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Yr 2.0 Sem 3 > Respiratory > Flashcards

Respiratory Flashcards

1
Q

1 What’s the point of the nasal conchae?

A

They induce turbulent airflow which maximizes exchange efficiency

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2
Q

1 What do the tubercles of each rib articulate with?

A

The transverse process of the inferior vertebra

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3
Q

1 What type of muscle is the diaphragm and what is it’s innervation?

A

Skeletal muscle - Phrenic nerve (C3,4,5)

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4
Q

1 Where in an intercostal space should you insert a chest drain?

A

Just above the inferior rib to avoid the neurovascular bundle

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5
Q

1 Describe the hiatuses of the diaphragm

A

Vena cava T8, Oesophagus T10, thoracic duct/aortic hiatus T12

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6
Q

1 Describe the venous drainage of the intercostal spaces around the heart

A

Intercostal veins -> azygous system -> superior vena cava

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7
Q

1 Which bronchus are aspirated objects more likely to settle in and why?

A

Right bronchus as it is more vertical

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8
Q

1 Which lobes of the lung are you listening to when you ausculate from the back?

A

Inferior

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9
Q

1 Name the 2 recesses of the pleural cavity

A

Costodiaphragmatic and retrosternal

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10
Q

1 Why should you consider the lungs when placing a central line?

A

Because the pleura extends above the 1st rib

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11
Q

1 How high up the anterior trunk does the diaphragm extend?

A

Highest point of dome is 4th intercostal space on R side and 5th ICS on L side

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12
Q

2 List the accessory muscles of breathing

A 
Sternocleidomastoid
Scalenes 
Pectoralis major and minor
Trapezius
Internal intercostal muscles
Muscles of Abdominal wall
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13
Q

2 How do you calculate alveolar ventilation rate?

A

(tidal volume - anatomical deadspace volume) x respiratory rate

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14
Q

2 What’s the physiological deadspace of the lungs?

A

The volume of air which is inhaled that does not take part in the gas exchange, either because it (1) remains in the conducting airways ( ie upper respiratory tract) or (2) reaches alveoli that are not perfused or poorly perfused.

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15
Q

2 What’s the Functional Residual Capacity?

A

Volume of air remaining in lungs at end of passive exhalation.

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16
Q

2 How does emphysema cause a barrel chested appearance?

A

Destruction of lung architecture results in increased compliance, causing hyperinflation of the lungs. Chest wall then becomes hyperexpanded and thus rounder or “barrel” shaped.

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17
Q

2 What potential pathophysiological features of the lung could cause an obstructive pattern on spirometry?

A

Mucus hypersecretion
Decreased radial traction / fewer attachments between airway and parenchyma
Hypertrophy of smooth muscle
Oedema (restrictive too)

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18
Q

2 What’s the formula for calculating airway resistance?

A

Pressure drop over airway divided by flow through airway

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19
Q

2 Why do we need a pleural seal?

A

Allows maintenance of negative pressure which forces lungs to follow expansion of chest wall while still allowing elasticity of lung to produce passive deflation when inspiratory muscles relax. Without it the lungs would collapse (pneumothorax).

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20
Q

3 List the parts of the diffusion barrier at the air-blood interface in the lung

A

Endothelium of capillary, collagen based extracellular matrix, surfactant and water layer and squamous epithelial cells of alvelous

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21
Q

3 How could you estimate total CONCENTRATION of oxygen in the blood?

A

Multiply partial pressure of gas in the blood by its solubility coefficient.
+
Estimated Amount of O2 bound to haemoglobin ( ie Hb concentration x Hb saturation x O2 carrying capacity of Hb)

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22
Q

3 Why does partial pressure of O2 in inspired air decrease as it passes through the upper respiratory tract?

A

Saturation with water vapour

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23
Q

3 Why does fast ascent from scuba diving risk decompression sickness / “the bends”?

A

Doesn’t give nitrogen enough time to be exhaled as it comes out of solution in the body fluids.

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24
Q

3 Explain how high altitude can cause hypoxia even through if % of oxygen is still roughly 21%

A

Air is less compressed at higher altitudes meansing that there is a lower amount of oxygen in the volume of inhaled air.

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25
Q

1st year What 3 factors will shift the oxygen-haemoglobin dissociation curve to the right?

A

Fall in pH / Bohr shift
Rise in temperature
Increased 2,3 BisPhosphoGlycerate

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26
Q

1st yr What are the 2 states of haemoglobin?

A

Tense / T / low affinity state

Relaxed / R / high affinity state

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27
Q

3 Why does haemoglobin readily give up oxygen where ppO2 is low?

A

Low pO2 causes Hb to shift into tense/T state which has a lower affinity for oxygen, and so some oxygen becomes unbound from Hb.

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28
Q

3 Why is pulse oximetery not helpful for diagnosing carbon monoxide poisoning?

A

Pulse oximetery measures % saturation of haemoglobin which will be normal regardless of pO2 in blood due to CO binding to Hb.

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29
Q

3 Impairment of which body systems can cause central cyanosis?

A

Pulmonary
Cardiovascular
CNS

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30
Q

3 How does emphysema cause a diffusion defect?

A

Parenchymal destruction reduces surface area available for diffusion

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31
Q

3 Give 3 reasons why pulmonary oedema can cause hypoxia

A
  1. Reduced compliance of lung due to reduced available volume for expansion
  2. Increased diffusion distance between air in alveloli and blood in capillary due to presence of fluid
  3. Oedema in bronchioles will cause increased resistance to air flow due to reduction of lumen diameter
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32
Q

4 How does hyperventilation change blood pH?

A

Decrease / more acidic

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33
Q

4 Where are the central chemoreceptors located?

A

Medulla of the brain

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34
Q

4 What do the choroid plexus cells do if pCO2 is persistently high? And why?

A

Permit movement of HCO3- across blood-brain barrier, stabilising pH to maintain favourable environment for the neurons

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35
Q

1st yr Around what kPa of O2 does the % saturation of haemoglobin approach 100? What happens to the dissociation curve at this point?

A

8kPa, dissociation curve flattens out

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36
Q

4 What do central chemoreceptors detect?

A

pH of CSF which is determined by the pCO2

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37
Q

4 How long does it take for the kidneys to compensate for a respiratory acidosis or alkalosis? How does it do this?

A

2-3 days

Changing excretion rate of HCO3-

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38
Q

4 How can alkalosis lead to tenany?

A

Drops free calcium concentration, which enhances neuromuscular excitability by increasing the permeability of neuronal membranes to Na+.

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39
Q

4 How is CO2 transported in the blood?

A
  1. Dissolved CO2
  2. As HCO3- after reacting with water
  3. Carbamino compounds (bound to amine groups of globin of Hb)
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40
Q

4 How are organic acids produced at tissues buffered in the blood?

A

React with HCO3- (bicarbonate ions), producing CO2 which is removed by breathing.

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41
Q

4 Where does all the HCO3- in the blood come from?

A

CO2 + H20 H+ + HCO3- in RBCs
HCO3- is transported into plasma
(H+ reacts w/ Hb)

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42
Q

4 Which state of haemoglobin can bind more H+?

A

T / tense state (when less O2 bound)

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43
Q

5 How can alkalaemia cause parathesia and tetany?

A

Increased pH lowers concentration of free/ionised calcium as more is bound to proteins. This increases neural excitability by lowering the threshold for depolarisation, resulting in parathesia and/or tetany.

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44
Q

5 Why does acideamia risk cardiac arrhythmia?

A

Reciprocal cation shift of K+ for H+ causes hyperkalaemia, increasing excitability esp in cardiac muscle. This causes irregular excitations which result in the irregular contractions of arrhythmia.

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45
Q

5 At what pH does acideamia become life threatening?

A

Below 7.0

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46
Q

5 How can acidaemia affect hepatic function?

A

Liver enzymes denatured by low pH

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47
Q

5 How is the ventilation rate usually controlled?

A

Via impulses from chemoreceptors detecting pH of CSF which is determined by pCO2.

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48
Q

5 How does pCO2 determine pH?

A

pCO2 reacts with H2O to form H+ (and HCO3-). H+ concentration is proportional to pH (pH=log[H+]).

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49
Q

5 How do kidneys control pH?

A

Variable recovery of hydrogen carbonate (HCO3-) and active

secretion of hydrogen ions (H+)

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50
Q

5 Where does most of the HCO3- in blood plasma come from?

A

Reaction of CO2 and H2O within red blood cells (where binding of H+ to Hb limits increases in free [H+])

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51
Q

5 How is H+ in the urine buffered?

A
  1. Filtered phosphate

2. Ammonia produced from amino acid breakdown in proximal convoluted tubule

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52
Q

5 In what causes of metabolic acidosis would you expect the anion gap to be normal?

A

Renal causes eg renal tubular acidosis

Severe persistent diarrhoea (lost HCO3- replaced by Cl-)

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53
Q

5 What has happened to HCO3- if there is an increased anion gap?

A

HCO3- will have been replaced by another organic anion from an acid (as it binds with the H+ from the acid)

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54
Q

5 Concentrations of which ions are measured to calculate the anion gap?

A

Na+ K+ Cl- and HCO3-

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55
Q

5 How would you define a patient’s acid-base status if [HCO3-] and pCO2 are low, and pH and anion gap are relatively normal?

A

Compensated respiratory alkalosis (generally associated w/ respiratory disease or altitude exposure)

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56
Q

5 How would you define a patient’s acid-base status if pCO2 is high, [HCO3-] is raised and pH is relatively normal?

A

Compensated respiratory acidosis

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57
Q

5 Can metabolic alkalosis be compensated?

A

Generally no, can’t reduce breathing much as need to maintain pO2

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58
Q

5 How can diabetic ketoacidosis lead to hypokalaemia?

A

K+ moves out of cells due to acidosis and lack of insulin. These move into the blood are subsequently lost in urine due to osmotic diuresis caused by high glucose.
This effect is not very common unless insulin is given w/o K+ replacement!

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59
Q

6 What is the cause of the majority of pulmonary embolisms?

A

90% from a DVT

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60
Q

6 What defines a “high risk” PE patient?

A

Presence of shock or hypotension

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61
Q

6 How can PE cause respiratory failure?

A
  1. Areas of ventilation-perfusion mismatch

2. Low R ventricle output

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62
Q

6 Explain how a PE can cause pleuritis

A

Small distal emboli may create areas of alveolar haemorrhage causing inflammation in the local pleura

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63
Q

6 What is the most common symptom of a PE?

A

Dyspnoea / shortness of breath / SoB

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64
Q

6 Give 2 signs of PE you may elicit on examination

A
  1. Pleural rub (if there is pulmonary infarction)

2. Raised JVP

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65
Q

6 What are your 3 main differentials for PE symptoms?

A
  1. MI
  2. Pneumothorax
  3. Pneumonia / pleurisy
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66
Q

6 What’s the utility of a Chest Xray in PE?

A

Can help exclude differential diganoses

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67
Q

6 What test could you use to rule out PE in a patient with low clinical likelihood of having one?

A

D dimer

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68
Q

6 What is the main type of imaging you would use to diagnose a PE?

A

CT Pulmonary Angiography

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69
Q

6 What would be your immediate management of a patient with confirmed PE?

A

Heparin and supportive treatment including oxygen

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70
Q

6 What are the “classic” ECG signs of a PE?

A

S1 Q2 T3 (deep S wave in lead I, Q wave in III, inverted T wave in III …but this isn’t diagnostic and not actually seen that often)

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71
Q

6 Why should a patient be seated for spirometry?

A

Just in case they faint from the maximal forced expiration (which can result in reduced cardiac output & cerebral blood flow)

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72
Q

6 What are the 4 most common reasons for pulmonary function tests?

A

Monitor serial changes in chronic / progressive diseases
Monitor response to therapy
Assessment for compensation (related to occupational lung damage)
Pre-surgical assessment

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73
Q

6 State 2 divisions of lung volume which together = total lung capacity

A

Inspiratory capacity + functional residual capacity

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74
Q

6 What is “functional residual capacity” of lung volume?

A

Resting end expiratory level

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75
Q

6 Define FEV1

A

Volume of air exhaled in the 1st second of maximal expiration

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76
Q

6 How would you describe the classic expiratory curve on spirometry in a obstructive defect?

A

Scalloped or scooped

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77
Q

6 What do the results of an incomplete vital capacity manoeuvre on spirometry look like?

A

Restrictive disease

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78
Q

6 What 2 graphs can you get from spirometry? Give the labels of the axes

A

Volume-time plot:-
Y: vol (l)
X: time (s)

Flow-Volume loop:-
Y: flow rate (l/sec)
X: lung vol (l)

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79
Q

6 Describe a restrictive pattern of FVC & FEV1 findings

A

FVC reduced
FEV1 appropriate for FVC
Ratio between them normal or high (hyperinflation)

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80
Q

6 Where on spirometry would an extra-thoracic obstruction cause an abnormality?

A

Inspiration / inspiratory curve / bottom bit of flow volume loop

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81
Q

6 Give 3 causes of extrathoracic causes of pulmonary obstruction

A

Vocal cord dysfunction (eg recurrent laryngeal nerve palsy / damage)
Laryngeal polyp
Tracheal stenosis
wiki says..
“foreign body aspiration, blunt laryngotracheal trauma, penetrating laryngotracheal trauma, tonsillar hypertrophy, acute laryngotracheitis such as viral croup, bacterial tracheitis, epiglottitis, peritonsillar abscess, pertussis, retropharyngeal abscess, spasmodic croup”

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82
Q

7 Give 2 ways that pulmonary oedema can cause respiratory failure

A
  1. Fluid in interstitial space increases diffusion distance for gas exchange between capillaries and alveoli
  2. Fluid in alveoli results in less ventilation of the lung, leading to ventilation-perfusion mismatch
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83
Q

7 Whats the difference between type 1 and type 2 respiratory failure?

A

In both types pO2 is low however in type 1 pCO2 is normal or low while in type 2 it is high.

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84
Q

7 Where on the body would you see signs of central cyanosis?

A

Oral mucosa, tongue and lips

AND fingers and toes as will also have peripheral cyanosis

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85
Q

7 Define hypoxia

A

O2 deficiency at tissue level (can occur w/o hypoxaemia!)

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86
Q

7 What changes happen in the blood to compensate for chronic hypoxaemia?

A

Increased haemoglobin ie polycythemia

Increased 2,3BPG

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87
Q

7 Give 2 CNS effects of hypoxaemia

A

Confusion and irritability

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88
Q

7 How can hypoxaemia cause right heart failure?

A

Cor pulmonale: Hypoxic vasoconstriction of pulmonary vessels leads to pulmonary hypertension increasing workload on R side of heart, which eventually will fail

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89
Q

7 How can a pulmonary embolism cause AF?

A

Reduced perfusion to lung -> hypoxaemia which can cause cardiac arythmias incl AF

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90
Q

7 Give 2 extra-pulmonary causes of hypoxia

A

Low inspired pO2

Right to Left CVS shunt eg due to cyanotic congential heart disease

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91
Q

7 Why would hypercapnia give you a headache?

A

Causes cerebral vasodilation

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92
Q

7 Give 3 signs of hypercapnia that you could elicit in the hands and wrists

A
  1. Flapping tremor
  2. Bounding pulse
  3. Warm hands
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93
Q

7 Explain the pO2 and pCO2 seen in ventilation-perfusion mismatch

A

Less gas exchange between affected alveoli and pulmonary capillaries results in low pO2 and high pCO2 in the blood. This increases respiratory drive causing hyperventilation in unaffected alveoli, which is enough to compensate the pCO2 as CO2 diffuses more easily than O2. pCO2 will be normal and pO2 will be low.

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94
Q

7 Explain how diffuse lung fibrosis can cause type 1 or type 2 respiratory failure

A

Fibrous tissue in interstitial space increases diffusion distance which alone would cause type 1 failure as pCO2 can be compensated by hyperventilation as it is much more soluble.
If fibrosis is severe however, lung expansion will be affected causing hypoventilation, resulting in type 2 failure.

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95
Q

7 Give 4 causes of acute type 2 respiratory failure

A

Very severe asthma attack
Head injury
Cervical spine fracture
Opiate overdose

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96
Q

7 What is the most common cause of type 2 respiratory failure?

A

Late stage Chronic Obstructive Pulmonary Disease

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97
Q

7 Give 4 neuromuscular causes of type 2 respiratory failure

A

Myasthenia gravis
Guillain Barre syndrome
Myopathies
Motor Neurone Disease

98
Q

7 Why is it important to monitor pCO2 in a patient with type 2 respiratory failure while they are being treated with O2?

A

Can lose hypoxic respiratory drive which would worsen their hypercapnia

99
Q

7 What’s the target sat for a patient in type 2 resp failure?

A

88-92%

100
Q

8 What, other than smoking, can cause COPD? 3 things

A

Occupational exposure to irritants eg coal dust
Pollution
Alpha-1-antitrypsin deficiency

101
Q

8 What % of smokers will develop COPD?

A

~15%

102
Q

8 How is severity of breathlessness assessed?

A

MRC dyspnoea score:
Graded 1-5 based on level of activity needed for onset of breathlessness 1 being strenuous exercise, 5 being unable to leave house or breathless while dressing or undressing

103
Q

8 Explain why you may see a COPD patient “purselip” breathing

A

Protective manoeuvre that increases the pressure within

the airways. This causes a reduction or delay in the airway closure. Makes the next breath easier

104
Q

8 Give 3 signs seen in advanced COPD

A
  1. Cyanosis
  2. CO2 retention flap
  3. Signs of Cor pulmonale / R heart failure
105
Q

8 What would you need to do to diagnose COPD?

A

Take good history and examination
Spirometry
Chest X ray to exclude other causes

106
Q

8 What range of FEV1 and FEV1:FVC would you see in a COPD patient?

A

FEV1 <80% of predicted

ratio <70%

107
Q

8 What range of FEV1 would indicate severe airflow obstruction, according to NICE?

A

Severe obstruction = FEV1 <30% of predicted

108
Q

8 Is it common for a COPD patient to wake up at night with breathlessness and wheeze?

A

No, uncommon (common in asthma)

109
Q

8 What 4 types of drugs would you use to manage stable COPD?

A

Bronchodilators (incl. methylxathines)
Anti-muscarinics,
Steroids,
Mucolytics

110
Q

8 / 1st year Explain the mechansim by which salbutamol dilates the airways

A

Beta 2 agonist, activating adenyl cylase on binding to its receptor. ->
Increasing cAMP
and activating Protein Kinase -> phosphorylation of
downstream targets (Myosin light chain kinase - MLCK) ->
relaxation of smooth muscle in airway → bronchodilation

111
Q

8 How can salbutamol affect the heart?

A

Can cause palpatations and/or tachycardia by stimulating atrial beta 2 receptors

112
Q

8 What serum electrolyte abnormality can beta 2 agonists cause and why?

A

Hypokalaemia due to increased skeletal muscle uptake of K+

113
Q

8 Give 4 side effects of salbutamol that a patient might notice

A

Increased heart rate
Tremor
Anxiety
Palpitations

114
Q

8 What are the 3 modes of action of methylaxanthines (eg Theophylline / Aminophylline) ?

A

Bronchodilatation
Increase respiratory drive
Anti-inflammatory effects

115
Q

8 How do Methylxanthines cause an increase in cAMP?

A

Inhibition of phosphodiesterases which break down cAMP

116
Q

8 What kind of dose of corticosteroids is likey to cause side effects?

A

Long term
AND
oral dose or >800mcg inhaled dose a day

117
Q

8 What is the danger if someone stops taking their steroids without medical guidance?

A

Adrenal insufficiency which could push them into an adrenal / Addisonian crisis, a life-threatening condition

118
Q

8 What are the signs and symptoms of an adrenal crisis?

A 
Malaise.
Fatigue.
Nausea or vomiting.
Abdominal pain.
Low-grade fever.
Muscle pains and cramps.
Then dehydration -> hypotension &amp; hypovolaemic shock.
\+/- confusion, loss of consciousness &amp; coma
119
Q

8 What are the requirements for long term O2 therapy (assuming there is clinical need)?

A

Non-smokers
Non CO2 retainers
Can use for 16+ hrs/day
Home passes fire safety assessment

120
Q

8 What 4 interventions improve mortality outcomes for COPD patients?

A

Smoking cessation
Long term O2
Lung volume reduction
Lung transplant

121
Q

8 What % saturation are you aiming for in management of an acute exacerbation of COPD?

A

88-92%

122
Q

8 What 3 things would you want to give a patient with an acute exacerbation of COPD with no infective features?

A

Controlled O2
Nebulised bronchodilators
Steroids (oral, sometimes IV)

123
Q

8 What interventions should you consider (ie not all patients need them) in acute exacerbations of COPD?

A

Antibiotics (if raised CRP or WCC, purulent sputum)
IV steroids
IV aminophilline / bronchodilators
ITU admission (if severe or not improving)
Non-invasive ventilation

124
Q

8 Define asthma

A

Asthma is a heterogeneous disease, usually characterized
by chronic airway inflammation.
It is defined by the history of respiratory symptoms (such as
wheeze, shortness of breath, chest tightness and cough)
that vary over time and in intensity, together with variable
expiratory airflow limitation.

125
Q

8 How is airflow restricted in asthma?

A

Airway / mucosal oedema
Mucus hypersecretion / plugging
Bronchoconstriction
Smooth muscle hyperplasia

126
Q

8 What are the 2 main types of inflammatory cells you might expect to see in asthma?

A

Eosinophils or neutrophils

127
Q

8 What factors of a patient’s respiratory symptoms would be suggestive of asthma?

A

> 1 type
Worse at night / early a.m.
Variation over time and in intensity
Identifiable triggers to symptoms eg viral infections, exercise, allergens, irritants

128
Q

8 What is/are the most likely finding/s on examination of a patient with asthma?

A

Normal findings or wheezing on auscultation esp on forced expiration

129
Q

8 What 2 investigation findings would confirm excessive variability of lung function in a suspected asthmatic asthma?

A

Excessive bronchodilator reversibility of airflow limitation

Excessive diurnal variability of peak flow

130
Q

8 What are the 4 main symptoms of asthma?

A

Expiratory wheeze
Cough
Dyspnoea
Chest tightness

131
Q

8 What are the 3 key questions to ask to assess asthma control?

A
  1. have you had difficulty sleeping because of your
    asthma symptoms (including cough)?
  2. have you had your usual asthma symptoms during the
    day (cough, wheeze, chest tightness or
    breathlessness)?
  3. has your asthma interfered with your usual activities
    (e.g. housework, work/school etc.)?
132
Q

8 Give 7 clinical signs of life-threatening asthma

A 
Altered consiousness / GCS
Exhaustion
Arrhythmia
Hypotension
Cyanosis
Silent chest 
Poor respiratory effort
133
Q

8 Below what O2 saturation % would you consider an asthma attack to be life threatening?

A

<92%

134
Q

8 Which 2 categories of medicines shouldn’t be used by asthmatics?

A

NSAIDs

Beta-blockers

135
Q

8 What would give to treat an acute moderate asthma attack?

A

High flow oxygen
Nebulised salbutamol
Oral prednisolone (40mg 10-14 day course)

136
Q

8 What O2 sats would you aim for when treating an asthma attack?

A

94-98%

137
Q

8 What drugs can you administer when an asthma attack doesn’t improve after initial treatment?

A

Nebulised ipratropium bromide
IV magnesium
IV aminophylline

138
Q

8 What are the 3 main signs of an acute severe asthma attack?

A

Heart rate > 110
Resp rate > 25
Inability to complete sentences in 1 breath

139
Q

8 If an asthma attack is “acute severe” what will the peak expiratory flow be?

A

33-50% of best or predicted

140
Q

8 What is bronchiectasis?

A

Chronic dilatation of one or more

bronchi with poor mucus clearance.

141
Q

8 What are the 2 most common symptoms of bronchietasis?

A

Chronic cough

Daily sputum production

142
Q

What are the most common causes of haemoptysis (in primary care)?

A

Acute and chronic bronchitis, Tuberculosis,

Lung cancer, Pneumonia, and Bronchiectasis.

143
Q

8 What are the 3 main categories of causes of bronchietasis?

A

Post-infective
Immune deficiency
Mucocilary clearence defects

144
Q

8 What is the most common type of primary immunodeficiency?

A

Hypogammaglobinaemia

145
Q

8 What are the 3 most common pathogens implicated in bronchietasis?

A

Haemophilus influenzae, Pseudomonas spp, and Streptococcus pneumoniae

146
Q

8 Describe the genetic defect that causes cystic fibrosis

A

Defect in long arm of BOTH (as recessive condition) copies of Chromosome 7 leads to mutation in Cystic Fibrosis Transmembrane conductance Regulator

147
Q

8 How does the CF defect cause thick dehydrated body fluids in the lungs, pancreas, GIT, joints and bones, liver and bilary tree, male reproductive tract and heart?

A

These organs have CFTR which is mutated in CF causing ineffective cell surface chloride ion transport

148
Q

8 What investigations are needed to diagnose Cystic fibrosis?

A

Sweat test

Genotyping - may need extended genotyping

149
Q

8 When did we start screening newborns for cystic fibrosis?

A

2006

150
Q

8 How can cystic fibrosis cause intestinal malabsorption

A

Severe deficiency of

pancreatic enzymes due to inadequate flow in pancreas / bile

151
Q

8 What is the most common complication of cystic fibrosis?

A

Chronic respiratory infection

152
Q

8 What are CF patients advised to avoid?

A 
Smoking
Other CF patients
Contacts with colds etc
Jacuzzis
Stables, compost &amp; rotting veg
153
Q

8 How, in principle, is cystic fibrosis managed?

A

MDTs often in CF specialist centres w/ holistic focus aiming to maintain lung health and nutritional state

154
Q

9 What is the most common cause of atypical pneumonia?

A

Mycoplasma pneumoniae

155
Q

9 What is atypical pneumonia?

A

Lung infection by pathogens lacking a cell wall

156
Q

9 What is the most common cause of community acquired pneumonia?

A

Streptococcus pneumoniae (these are gram pos cocci)

157
Q

9 What type/s of antibiotics do you need to treat community acquired pneumonia?

A

Agents that work on protein synthesis i.e.
Macrolides eg clarithomycin and erythromycin
Tetracyclines eg doxycycline

158
Q

9 What defines a hospital acquired pneumonia?

A

Occurs >48 hours after admission and was not incubating at time of admission

159
Q

9 What is pneumonia?

A

Infection in lung alveoli leading to inflammation

160
Q

9 What are the main 5 organisms causing community acquired pneumonia?

A 
Streptococcus pneumoniae
Haemophilus influenzae
Moraxella catarrhalis
Staphylococcus aureus
Klebsiella pneumoniae
161
Q

9 What are the common systemic symptoms of pneumonia?

A

Fever
Rigors
Malaise
Nausea and vomiting

162
Q

9 Why might you get sharp chest pain that is worse on breathing if you have pneumnoia?

A

This is pleuritic chest pain/pleurisy, caused by inflammation of pleura due to infection

163
Q

9 Give 5 causes of hospital acquired pneumonia

A 
Staphylococcus aureus and MRSA 
Enterobacteriaciae
Pseudomonas spp
Haemophilus influenzae
Acinetobacter baumanii
164
Q

9 Give 4 types of patients who are at risk of aspiration pneumonia

A

Stroke patients (with neurological dysphagia)
Epileptics
Alcoholics and drug addicts
Drowning victims

165
Q

9 What antibiotic do you use to treat aspiration pneumonia? UHL

A

Co-amoxiclav

166
Q

9 Give 4 localising signs of pneumonia

A

Dullness to percussion
Tactile vocal fremitus
Bronchial breathing
Crackles

167
Q

9 When would you take nose and throat swabs when investigating pneumonia?

A

If you suspect viral cause (10% cases)

168
Q

9 How would you decide whether to admit someone with pneumonia to hospital?

A

Assess their CURB-65 score, if 2 or more admit (manage as severe if 2-5)

169
Q

9 What are the criteria of the CURB65 score?

A 
Confusion
Urea >7 mmol/l
Respiratory Rate >30
Blood Pressure <90 systolic <60 diastolic
>65 years old
170
Q

9 In UHL (2017) what antibiotics would you use for mild-moderate community acquired pneumonia?

A

Amoxicillin
– Or doxycycline or erythromycin /
clarithromycin if penicillin allergy

171
Q

9 What complications of pneumonia can arise in the lung? Give 3

A

Lung abscess
Bronchiectasis
Empyema

172
Q

9 Why do penicillins not work on atypical pneumonia?

A

Penicillins act on cell wall which atypicals don’t have

173
Q

9 What does viral pneumonia look like on chest X-ray?

A

Patchy or diffuse ground glass opacity

174
Q

9 Why is it better to culture a sample from bronchial lavage instead of sputum in hospital acquired pneumonia?

A

Bronchial lavage desirable to differentiate upper respiratory from lower respiratory flora

175
Q

9 What’s the 1st line treatment for hospital-acquired

pneumonia in UHL?

A

Co-amoxiclav
(Second line/ITU: Pipperacilin /
tazobactam Or Meropenem)

176
Q

9 What type of organism is the likely cause of lower respiratory tract infection in neutropenic patients?

A

Fungi e.g. Aspergillus spp

177
Q

9 What type of patients get pneumocystis pneumonia (PCP)?

A

Those with weakened immune system eg HIV, cancer, immunosuppressed

178
Q

9 What medicial interventions can help prevent pneumonia in high risk patients?

A

Annual flu vaccine Pneumococcal vaccine (every 5 years)
Chemoprophylaxis (oral pencillin / erythromycin)
Smoking cessation advice

179
Q

9 What is the most likely outcome of acute bacterial pneumonia?

A

Resolution with organisation / fibrous scarring

180
Q

9 Why are lungs with pneumonia less compliant?

A

Acute inflammatory
response to infection:
Exudation of fibrin-rich fluid
Neutrophil and macrophage infiltration

181
Q

9 What are the 4 histopathological stages of pneumonia?

A

Congestion
Red hepatisation (fibrinous alveolitis)
Grey hepatisation (leukocytic alveolitis)
Resolution

182
Q

9 When would you expect to see signs of resolution on histology of pneumonia?

A

7-8 days

183
Q

9 What 4 groups are at most at risk of tubercluosis?

A

Immunocompromised eg HIV
Non-UK born
Homeless
Those with friends and family who have been diagnosed with TB

184
Q

9 What is the primary complex of TB?

A

Ghon’s focus and draining lymph nodes

185
Q

9 Give 7 possible risk factors for reactivation of a latent TB infection

A 
HIV
Immunosuppressive therapy
Corticosteroids
Silicosis
Diabetes
Severe kidney disease
Substance abuse
186
Q

9 What % of latent TB infections heal or self cure?

A

95%

187
Q

9 Does a positive tuberculin skin test or IFN gamma test mean the patient is infectious?

A

No, could be latent infection (non infectious and not classed a case of TB)

188
Q

9 Describe the process of the formation of a Ghon’s focus in TB

A

Infectious droplets inhaled and engulfed by alveolar macrophages. Other lymphocytes are recruited and bacilli are isolated within a tubercle. Wall of tubercule consists of epitheliod lymphocytes and Langhan’s giant cells. Caseous necosis then develops in the centre.

189
Q

9 How likely is it that infection with tuberculosis will lead to active primary disease?

A

Not very (only 5% do, more likely if high infectious dose, virulent strain and/or weak host response)

190
Q

9 In what groups is extra-pulmonary TB more common (than pulmonary)?

A

HIV + or otherwise immunocompromised

Young kids

191
Q

9 What are the systemic signs of pulmonary TB?

A

Fever, Night sweats, Weight loss, Anorexia

Fatigue, Malaise

192
Q

9 What is the main cause of breathlessness in pulmonary TB?

A

Pleural effusion due to pleural involvement

193
Q

9 What is the most common symptom of pulmonary TB?

A

Cough

194
Q

9 Why does post primary (reactivated) TB tend to cause more signs and symptoms?

A

Immune system hyper sensitised to bacilli resulting in massive destruction of the lung

195
Q

9 What is the risk of re-exposure to TB in a patient that has had latent TB that has healed?

A

Re-infection likely to cause post primary TB which is more severe than primary TB

196
Q

9 What investigations are needed for suspected pulmonary TB?

A

Chest X Ray
Sputum sampling for culture
(3 early morning samples minimum volume 5ml / Induced Sputum or Bronchoscopy if needed )
HIV test

197
Q

9 What are the signs of TB on a chest xray?

A

Ill defined patchy consolidation often with cavitation (often in apicies)
+/- pleural effusion white out
+/- fibrosis

198
Q

9 Why do normal stains not work on TB?

A

Cell wall is acid and alcohol fast (due to composition of long chain fatty acids, complex waxes and glycolipids)

199
Q

9 What stain is used for TB?

A

Ziehl Neeson

200
Q

9 Suggest why upper lobes of lung are more often affected by TB than lower lobes?

A

TB is obligate aerobe, more air in apexes of lung

201
Q

9 What is the 1st line treatment for TB?

A 
4 drugs:
Rifampicin
Isoniazid
Pyrazinamide
Ethambutol
All for 6 months then just the 1st 2 for another 6 months
202
Q

9 Why would being treated for TB make your sweat change colour?

A

Rifampicin causes bodily secretions to go red-orange

203
Q

9 What are the respiratory symptoms like in miliary TB?

A

Often few, dry cough most common

204
Q

9 What is Pott’s disease?

A

TB infection in spine (most common form of extra-pulmonary TB)

205
Q

12 Give 4 risk factors for lung cancer, other than smoking!

A

Asbestos exposure
Radon
Occupational heavy metal exposure
Genetic factors

206
Q

12 List 7 common symptoms caused by a primary lung tumour

A 
Cough +/- blood
Wheeze
Shortness of breath / dyspnoea
Recurring or unresolving lung infections
Chest and shoulder pain
Lethargy &amp; malaise
Weight loss
207
Q

12 How can lung cancer cause a bloated face?

A

Tumours may compress superior vena cava, impeding venous drainage of the face causing oedema

208
Q

12 Give 5 ways in which lung cancer can cause shortness of breath

A 
Directly via obstruction of airflow by tumours
Or may cause:
Pleural effusion
Pericardial effusion
Aneamia
Lung infections
209
Q

12 What 3 symptoms would suggest the presence of a tumour in the apex of the lung

A

(Horner’s syndrome:)
Unilaterial ptosis, mydriasis and anhydriasis
( one sided drooping eyelid, blown pupil, no sweat)

210
Q

12 How can lung cancer cause a patient’s voice to become hoarse?

A

Compression of L laryngeal nerve which passes near the hilum of L lung causing unilateral paralysis of vocal cords

211
Q

12 Give 3 paraneoplastic syndromes caused by lung cancer that affect the endocrine system

A

Cushing’s
SIADH
Hypercalceamia

212
Q

12 What is the most common cause of finger clubbing?

A 
Lung cancer 
(Congenital heart defects and chronic lung infections can also cause it)
213
Q

12 Why might you get seizures in lung cancer?

A

Small cell lung cancer can cause SIADH which can lead to hyponatreamia, causing seizures

214
Q

12 What signs of lung cancer may be elicited from examination of the chest?

A

Signs of consolidation - including crackles and dullness to percussion
Signs of pleural effusion - stony dull to percussion
Muffled heart sounds
Hepatomegaly
Cachexia
May see skin metastases

215
Q

12 What signs do most lung cancer patients have?

A

None!

216
Q

12 What is the most common type of lung cancer in people who have never smoked?

A

Adenocarcinoma

217
Q

12 Which is the most aggressive type of lung cancer?

A

Small cell lung cancer

218
Q

12 Which 2 types of lung cancer are usually caused by smoking?

A

Small cell and squamous

219
Q

12 Which 4 locations (outside cardio-resp system) does lung cancer tend to spread to?

A

Brain, liver, adrenals and bone

220
Q

12 What are the 2 main imaging techniques used in lung cancer?

A

Chest X rays

Staging chest CTs

221
Q

12 What should all patients potentially suitable for treatment with curative intent be offered first and why?

A

CT-PET and/or MRI to look for metastases

222
Q

12 What is the “performance status” of a cancer patient?

A

An attempt to quantify their general well-being and ability to perform activities of daily life.
(Zubrob / ECOG scale:
0 no symptoms
1 symptoms but no limitation on daily activities
2 limited to bed / chair <50% day
3 limited to bed / chair >50% day
4 bedridden)

223
Q

12 Give 5 palliative treatments for lung cancer that can directly improve or control symptoms

A 
Analgesia
Nutritional support
Airway stents
Radiotherapy
Anxiolytics
224
Q

12 What are the 4 main factors in deciding the management of a patient with lung cancer?

A

TMN staging
Performance status
Co-morbidities
Patient’s wishes

225
Q

12 Is chemotherapy likely to cure a lung cancer?

A

No, sometimes does in small cell however will control tumour growth

226
Q

12 What treatment for lung cancer has the best chance of cure? and why do all patients not recieve this?

A

Surgery, patient may have distant metastases (very common in small cell), may not be fit for or decide against surgery

227
Q

12 What are neo-adjuvant and adjuvant chemotherapies?

A

Where chemotherapy is given alongside other therapies to boost efficacy
Neo-adjuvant - chemo given before surgery to shrink tumour & treat micromets
Adjuvent - chemo given after to reduce risk of recurrence

228
Q

12 Give 4 local sites of lung cancer metastases

A

Contra- or ipsi-lateral lung
Draining lymph nodes
Pleura
Pericardium

229
Q

11 A break in which layer of the pleura is the most common cause of pneumothorax?

A

Visceral (air enters pleural cavity from lungs)

230
Q

11 What 3 risk factors are associated with primary pneumothorax?

A

Smoking
Young thin and male
Connective tissue disorders eg Marfan’s

231
Q

1st year A patient with Marfan’s syndrome has come to you for family planning advice. They ask, what is the risk of their children having the condition?

A

50% If their partner is healthy, 100% if partner has Marfan’s (autosomal dominant)

232
Q

11 What does a pneumothorax look like on chest Xray?

A

Black-out, no lung markings

Tracheal / mediastinal shift if tension pneumothorax

233
Q

11 What are 3 common risk factors for empyema?

A

Pre-existing pulmonary disease
Alcoholism
Drug use

234
Q

11 What is a pleural effusion?

A

Accumulation of fluid within pleural space

235
Q

11 What does a pleural effusion look like X ray?

A

White out

236
Q

11 Is a pleural effusion more likely to be transudate or exudate if it is bilateral?

A

Transudate

237
Q

11 What are the most likely types of causes of an exudate within the pleura?

A

Infective
Malignant
Inflammatory
Infarction eg Secondary to Pulmonary Embolism

238
Q

11 Why do you remove chest drain at end of expriation?

A

Lower intra-pulmonary pressure

239
Q

11 What’s a “swinging” chest drain?

A

Fluid level in tube rising and falling with breathing

240
Q

11 How do you treat a tension pneumothorax?

A

Venflon in 2nd intercostal space mid clavicular line, just above 3rd rib (t

241
Q

11 Why do you put a chest drain in just above a rib / inferior in intercostal space?

A

To avoid neurovascular bundle which passes along inferior edge of each rib

242
Q

11 What’s a chylothorax?

A

Lymph in pleural space

Yr 2.0 Sem 3 (5 decks)

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