12
From most the lung outwards name all the layers and structures in between ribs.
Lung, visceral pleura, pleural cavity, parietal pleura, innermost intercostal, internal intercostal, external intercosta, fat, fascia, skin. In intercostal groove of rib(inferior edge) sits the neuromuscular bundle Vein, Artery, Nerve. There is a smaller collateral bundle on the superior edge of the rib
Describe the process of a thoracentesis
Procedure to remove fluid or air from the pleural space. Administer local anaesthetic to the following layers: Skin, fat, intercostals,, parietal pleura. Insert need above rib to avoid main neuromuscular bundle. Fluid will normally be drained around 5th intercostal space, air mid clavicular.
What are some indicators that support an asthmatic diagnosis over a COPD diagnosis
Hx of atopy Nocturnal pattern Sudden onset No smoking/ recent onset of smoking Age
Identify common symptoms of asthma
Sudden onset of SOB Nocturnal Wheezing Cough Sputum production
Name the classes of bronchodilators
Long and short acting beta 2 agonists (adrenaline and salbutamol), anticholinergics (atropine), theophylline
Name the anti-inflammatory drugs use in asthma treatment
Glucocorticoids
Inhaled cortisone, prednisone
Systemic
Pulmicort, flixotide
Phamacological action of b2 agonists
Stimulates cAMP resulting in smooth muscle relaxation
Phamalogical action of Anticholinergics
M3 antagonist, blocks ACh resulting in smooth muscle reaxation and reduced mucous
Theophylline pharmacology
Phosphodiesterase inhibitor, blocks the degradation of cAMP
Phamacological actions of glucocorticoids
Bind to glucocorticoid receptor which then activated up regulates anti-inflammatory proteins (transactivation) and represses expression of pro-inflammatory proteins (transrepression)
Define mild, moderate and severe COPD
Mild FEV1 60-80%, moderate 40-59%, severe
Pathogenesis of COPD
Smoking- more oxidants, fewer antioxidants—> lung inflammation–>neutrophil mediated release of enzymes that destruct elastic tissue in lungs–> airway collapse and increased FRC
Outline the management plan for COPD, including pharmaceutical treatments, potential lifestyle changes, and plans for possible future deterioration
Pharmaceuticals: inhaled bronchodilator, corticosteroids as prn.
Prevent deterioration- flu vaccination, pneumococcal vaccination, quit smoking (offering help if required), look to continue exercise as much as possible, assess occupation e.g. dustiness, schedule follow up visits, look to negate negative impact on life
Plan: possibility of psychosocial problems addressed, look at home suitability, possible oxygen admin, ensure multidisciplinary plans, nutrition, sleep apnoea. O2 therapy?
In the absence of the stress response (an acute event), and assuming they are trying to minimise the work of breathing would you expect a COPD patients respiratory rate to increase or decrease?
Decrease- COPD patient has increased airway resistance. A slower respiratory rate means lower resistance to flow.
Name three effects of significant weight loss on spirometry findings
1: Increased functional lung capacity and total lung capacity due to less weight on chest wall (inward pressure)
2: Quicker expiratory flow due to more outward pressure (tethering) on airway decreasing resistance and reducing likelihood of aw collapse
Where in the respiratory tract would you find goblet cells?
In conducting airways from trachea to terminal bronchus
Where in the respiratory tract would you find smooth muscle cells and elastic fibres?
All airways from trachea to respiratory bronchioles
Where in the resp tract do you find type 1 pneumocytes
Alveoli walls
C shaped cartilage rings
Trachea
pseudostratified ciliated columnar epithelium
Trachea to segmental bronchi
Vibrissae
Nose
ciliated cells and smooth muscle, but no hyaline cartilage
terminal bronchi and respiratory bronchi
What stage of lung development and at what gestation does surfactant begin to be produced?
Saccular stage, 24 weeks
