MAPAS

Question 1

Why would you not give a COPD patient oxygen?

Answer 1

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.

Question 2

Describe the mechanism of respiratory drive mediated by CO2 levels and how this is affected in COPD

Answer 2

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.

Question 3

What are the effects to the patient of hypercapnia

Answer 3

Headache, confusion, lethargy and death

Question 4

Where are the peripheral chemoreceptors located and what do they detect? What nerve do they convey their messages via?

Answer 4

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.

Question 5

Where are the central chemoreceptors located, what do they detect and what is their effect

Answer 5

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.

Question 6

Name the true, false and floating ribs

Answer 6

True ribs first seven (directly attached to sternum)
False ribs ribs 8-10
Floating ribs 11-12

Question 7

From most the lung outwards name all the layers and structures in between ribs.

Answer 7

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

Question 8

Describe the process of a thoracentesis

Answer 8

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.

Question 9

What are some indicators that support an asthmatic diagnosis over a COPD diagnosis

Answer 9

Hx of atopy
Nocturnal pattern
Sudden onset
No smoking/ recent onset of smoking
Age

Question 10

Identify common symptoms of asthma

Answer 10

Sudden onset of SOB
Nocturnal 
Wheezing
Cough
Sputum production

Question 11

Name the classes of bronchodilators

Answer 11

Long and short acting beta 2 agonists (adrenaline and salbutamol), anticholinergics (atropine), theophylline

Question 12

Name the anti-inflammatory drugs use in asthma treatment

Answer 12

Glucocorticoids
Inhaled cortisone, prednisone
Systemic
Pulmicort, flixotide

Question 13

Phamacological action of b2 agonists

Answer 13

Stimulates cAMP resulting in smooth muscle relaxation

Question 14

Phamalogical action of Anticholinergics

Answer 14

M3 antagonist, blocks ACh resulting in smooth muscle reaxation and reduced mucous

Question 15

Theophylline pharmacology

Answer 15

Phosphodiesterase inhibitor, blocks the degradation of cAMP

Question 16

Phamacological actions of glucocorticoids

Answer 16

Bind to glucocorticoid receptor which then activated up regulates anti-inflammatory proteins (transactivation) and represses expression of pro-inflammatory proteins (transrepression)

Question 17

Define mild, moderate and severe COPD

Answer 17

Mild FEV1 60-80%, moderate 40-59%, severe

Question 18

Pathogenesis of COPD

Answer 18

Smoking- more oxidants, fewer antioxidants—> lung inflammation–>neutrophil mediated release of enzymes that destruct elastic tissue in lungs–> airway collapse and increased FRC

Question 19

Outline the management plan for COPD, including pharmaceutical treatments, potential lifestyle changes, and plans for possible future deterioration

Answer 19

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?

Question 20

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?

Answer 20

Decrease- COPD patient has increased airway resistance. A slower respiratory rate means lower resistance to flow.

Question 21

Name three effects of significant weight loss on spirometry findings

Answer 21

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

Question 22

Where in the respiratory tract would you find goblet cells?

Answer 22

In conducting airways from trachea to terminal bronchus

Question 23

Where in the respiratory tract would you find smooth muscle cells and elastic fibres?

Answer 23

All airways from trachea to respiratory bronchioles

Question 24

Where in the resp tract do you find type 1 pneumocytes

Answer 24

Alveoli walls

Question 25

C shaped cartilage rings

Answer 25

Trachea

Question 26

pseudostratified ciliated columnar epithelium

Answer 26

Trachea to segmental bronchi

Question 27

Vibrissae

Answer 27

Nose

Question 28

ciliated cells and smooth muscle, but no hyaline cartilage

Answer 28

terminal bronchi and respiratory bronchi

Question 29

What stage of lung development and at what gestation does surfactant begin to be produced?

Answer 29

Saccular stage, 24 weeks