Conditions Flashcards
Surface markings.
Domes of the diaphragm.
I 8 10 EGGS AT 12?
Difference in blood supply to the parietal and visceral pleura.
Which lymph nodes can widen to lead to widening of the angle of carina?
What are the surface markings for the two fissures?
What are the inferior borders of the lungs?
Right 5th rib
Left - ~5th IC
IVC T8
Esophagus/vagus T10
Aorta/Azygous vein/ Thoracic duct T12
Visceral = bronchial arteries Parietal = intercostal arteries.
Tracheobronchial lymph nodes.
4th rib from mid axillary line = horizontal fissure
T2 to 6th costal cartilage.
6th rib MCL
8th rib MAL
10th rib MSL
+2 for pleura
Azygous system.
What two veins form the azygous vein and hemiazygous vein at the level of T12?
Where does the hemiazygous vein drain into?
Where does the accessory hemiazygous vein drain into?
Ascending lumbar vein and the subcostal vein
Azygous vein
Azygous vein
Respiratory distress syndrome.
By when is surfactant production sufficient in the newborn
Give some symptoms.
Treatment for the baby?
Give two riskfactors.
35-36 weeks.
Tachypnoea Intercostal recessions Grunting Nasal flaring Cyanosis
Endotracheal tube surfactant for replacement and oxygen.
Premature delivery
Diabetes in mother
Interstitial lung disease.
Give some causes.
Give some drugs that can cause it?
Why is airway obstruction worse on expiration?
What defines barrel chest?
What would you find on examination in interstitial lung disease?
Asbestos/ silicosis exposure Idiopathic Auto-immune mediated Sarcoidosis Methotrexate, amiodarone and nitrofurantoin
Positive intrapulmonary pressure exacerbates narrowing of the intra thoracic airways.
AP:Lateral diameter 1:1 as opposed to 1:2
Bilaterally reduced lung expansion
Atelactasis.
Give 3 causes.
Fluid/ air in the pleural cavity leading to mechanical collapse - relaxation or compression
Resorption due to obstruction
Post surgical
Cicatrization- fibrotic changes
Why is the pH of plasma normally alkaline?
Why is HCO3- higher in the plasma than H+?
What is the HCO3- concentration in plasma mainly determined by?
Why is there more CO2 in venous blood compared to plasma both in dissolved and reacted form?
Why can CO2 be breathed off at the lungs?
Why are more carbamino compounds formed at the tissues?
Because there is a high concentrating of HCO3- driving the reverse reaction which is favoured.
Because HCO3- is pumped out via AE whilst H+ binds to Hb inside the RBC
Determined by the ability of Hb to bind H+ NOT pCO2
At tissues - lower O2 - means more H+ can bind to haemoglobin allowing for more HCO3- to be produced.
High O2 - means more binds to Hb - relaxed state - more H+ given up - reacts with HCO3- forming CO2 which can be breathed off
Because of unloading of oxygen allows more CO2 to bind
Because high pCO2
Acid Base Balance.
What symptoms may alkalaemia present with?
What is the difference in the way the PCT and DCT make HCO3-?
Give two things that buffer H+ in the kidney?
Why can we not compensate for a metabolic alkalosis?
Paraesthesia and tetany
PCT - from glutamine (broken down to NH3 and H+ which combine to form NH4+ in the lumen whilst the aKG gets broken down to two HCO3- and is pumped out basolaterally into the ECF by Na+/HCO3- exchanger).
DCT - from CO2 and H2O
Phosphate and NH3.
Can not breath less due to the need to maintain pO2
Renal tubular acidosis.
Type I cause?
Type II cause?
Acid base status?
Another cause with this base status?
When type II is combined with other things phosphaturia, glycosuria, amunoaciduria etc what is it known as?
Issues?
Decreased H+ excretion in the DCT (malfunctioning HKATPase and H+ pumps)
Decreased reabsopriton of Na in the PCT (malfunctioning of basolateral Na HCO3- symporter)
Metabolic acidosis with NORMAL anion gap
Severe persistent diarrhoea
Acetazolamide
Fanconi syndrome
Osteomalacia due to loss of phosphate.
Metabolic alkalosis.
Give 3 causes.
Why does hyperaldosteronism cause it?
How is it normally corrected and why may it be hard to correct?
Persistent vomiting Diuretics (loops/ thiazides) Cushing s Primary hyperaldosteronism Hypokalemia
Because more Na H exchanger activity in the DCT - more H+ secreted into urine - alkalosis.
Normally corrected due to less H+ excretion and reduced HCO3- recovery.
In the case of volume depletion - Na+ reabsorption favoured - more Na+ reabsorption via NaH exchanger favours more HCO3- absorption.
X ray.
What can an increased right paratracheal stripe width mean?
How can you assess whether sufficient penetration has occured?
What can you use to assess adequacy of an X-ray?
What is silhouette sign?
Two signs of a tension PT?
When may a meniscus not be seen?
What two signs are seen when left upper lobe collapses on lower lobe? Left lower lobe collapse?
Paratracheal Lymphadenopathy
Lipoma
Vertebrae visible through heart
Left hemidiaphragm not visible
RIP - rotation, inspiration and penetration.
Adjacent structures of differing density form a crisp contour.
Depressed hemidiaphragm
Mediastinal shift
When the CXR is taken supine position.
Veil like opacity
Luftsickle sign
Sail sign
Respiratory control.
Give 4 sensors that feed to the respiratory centre.
Other than increased heart rate and increased breathing what other change can be bought about by peripheral chemoreceptors in response to fall of pO2?
Peripheral chemoreceptors (O2 CO2 and H+) Central chemoreceptors (H+) Pulmonary receptors (stretch) joint and muscle receptors (stretch and tension)
Changes in blood flow distribution - brain and kidneys prioritised for example.
Spirometry.
What does FEV1 decrease in obstructive volume time graph? FEV1:FVC ratio?
FEV1 in restrictive?
Difference between variable upper airway obstruction as opposed to fixed obstruction?
Why may flow volume in obstructive airway disease be moved to the left?
Because narrowed airways reduce the speed at which air can be breathed out.
Less than 70%.
more than or equal to 70% in restrictive
FEV1 normal or greater than normal (increased elastic recoil)?
Variable - inspiration blunted (bottom of flow volume loop) Fixed - both bottom and top blunted
Due to increased total lung capacity due to hyperinflation occurring.
Ventilation perfusion mismatch.
Give some causes of V/Q mismatch.
Why may left sided heart failure result from right sided failure in the context of a PE?
Give two signs that may be seen in RV failure.
Why may pulmonary infarction lead to death in PE?
Give four X ray findings that might be seen on PE?
What criteria is used for PE? Relevance?
Why is D dimer not used to rule out PE in those with high likelihood?
How does heparinisation reduce mortality?
Pneumonia Pulmonary embolism COPD RDS Pulmonary oedema
Due to shift of the interventricular septum
JVP distension
Hepatosplenomegaly
Oedema
Haemoptysis, pleuritis and pleural effusion occurs impairing lung function.
Wedge shaped opacity
Enlarged pulmonary artery
Pleural effusion
Elevated hemidiaphragm.
Well’s criteria
Score more than 4 - imaging
Score less 0-4 - D diner - no further investigation.
Negative predictive value of D dimer is too low to use.
Reduce propagation at site and source
Hypoventilation
.
Give 5 main causes for hypoxaemia.
What type of respiratory failure caused by hypoventilation?
Give an acute and chornic cause.
Give two reasons why treating hypoxia in chronic TII resp failure is bad?
V/Q mismatch Altitude Hypoventilation (ENTIRE LUNG) Diffusion defect Right to left shunt
Type 2 ALWAYS.
Acute - asthma attack (VSA), opiate overdose, head injury
Chronic - kyphoscoliosis, MND, myopathy, late stage COPD, lung fibrosis
Oxygen removes the stimulus for the hypoxic respiratory drive
Correction of hypoxia removes pulmonary vasoconstriction
V/Q mismatch.
Why is O2 low but CO2 Normal/ low?
Why do certain segments have increased ventilation in V/Q mismatch pathologies?
Why do diffusion defects cause Type I respiratory failure?
Give two conditions where this is the case? Differences in pathogenesis?
Give the two different mechanisms by which these can cause respiratory failure.
O2 low because increased areas of ventilation (V/Q>1) increase the dissolved O2 by a very small amount but since Hb is already fully saturated above 10kPa it is insuffienct to compensate for areas with V/Q <1.
CO2 normal or low because in areas of increased ventilation (V/Q <1) more CO2 will be breathed out - sufficient enough to compensate for CO2 retention in areas with V/Q of less than 1.
Because areas where ventilation is decreased cause low O2 and CO2 retention which will cause stimulation of chemoreceptors and thus hyperventilation to unaffected segments.
Due to CO2 being more soluble than O2 and allowing for for diffusion of CO2 whilst O2 diffusion is still affected. This results in type 1 respiratory failure.
Pulmonary oedema, fibrotic lung disease.
Pulmonary oedema - more fluid in interstitium
Fibrotic lung disease - thickened membrane.
Pulmonary oedema - diffusion defectand V/Q mismatch
Lung fibrosis - diffusion defect and hypoventilation.
