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Year 2 > Case 5 > Flashcards

Case 5 Flashcards

1
Q

Compensating organ response to increased pCO2 as a result of hypoventilation in COPD

A

Kidney retains HCO3- (slow response - hours/days)

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2
Q

Compensating organ response to decreased pCO2 as a result of a panic attack (hyperventilation)

A

Kidneys decrease retention of HCO3- in the tubules.

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3
Q

Compensating organ response to decreased HCO3- and increased CO2 in metabolic acidosis (e.g. DKA)

A

Hyperventilation by lungs, to drive off CO2

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4
Q

Compensating organ response to metabolic acidosis due to severe vomiting

A

Hypoventilation to reduce loss of CO2

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5
Q

Inspiration

A 
Contraction of diaphragm and external intercostal muscles.
Increased volume of thorax 
Decreased intrapleural pressure 
Draws air into lungs
Decreased pressure in alveoli 
Therefore, expansion of alveoli
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6
Q

Expiration

A 
Relaxation of diaphragm and external intercostal muscles 
Decreased volume of thorax 
Increased intrapleural pressure 
Forces air out of lungs 
Increased pressure in alveoli
Therefore, recoil of alveoli
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7
Q

Compliance

A

Ease at which the chest volume can be changed

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8
Q

Elastic recoil

A

Ability of the lungs to recover their original shape after stretching

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9
Q

What is the function of lung surfactant?

A

Since alveoli have a small radius and moist walls, surface tension can be generated causing walls to collapse.
Lung surfactant forms a fluid layer that lines the alveoli, decreasing surface tension and preventing collapse of alveoli. Therefore, increased compliance of lungs.

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10
Q

Lung surfactant is secreted by…

A

Type II epithelial cells

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11
Q

Factors which affect lung compliance

A

Elasticity of lung tissue (e.g. pulmonary fibrosis decreases compliance)
Obesity (reduces contraction of diaphragm)
Pulmonary blood flow
Bronchial smooth muscle tone
Changes in bone structure around lungs (e.g. rub fracture)

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12
Q

Maximum airway resistance in the respiratory tract

A

Segmental bronchi - airflow is high but cross sectional area is low

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13
Q

Factors affecting airway resistance

A

Radius of airway
Flow pattern - laminar or turbulent (mucus will cause turbulent flow)
Obstruction (e.g. tumor, inhaled particle)
Viscosity and density of gas mixture

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14
Q

FEV1

A

Volume of air forcefully exhaled in 1 second

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15
Q

FVC

A

Volume of air that can be maximally forcefully exhaled

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16
Q

Silicosis

A

Caused by inhalation of silicon dioxide.
Toxic to macrophages
Readily initiates fibrosis (may also have some streaks of calcification around hilar lymph nodes)

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17
Q

Asbestosis

A

Fibrosis caused by asbestos

Other symptoms: clubbing, inspiratory crackles

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18
Q

Mesothelioma of the lung

A

Commonly presents as pleural effusion with chest wall pain

Also caused by asbestos

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19
Q

Pneumoconiosis

A

Dust particles retained in small airways and alveoli. Common in coal workers. Has an immediate fibrogenic effect.

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20
Q

Pulmonary fibrosis on an X-ray

A

Reticular (net-like) shadowing of lung peripheries, typically more prominent towards lung bases.
Contours of the heart less distinct (‘shaggy’)

Later becomes more widespread, leading to lung volume loss.

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21
Q

Production of mucus in the lungs…

A

Goblet cells in epithelium of respiratory tract

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22
Q

Function of mucus in the lungs

A

Trap inhaled particles, preventing them from entering the lungs. Combination of mucus and inhaled particles can be swallowed.

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23
Q

Area of greatest ventilation in the lungs

A

Apex - since intrapleural pressure is greater here.

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24
Q

Area of greatest perfusion in the lungs

A

Base - since blood pressure is greatest here.

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25
Q

Bohr Shift

A 
Increased unloading of oxygen in response to:
Increased pCO2
Increased [H+]
Increased temperature 
Increased 2-3 BPG

Occurs at metabolising cells to supply them with oxygen.

Oxygen dissociation curve shifted to the right.

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26
Q

Hypoventilation

A

Ventilation does not meet metabolic demand.

Occurs in diseases which increase physiological dead space and in paralysis of respiratory muscles

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27
Q

Hyperventilation

A

Ventilation in excess of metabolic needs OR CO2 exhaled at a greater rate than production.
Occurs during acute asthma attacks, under stress and at high altitude.

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28
Q

Functions of conducting portion of respiratory tract

A

Humidify - by serous and mucous secretions
Warmed - by underlying blood vessels
Filtered - i.e. particles become trapped in mucous to be swallowed

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29
Q

Structures which make up the conducting portion of respiratory tract

A 
Nasal cavities
Nasopharynx 
Larynx 
Trachea 
Bronchi 
Bronchioles
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30
Q

Function of respiratory portion of respiratory tract

A

Interface for passive exchange of gases between the atmosphere and blood

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31
Q

Structures which make up the respiratory portion of the respiratory tract

A

Respiratory bronchioles
Alveolar ducts
Alveolar sacs
Alveoli

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32
Q

Epithelium found in respiratory portion of tract

A

Ciliated cuboidal epithelium, containing some secretory cells called CLARA cells

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33
Q

Type I pneumocytes

A

Large flattened cells (thin barrier to gaseous exchange)
95% of total alveolar area
Connected to each other by tight junctions.
Involved in gaseous exchange

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34
Q

Type II pneumocytes

A

5% of total area
60% of total number of cells (very small)
Secrete lung surfactant to reduce surface tension
Connected to epithelium and other cells by tight junctions.
Foamy cytoplasm due to lamella bodies (GAGs, proteins, phospholipids)

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35
Q

Composition of lung surfactant

A

80% Phospholipids (inc DPCC)
10% Neutrolipids (mostly cholesterol)
10% Surfactant proteins

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36
Q

Left lung lies in close proximity to…

A

Heart
Arch of aorta
Thoracic aorta
Oesophagus

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37
Q

Right lung lies in close proximity to…

A

Heart
Oesophagus
IVC and SVC
Azygous vein

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38
Q

Lobes of the left lung…

A

Superior and inferior

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39
Q

Lobes of the right lung

A

Superior, middle and inferior

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40
Q

Outer surfaces of lungs:

A

Mediastinal (between the two lungs)
Cervical (upper, lateral)
Costal (lower, lateral) - smooth, convex and separated from ribs by costal pleura
Diaphragmatic

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41
Q

Blood supply to the lung parenchyma

A

Deoxygenated blood enters via 2 pulmonary arteries.

Oxygenated blood leaves via 4 pulmonary veins.

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42
Q

Blood supply to bronchi

A

Bronchial arteries arise from descending aorta .

Venous drainage via bronchial veins into azygous (right) and hemiazygous (left) veins

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43
Q

Sympathetic innervaton of lungs

A

Derived from sympathetic trunk.

Stimulates relaxation of bronchial smooth muscle and vasoconstriction of pulmonary vessels.

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44
Q

Parasympathetic innervation of lungs

A

Supplied by vagus nerve.

Stimulates secretion from bronchial glands, contraction of bronchial smooth muscle and vasodilation of pulmonary vessels.

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45
Q

Visceral afferents of lungs

A

Conduct pain impulses to sensory ganglion of vagus nerve.

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46
Q

What is a pulmonary embolism?

A

Obstruction of pulmonary artery by a substance travelled from elsewhere in the body.
Most commonly thrombus.
Can be fat (following bone fracture/orthopod surgery) or air (following cannulation in the neck).

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47
Q

Clinical features of Pulmonary Embolism

A

Dyspnoea
Chesty cough
Haemoptysis
Tachypnoea

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48
Q

Well’s Score

A

Calculates risk of DVT/PE

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49
Q

Treatment of Pulmonary Embolism

A

Anticoagulation and thrombolytic therapy (decrease size of embolism)

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50
Q

What are pleura?

A

Serous membrane enfolding both lungs. Reflected upon the walls of the thorax and diaphragm.
Visceral - covers lungs, extending into interlobular fissures.
Parietal - covers internal surface of thoracic cavity (mediastinal, cervical, costal and diaphragmatic)

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51
Q

Pleural Cavity

A

Space between parietal and visceral pleura.
Contains serous fluid which lubricates surfaces of pleurae and generates surface tension (so that when thorax expands, the lungs also expand).

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52
Q

Pleural recesses

A

Where opposing surfaces of parietal pleura meet.

Costomediastinal and costodiaphragmatic

Of clinical importance since they provide a location for fluid collection.

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53
Q

How does nervous supply differ between parietal and visceral pleura?

A

Parietal - innervated by phrenic and intercostal nerves. Sensitive to pain, temp and pressure. Produces a well localised pain.

Visceral - autonomic innervation from vagus nerve and sympathetic trunk only. Sensitive only to stretch.

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54
Q

Blood supply to parietal pleura

A

Intercostal arteries

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55
Q

Blood supply to visceral pleura

A

Internal thoracic arteries (bronchial circulation which also supplies lung parenchyma)

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56
Q

What is a Pneumothorax?

A

When air or gas is present within pleural space.

Can be spontaneous (w/ or w/o underlying respiratory disease) or traumatic

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57
Q

Clinical features of pneumothorax

A

Chest pain
Shortness of breath
Asymmetrical chest expansion
Hyperresonance on affected side due to excess air.

58
Q

Normal response to allergens in the lungs

A

Driven by Th2 lymphocytes.

Facilitate IgE synthesis (via IL4) and eosinophilic inflammation (via IL-5)

59
Q

Why can exercise cause coughing?

A

When out of breath, people often start to breath in through their mouth - breathing in cold, dry, unconditioned air. Results in bronchospasm.

60
Q

Trachealis muscle

A

Smooth muscle that bridges the gap between the free ends of C-shaped cartilages at the posterior border of the trachea.
Contracts to constrict trachea, allowing air to be expelled with more force e.g. during coughing.

61
Q

Structure of large central airways

A

Pseudostratified epithelium

Surrounded by mucous secreting and serous (water secreting) cells

Surrounded by C-shaped cartilagenous ring, joined at each end by trachealis muscle.

62
Q

How does structure of tertiary bronchus differ from large central airways?

A

Contains columnar epithelium rather than pseudostratified.
Contains less cartilage and its cartilage is discontinuous.
More collapsible, easier to change diameter.

63
Q

How does structure of bronchioles differ from tertiary bronchus?

A

No cartilage
More smooth muscle
Clara cells

64
Q

Clara cells

A

Club cells/Bronchiolar exocrine cells
Dome shaped with short microvilli
Protect bronchiolar epithelium - secrete uteroglobulin and detoxify harmful substances (protect against oxidative pollution)
Also act as a stem cell, multiplying and differentiating into ciliated cells to regenerate bronchiolar epithelium.

65
Q

Mucus secretion into the bronchioles

A

Vagal nerve ending releases ACh (parasypathetic)
ACh binds to M3 receptor on serous cells.
Cl- secreted into lumen of submucosal gland. Promotes secretion of fluid into lumen.

66
Q

Effect of parasympathetic activation on the lungs

A

Fight and prevent infection

Bronchoconstriction
Vasodilation (ready to mobilise neutrophils during infection)
Mucus gland and goblet cell secretion

67
Q

Effect of sympathetic activation on the lungs

A

Fight or flight response

Bronchodilation
Vasoconstriction
Modulate cholinergic transmission.

68
Q

Cough Reflex

A

Defensive reflex within respiratory tract.
Forced expulsive manouvre usually against a closed epiglottis which aims to actively repel irritant or foreign body from lungs e.g. sputum

69
Q

Expiratory reflex

A

Strong expiration without a preceding in-draw of breath.

Aims to prevent aspiration into lungs.

70
Q

C fibres in the lungs

A

Arise from Jugular neurons
Thin, unmyelinated (slow, <2m/s)
Contain neuropeptides: Substance P, CGRP and neurokinin A

Also contain tachykinin.

71
Q

How does activation of C-fibres generate a proinflammatory environment?

A

C fibres release substance P, CGRP and neurokinin A.

These neuropeptides act on neurokinin 1, 2 or 3

Activation of NK1 = mucus hypersecretion and airway smooth muscle contraction.

Activation of NK1 = extremely potent bronchoconstriction

72
Q

Definition of chronic cough

A

Duration >8wks

73
Q

Definition of acute cough

A

Sudden onset

Duration up to 3 weeks

74
Q

Definition of sub-acute cough

A

3-8weeks duration

75
Q

Emphysema

A

Abnormal and permanent dilatation of alveoli with destruction of walls

76
Q

Pathophysiology of emphysema

A

Degradation of elastin due to:
Hyperinflation of alveoli
Destruction of alveolar and capillary walls

Therefore, loss of elastic recoil and collapse of small airways.

77
Q

Chronic bronchitis

A

Inflammation of bronchi and bronchioles

78
Q

Pathphysiology of chronic bronchitis

A

Hypertrophy of mucosal glands and increased number of goblet cells causing mucus hypersecretion.

Mucociliary escalator dysfunction - mucus is not removed from lumen causing an obstruction.

Thickening of bronchial wall due to inflammation also causes narrowing - therefore further obstruction.

79
Q

Causes of COPD

A

Smoking (only occurs in 30% of smokers)
Genetic factors (alpha-trypsin deficiency causes emphysema)
Occupational (silica, coal dust)
Biomass fuel emission
Nutrition - diet low in antioxidant vitamins
Low birth weight
Maternal smoking

80
Q

Clinical features on examination of a patient with COPD

A 
Hyperinflated chest (air trapping)
Breathing quickly
Using accessory muscles of respiration 
Cachectic 
Reduced breathing sounds/wheezing
81
Q

Symptoms of COPD

A 
Progressive dyspnoea 
Reduced exercise tolerance 
Productive cough
Wheeze
Winter exacerbation 
Fatigue
Weight loss/loss of appetite
Oedema
82
Q

Conditions associated with COPD

A 
Osteoporosis (stimulation of osteoclasts by inflammatory cytokines)
Type II diabetes 
Peptic ulcers 
CVD (25% chance)
Renal Failure
Lung cancer 
Reduced wound healing
83
Q

CXR of COPD

A

Flattening of diaphragm (extreme case - floating heart sign)
Difficult to see ribs - osteopenic due to long term steroid use
Bullous Emphysema - upper zones contain areas of low density (black) with thinning of pulmonary vessels
May have consolidation due to infection.

84
Q

FEV1/FVC ratio > 0.7

A

Normal or restrictive (if both values are low)

85
Q

FEV1/FVC ratio < 0.7

A

Obstructive e.g. Emphysema

86
Q

How does alpha 1 antitrypsin deficiency cause emphysema?

A

Alpha 1 antitrypsin inhibits elastase which breaks down elastin.

When A1A is deficient, elastase breaks down more elastin in the lungs causing loss of elasticity.

87
Q

Physical mechanisms of lung defence

A

Humidification

Particle expulsion - cough or sneeze

88
Q

Pathophysiology of bronchiectasis

A

External insult (infectious or toxic) causing bronchial wall inflammation or destruction.
Ciliary dyskinesia +/- altered bronchiodynamics (smooth muscle cannot expand/contract as easily.
Ineffective mucus clearance due to loss of cilia.
Bacteria in mucus are able to colonise airway - results in chronic or recurrent infection.

89
Q

Cause of bronchiectasis

A 
Any lung damage:
Pneumonia 
Large PE
Immune deficiency
RA
Inhalation of foreign body
Alpha 1 antitrypsin deficiency
Allergic Bronchopulmonary Aspergillosis 
Idiopathic (32%)
90
Q

Symptoms of Bronchiectasis

A 
Chest pain (31%)
Breathlessnes (83%)
Cough w/ daily sputum  (75%)
Haemoptysis (50%) - new fragile blood vessels generated to help damaged organ.
Weight loss
Malaise 
Low energy
91
Q

Signs of bronchiectasis

A

Course crackles on early inspiration in lower lobes (50%)
Large airway rhonchi (44%) - low pitched, snore like sounds
Finger clubbing (rare)

92
Q

Clinical features of bronchiectasis

A

Young age of onset of symptoms (have had symptoms for many years)
No history of smoking
Pseudomonas aeruginosa in sputum

93
Q

Investigations used in diagnosis of bronchiectasis

A

CXR (abnormal in 90% of cases)
CT scan - shows signet rings due thickening of walls of bronchioles
Tests for CF, A1A deficiency and other assoc. conditions
Serum antibodies
FBC and CRP

94
Q

CXR in Bronchiectasis

A

Coarsening of lung markings.

BUT may have a normal CXR, CT is needed to confirm diagnosis.

95
Q

Indication for salbutamol

A

Acute exacerbation of COPD/Asthma

96
Q

Route of administration of salbutamol

A

Asthma/COPD - inhalation

Status asthmaticus - IV or nebulised

97
Q

ADRs of salbutamol

A 
Hand tremor 
Headache 
Hypokalaemia 
Cardiac arrhythmia 
Uticaria (itchy rash)
98
Q

Contraindications of salbutamol

A

Arrhythmia
CVD
Hypokalaemia

99
Q

MOA of salbutamol

A

Short acting Beta 2 agonist causing bronchodilation (relaxation of smooth muscle)

100
Q

MOA of ipratropium

A

Short acting inhibition of M1-3 muscarinic receptors causing bronchodilation through relaxation of smooth muscle

101
Q

Indication for Ipratropium

A

Acute, rescue drug for exacerbations of asthma/COPD

102
Q

ADRs of Ipratropium

A 
Constipation 
Cough
Dry mouth
diarrhoea 
GI disturbance 
Headache
103
Q

Contraindications of Ipratropium

A

Arrhythmia

Cardiac failure or MI in last 6 months

104
Q

MOA of beclametasone

A

Steroid - forms a complex with corticosteroid receptor. Complex acts as a transcriptional regulator. Upregulates anti inflammatory proteins and down regulates pro inflammatory mediators.

105
Q

Indication for beclametasone

A

Preventative anti inflammatory drug

Used in conjunction with preventers

106
Q

ADRs of beclametasone

A

Long term immunosuppression
Cushing’s Syndrome
Osteoporosis
Oral Thrush
Potentially decreased growth velocity in children
Increased risk of pneumonia in COPD patients

107
Q

Contraindications of beclametasone

A

Immunocompromised

Diabetic

108
Q

Management of infective exacerbation of bronchiectasis

A
  1. Sputum culture and sensitivity testing
  2. Abx - 1st line: Amoxicillin. If contraindicated: Clarythromycin
  3. SABA - Salbutamol
  4. ICS if asthmatic or COPD
  5. Ensure suitable airway clearance technique taught by physio
109
Q

General management of COPD

A

Smoking cessation
Annual flu vaccination
Pneumococcal Vaccination
First line: SABA or SAMA

110
Q

Patient with COPD is receiving a SABA/SAMA which is not effectively managing their symptoms. What alternative treatment can be offered?

A

If FEV1 > 50%: LABA (salmeterol) or LAMA (tiotropium)

If FEV1 < 50%: LABA (salmeterol) + ICS (Fluticasone) OR LAMA (tiotropium)

111
Q

Indication for theophylline in management of COPD

A

Only when all other treatment options have been tried

112
Q

Indication for mucolytics (Mucodiene, Bromhexine) in management of COPD

A

Only for patients with chronic productive cough and only continued if symptoms improve with treatment.

113
Q

Common causes of infectious exacerbations of COPD

A

Haemophilus influenza
Streptococcus Pneumoniae
Moraxella Catarrhalis

114
Q

Management of infectious exacerbation of COPD

A

Increase frequency of bronchodilator (and consider giving via nebuliser rather than inhaler)
Prednisolone

NICE do not support treatment with oral antibiotics. Only given when sputum is purulent or there are clinical signs of pneumoniae.

115
Q

What are the advantages of nebulised antibiotics over oral?

A

Targeted - therefore reduced systemic side effects (but increased local side effects) and smaller dose is required

116
Q

What are the advantages of oral antibiotics over nebulised?

A

Cheap

Quicker and easier

117
Q

Symptoms of pneumoniae

A 
Dyspnoea
Chest pain (pleuritic)
Cough (with purulent sputum)
Fever
General malaise 
Confusion or delirium
118
Q

MOA of salmeterol

A

Long acting inhaled B2 agonist (LABA)

119
Q

ADRs of salmeterol

A 
Angioedema 
Cardiac arrhythmias 
Hand tremors 
Uticaria (itchy rash)
Hypokalaemia
120
Q

Contraindications of Salmeterol

A

CVD
Arrhythmia
Hypokalaemia

121
Q

MOA of Tiotropium

A

Long acting inhibition of muscarinic (M3) receptors (LAMA)

122
Q

ADRs of Tiotropium

A 
Constipation
Diarrhoea
Dry mouth
GI disturbance 
Headache
123
Q

Contraindications of Tiotropium

A

Arrhythmias

Cardiac failure or MI in the past 6 months

124
Q

Components of respiratory epithelum

A

Pseudostratified ciliated columnar with goblet cells

125
Q

Anatomical dead space V:Q ratio

A

Ventilated alveoli which are not perfused e.g. pulmonary embolism
Va:Q = infinite

126
Q

Shunting V:Q ratio

A

Perfused tissue which is not ventilated

Va:Q = 0

127
Q

Physiological shunting

A

Bronchial arteries which supply lung tissue

128
Q

Pathophysiological shunting

A

Fluid filled alveoli

129
Q

How does the body maintain V:Q ratio?

A

Modulation of blood flow - if pO2 decreases, vasoconstriction occurs. Therefore, redirecting blood flow away from poorly perfused areas.

This is the opposite to systemic circulation

130
Q

Ideal V:Q

A

1

131
Q

Change in breathing pattern as a result of damage to the pons

A

Ataxic breathing with irregular period apnoea - Pons is involved in fine tuning

132
Q

Central chemoreceptors are located in…

A

Ventrolateral surface of the medulla

133
Q

Central chemoreceptors detect…

A

Changes in pH of the surrounding CSF which is proportional to pCO2

134
Q

Changes in pulmonary vascular resistance

A

PVR decreases as blood pressure increases as pulmonary capillaries which were closed at rest will open.

Ensures that there is sufficient time for gaseous exchange to occur.

135
Q

Pulmonary wedge pressure

A

Indirect measurement of pressure of blood in left atrium

136
Q

Why is intrapleural pressure higher in base of lungs than in the apex?

A

Lung base weighs more than the apex

137
Q

Flow of blood in pulmonary capillaries 3cm above the heart

A

Pulsatory

Pressure in artery > Pressure in alveoli > Pressure in vein

138
Q

Core pulmonale

A

Enlargement or failure of right ventricle caused by increased vascular resistance or high lung blood pressure.

139
Q

Signs of cor pulmonale

A 
Cyanosis 
Oedema 
Raised JVP
Ascites 
SOB
Prominent neck and facial veins
140
Q

Type I Respiratory failure

A

Oxygenation failure
Hypoxia without hypercapnia
Due to V:Q mismatch, shunting or low altitude

141
Q

Type II Respiratory failure

A

Ventilation failure
Hypoxia with hypercapnia
Due to COPD and pulmonary fibrosis

Year 2 (17 decks)

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