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MLA Revision > Lungs (HLB) > Flashcards

Lungs (HLB) Flashcards

1
Q

What is VE?

A

Minute ventilation - the amount of air entering or exiting the lung each minute

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2
Q

What is the A-a gradient?

A

Alveolar and arterial O2 gradient - difference between the O2 in the alveoli and the arteries.

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3
Q

What is the V/Q ratio?

A

Ventilation / Perfusion

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4
Q

What happens when there is reduced O2 available?

A

Hypoxic pulmonary vasoconstriction - constriction of the pulmonary arteries in the presence of alveolar hypoxia = redirects blood to areas that are poorly ventilated to areas which are more O2 rich & better ventilated.

Hypoxic pulmonary vasoconstriction (HPV) is a homeostatic mechanism that is intrinsic to the pulmonary vasculature. Intrapulmonary arteries constrict in response to alveolar hypoxia, diverting blood to better-oxygenated lung segments, thereby optimizing ventilation/perfusion matching and systemic oxygen delivery.

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5
Q

What is the definition of respiratory failure?

A

Hypoxaemia with PaO2 <8.0kPA

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6
Q

What is the difference between T1 and T2 respiratory failure

A

T1 = hypoxaemia with normal CO2

T2 = hypoxaemia with high CO2

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7
Q

What causes acute upon chronic respiratory failure?

A

Acute worsening of existing abnormalities (e.g. infection on top of COPD)

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8
Q

What are the two mechanisms behind respiratory failure?

A

Lung failure = hypoxaemia

Pump failure - hypercapnoea

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9
Q

What causes T1 RF?

A

Disease of the lungs - preventing adequate oxygenation of the blood = low O2 but normal or low CO2.

PaO2 = <8 with normal or low CO2

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10
Q

What are the 5 mechanisms of hypoxaemia in T1RF?

A

Hypoventilation
Low FIO2
Diffusion Impairment
Shunt
V/Q Mismatch

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11
Q

How does hypoventilation cause respiratory failure?

What causes hypoventilation?

A

Inadequate ventilation = low PaO2 and high CO2
Can cause T1 or T2 failure

Hypoventilation - caused by head injury, respiratory centre depression, respiratory muscle weakness, COPD, NMD, MSK disease

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12
Q

Why is high altitude a problem for FiO2?

How do we treat this?

A

Higher altitudes - the atmospheric pressure decreases = this decreases the partial pressure of O2 in blood

Treatment = supplemental O2

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13
Q

How does diffusion impairment cause respiratory failure?

A

Disease or damage to the basement membrane in alveoli & capillaries = reduces the amount of O2 that can cross = hypoxaemia.

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14
Q

How can we measure diffusion across the intersitium of the alveoli?

A

Measured by diffusing capacity called Transfer Factor = measures how much CO can pass over.

The Alveolar - arterial gradient can also tell us if there is a problem.

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15
Q

What factors can cause impaired diffusion of gases across the alveolar membrane?

A

Decreased SA (emphysema)
Inc thickness of membrane (pulmonary fibrosis)
Diffusion coefficient
pp & gradient of the gas

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16
Q

How is diffusion impairment treated?

A
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17
Q

Why do shunts cause hypoxaemia?

A

Because the arterial and venous bloods can mix - thereby reducing the amount of oxygenated blood to travel around the body.

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18
Q

What is a pulmonary shunt?

A

A shunt of deoxygenated blood from the RHS of the heart to the LHS without participating in gas exchange in the lungs

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19
Q

What is a physiological shunt?

A

Can happen with consolidation (causing hypoxia pulmonary vasoconstriction) or an AVM - causes hypoxaemia.

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20
Q

What is the normal V/Q ratio?

A

0.8

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21
Q

What is ventilation?

A

Volume of gas inhaled and exhaled over a given time period

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22
Q

What is perfusion?

A

Total blood vol reaching the pulmonary capillaries in a given time period

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23
Q

Complete the following for ventilation and perfusion in the lung:

Apex - V Q
Middle - V Q
Base - V Q

A

Apex = V > Q (over ventilated)
Middle = V = Q
Base = V < Q (over perfused)

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24
Q

In healthy lungs, what is VQ mismatch minimised by?

A

Minimised by hypoxic vasoconstriction - this directs blood away from poorly ventilated areas.

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25
Q

What is the management of T1 RF?

A

Treat underlying cause - bronchodilators, diuretics etc
Give Supplemental O2
Maintain Sats at 94-98%

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26
Q

What is the definition of T2RF?

A

pO2 <8.0KPA
pCO2 > 6.5 KPA

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27
Q

What causes T2RF?

A

Failure of ventilation - causing alveolar hypoventilation

Chronic Lung Disease
Chest Wall Deformity
Neuromuscular and Peripheral Nerve Disorders
Neuromuscular Lung Disorders
Disorders of the Respiratory Centre

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28
Q

What is the difference between acute and chronic T2RF?

A

Acute - renal buffering doesn’t have time to act - therefore HCO3 is normal and pH decreases.

Chronic - kidneys excrete H2CO3 and reabsorb HCO3 - increasing levels and pH only falls slightly

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29
Q

What is the Henderson-Hesselbach Equation?

A
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30
Q

How is T2RF Managed?

A
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31
Q

What is the problem of giving O2 to a patient with a hypoxic drive?

A

Control of ventilation is mediated via central and peripheral chemoreceptors. Central detect pCO2 and pH. Peripheral - also monitor PO2 as well as pCO2 and pH.

When there are high chronic levels of CO2 - brain starts to ignore central chemoreceptors due to inc in HCO3 in the blood and controls ventilation by levels of O2 from peripheral chemoreceptors alone = hypoxic drive. If lots of O2 are given - this suppresses the O2
chemoreceptors in the P and therefore ventilation in the P stops.

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32
Q

What type of RF does asthma usually cause?

A

Normally presents as T1 but if severe and chronic - can present as T2.

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33
Q

What are the following types of hypoxia caused by?
- Cytotoxic hypoxia
- Circulatory / Stagnant hypoxia
- Anaemic hypoxia
- Hypoxic hypoxia (hypoxaemic hypoxia)

A
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34
Q

What is
- Anatomical dead space
- Alveolar dead space
- Physiological dead space
in the lungs?

A

Anatomical = upper respiratory tract to the terminal bronchioles that do not take part in gas exchange (warm and humidify air instead)

Alveolar = alveoli that have lost blood supply and do not participate in gas exchange

Physiological = Anatomical dead space + Alveolar dead space

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35
Q

In healthy lungs, what does physiological dead space equate to?

A

Physiological dead space = Anatomical dead space (i.e. no alveolar dead space)

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36
Q

What will the FEV / FVC ratio be in an asthma P?

A

<70%

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37
Q

What are obstructive airways diseases caused by?

Which lung diseases are considered obstructive?

A

Narrowing of the airways - leads to air trapping and hyperinflation.

Asthma, COPD and BET are obstructive diseases

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38
Q

How are FEV and FVC affected by obstructive lung disease?

A

Narrow airways = cannot blow air out forcefully

FEV1 ⬇
FVC ↔
FEV1 : FVC <70%

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39
Q

What is
- FEV1
- FVC

A

FEV1 = Forced expiratory volume in 1 second
FVC = Forced vital capacity is the amount of air that can be forcibly exhaled from your lungs after taking the deepest breath possible.

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40
Q

Which lung disease is
- caused by inflammation, hyper-responsiveness and narrowing of the bronchial tree and is characterised by attacks of breathlessness and wheezing?

A

Asthma

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41
Q

What is the difference between asthma and COPD?

A

Asthma - breathlessness is recurrent and reversible. COPD - breathless all the time.

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42
Q

What are the symptoms of asthma?

A

Wheeze, breathlessness, chest tightness, cough, variable airway obstruction. Between exacerbations - Ps are completely well - with possible mild chest tightness, wheeze or dry cough.

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43
Q

What is atopy?

A

The tendancy to produce high amounts of IgE when exposed to a small amount of antigen. Atopic individuals have high prevalence of asthma, allergic rhinitis, urticaria and eczema.

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44
Q

What chromosome is asthma linked to?

A

Chromosome 11q13

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45
Q

What theory tries to explain asthma?

A

The hygiene hypothesis - that lack of infections in childhood = altered T cell function and a predisposition to developing asthma.

Also - that allergen exposure in early life may determine sensitisation.

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46
Q

What is the pathophysiology of asthma?

A

Individual has been sensitised to an allergen - this is later inhaled. Th cells secrete Its which cause release of IgE by plasma cells.

2 phase reaction - early (20mins) and late (6-12 hours later)

Early phase:
IgE - binds to receptors on mast cells & eosinophils - stimulate release of - histamine, prostaglandins, leukotrienes and other inflammatory factors.

These cause bronchoconstriction within minutes.

Late phase:
Infiltration of smooth muscle layer by Es, Bs, Ns, Monos and DCs = desquamation of epithelial cells = inc in mucus glands and goblet cell hyperplasia.

This causes hypertrophy and hyperplasia of airway smooth muscle.
Cytokines = contraction of smooth muscle and narrowing of airways, inc BV permeability, and inc mucus production. Acute inflammation occurs = oedema.

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47
Q

What causes polyphonic wheezing in asthma?

A

The narrowing of bronchi of different sizes

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48
Q

What is dynamic hyperinflation and why is it caused by asthma?

A

Dynamic hyperinflation = air trapping in the lung. Bronchi <2cm can completely close in asthma - trapping air - increasing residual volume and increasing total lung capacity.

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49
Q

Why can severe and chronic asthma sometimes behave like COPD?

A

Leads to collagen deposition, fibrosis of airways & fixed narrowing = remodelling of the airways – can behave like COPD.

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50
Q

Which type of cell are most associated with
- Acute asthma?
- Persistent inflammation and steroid dependent asthma?

A

Acute = Eosinophils

Persistent airway inflammation & Steroid-Dependent = Neutrophils

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51
Q

What are the triggers for asthma?

A

Environmental (see attached slide)

Drugs = Aspirin, NSAIDs, β blockers

Physiological = Pregnancy, Premenstrual, Exercise

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52
Q

What is a good indicator of asthma clinically?

A

Diurnal variation - worse and night and in early morning

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53
Q

What are the signs of
- Acute Asthma
- Severe Asthma

A

Acute asthma = Tachypnoea, Tachycardia, Polyphonic wheeze, Signs of hyperinflation

Severe asthma = cyanosis, silent chest, bradycardia

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54
Q

What investigations can be done for suspected asthma?

A

FBC - Es raised?
Peak flow
Spirometry
Full lung function tests with reversibility

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55
Q

What degree of diurnal variance suggests asthma?

A

> 20% diurnal variation is suggestive of asthma
Lower value in the morning compared to the evening

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56
Q

What will lung function tests show with asthma?

A

Increased TLC and RV - due to air trapping
Normal TLCO / DLCO
Reduced FEV1
FEV1:FVC <70%

Reversibility with bronchodilator - FEV1 should increase by at least 15% or 200ml

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57
Q

How can asthma appear on CXR?

A

May be normal in mild asthma

May show hyperinflation with inc lung flumes and flat diaphragms (seen as >6 anterior or 10 posterior ribs in MCL). Heart can appear vertical and narrow.

HRCT - will show air trapping

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58
Q

Which guidelines are used in the management of asthma?

A

BTS Guidelines (British Thoracic Society)

Avoid allergens, inhaled therapy, oral therapy, smoking cessation, self-management plan, regular reviews. Want good symptom control & QOL, best possible pulmonary function (FEV1 at 80% of predicted or best), prevent exacerbations, reduce M&M, minimal side effects.

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59
Q

Which receptors are present in bronchial mucosa?

A

β adrenoreceptors

Muscarinic cholinergic receptors

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60
Q

What factors determine drug deposition in lungs?

A
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61
Q

How do β 2 agonists (SABA and LABA) work?

A

Act on β 2 receptors - inc AC - inc cAMP - inc PKA = phosphorylation = dec Ca levels intracellularly.

Causes bronchodilation
Stabilises mast cells, inhibits inflammatory mediator release = enhanced mucociliary clearance and decreased vascular permeability.

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62
Q

Name a SABA and a LABA

A

SABA
- Salbutamol (Ventolin)
- Terbutaline (Bricanyl)

LABA
- Salmeterol
- Formoterol

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63
Q

How to SAMA and LAMAs work?

A

They act on muscarinic receptors which use the M3 - Gαq pathway – Phospholipase C (+), IP3 and DAG = increase of Ca2+ - they are ANATGONISTS – so decrease levels of Ca2+ by inhibiting this pathway – therefore cause bronchodilation. (Agonists cause bronchoconstriction).

Therefore - antagonists of Gq path

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64
Q

What are the side effects of salbutamol?

How long does onset of action take?
How long do the effects of salbutamol last?

A

Tachycardia (β1 receptors in heart)
Tremor (β3 receptors in skeletal muscle)
Agitation

Rapid onset - 10 mins
Lasts 3-5 hours

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65
Q

What is the time for onset of action of salmeterol?
How long do the effects of salmeterol last?

What is it always used in combination with?

A

Takes 30 mins for onset
Effects = 10-12 hours

Always used in combo with ICS +/- LAMA - suppresses chronic inflammation and reduces airways hyper-responsiveness

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66
Q

When is ipratropium bromide used in asthma?

A

Only in acute exacerbation

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67
Q

How do glucocorticoids work?

A

GCS taken into cells - binds to target genes and changes transcription of inflammation / anti-inflammatory components.

GCS receptors found in most cells of the body

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68
Q

Which steriods for asthma can be given
= Orally
= Inhaled
= Intravenous

A

Oral = prednisolone, dexamethasone

Inhaled = beclomethasone

IV = methylprednisolone, hydrocortisone

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69
Q

What are the side effects of oral steroids?

A
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70
Q

Which is the most effective preventer drug for asthma in adults and children?

What are the common side effects? How can these be prevented?

A

ICS
Beclomethasone - BPD

SE = Oral candidiasis (bodys ability to fight infection reduced), Dysophonia

Prevent by gargling after use and using a spacer

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71
Q

Why do we use combination therapy in asthma?

A
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72
Q

What do spacers do?

A

Inc distance - allows particles time to evaporate and slow down before inhalation = larger proportion of particles deposited in lungs and minimises oral deposition - reducing incidence of thrush

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73
Q

What type of drug is theophylline? How does it work?

A

Is a methyxanthine

Inc intracellular cAMP conc - blocks adenosine receptors and dec bronchoconstriction.

Many side effects!

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74
Q

What type of drug is Montelukast?

A

Is a leukotriene inhibitor - used for allergic and exercise-induced asthma

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75
Q

What are the initial steps in asthma management?

A

Smoking cessation + avoid triggers

Step 1 = ICS
Step 2 = add LABA if still symptomatic
Can add Leukotrine inhibitor, oral theophylline later if needed

Use SABA for immediate relief of Sx as needed

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76
Q

What Tx is given for acute asthma?

A

Nebulised SABA (salbutomol) and SAMA (Iprotropium bromide)
Systemic corticosteriods
Magnesium sulphate if severe
Aminophylline
ABx

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77
Q

What can Ps use to self-manage their asthma?

A

A Personalised Asthma Action Plan (PAAP)

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78
Q

When can asthma Ps be discharged after admission for acute asthma?

A

If PEFR is >75% of best
There is less than 25% diurnal variability

Oral steroids need to be given and reduced over following 2w

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79
Q

What is an allergy?

A

A damaging immune response by the body to a substance to which it has become hypersensitive

80
Q

What are the four categories of hypersensitivity?

A

Type 1 - IgE (Antibody mediated)
Type 2 - Cytotoxic (IgG)
Type 3 - Immune complex-mediated
Type 4 - Delayed Cell Mediated

81
Q

What is the pathophysiology behind Type 1 reactions?

A

IgE binds to the receptors (FcεRI) on mast cells, Bs and Es - causes cross-linkage of receptors (brings them close together so they phosphorylate) ➡ signalling cascades à mast cell and B degranulation ➡ release of inflammatory mediators – activates local immune response (vascular permeability etc).

Non-allergic people generally produce IgE antibodies only in response to parasitic infections.

First exposure – don’t get large response – but B-cells (after exposure to antigen from antigen-presenting cells) will make memory cells. – On second exposure - that you activate and get a large production of B cells (that produce IgE) in response to recognition of the allergen. IgE ➡ mast cell degranulation ➡ contraction of smooth muscle cells, vasc perm, secretions by mucous cells, aggregation of platelets, sensation of sensory nerve endings & infiltration of Es.

82
Q

Why is asthma a Type 1 hypersensitivity?

A

Because IgE is released in response to the allergen - this mediates mast cells to release histamine - this binds to the H1 receptors initiating vascular permeability and mucous secretion.

Also releases phospholipase - this results in the release of leukotrienes and prostaglandins - triggers bronchoconstriction.

83
Q

In humans - what is though to significantly contribute to prolonged bronchospasm and build up of mucous?

A

Leukotrienes.

84
Q

What is the pathophysiology of Type II hypersensitivities?

A

Involves AB mediate destruction of cells by AB classes OTHER than IgE.

AB released - activates complement cascade ➡ antibody cell mediated cytotoxicity (AB binds to the target cell and activates phagocytic cells to kill them by opsonization.

85
Q

Which allergies are associated with Type 1 hypersensitivity?

A
86
Q

Which allergies are associated with Type II hypersensitivity?

A
87
Q

What is the pathophysiology behind Type III hypersensitivities?

A

Immune-complex mediated

Immune-complexes can induce degranulation of mast cells ➡ inflammation and complement activation and Ns ➡ if deposited in capillary beds, immune complexes can cause vasculitis, or glomerulonephritis or arthritis.

88
Q

Which allergies are associated with Type III hypersensitivity?

A
89
Q

What is the pathophysiology behind Type IV hypersensitivities?

A

Purely cell mediated - no Igs

T-cell get sensitised to the antigen - subsequent re-exposure results in cytokines, inflammation and recruitment of Macs. Sx occur 24-48hr later.

90
Q

What allergies are considered to be Type IV hypersensitivities?

A
91
Q

What are the red flags for cough?

A
92
Q

What is COPD characterised by?

A
  • Progressive airflow obstruction
  • Not fully reversible
  • Does not change markedly over several months
93
Q

What are the causes of COPD?

A

Cigarette smoking - 90% of cases caused by this

Also - occupational exposure, air pollution

1-2% = α-1 antitrypsin deficiency

94
Q

What is the definition of chronic bronchitis?

A

Sputum - for at least 3 months per year for at least 2 consecutive years

95
Q

What is the definition of emphysema?

A

Destruction of alveoli distal to the terminal bronchiole resulting in loss of elastic supporting tissue. Gas exchanged affected - interstitium is destroyed = REDUCTION IN TLCO

96
Q

What is the pathophysiology of emphysema?

A

Healthy lungs = α-1 antitrypsin protects from elastase (secreted by Ns).

Smoking - activates Ns - more numbers of them - secrete more elastase & collagenase than can be controlled by α1 antitrypsin. This damages alveolar sacs ➡ bullae = emphysema.

Much of the alveolar surface of lung is destroyed - therefore reduced SA for gas exchange.

97
Q

What is the pathophysiology of chronic bronchitis?

A
98
Q

What is the pathophysiology of COPD?

A

Airways are thicker, hypertrophied, fixed and narrowed – tendency to collapse (esp expiration) ➡ air trapping & hyperinflation \ breathing is harder work.

COPD Ps – tend to be breathless all the time – will use accessory muscles & pursed lip breathing.
End stage – develop RHF (cor pulmonale) ➡ pulmonary hypertension

99
Q

How is COPD diagnosed?

A

Spirometry that shows an FEV1 : FVC ratio <70 that is not reversible with a SABA or SAMA.

Reduced FEV1
Inc in TLC and RV
Reduced TLCO / DLCO

100
Q

What are the Sx of COPD?

A
101
Q

What are the signs of COPD?

A
102
Q

What is the extent of breathlessness assessed by?

A

The mMRC Dyspnoea Scale

103
Q

What is the severity of COPD graded by?

A

Global initiative for COPD

104
Q

What will a CXR show in COPD?

A

Hyperinflation
- Flat diaphragm and anterior ribs

105
Q

What will a HRCT show in COPD?

A

Bullae

106
Q

What is cor pulmonale?

A

Right heart failure secondary to lung disease

Cor pulmonale is an enlarged right ventricle in your heart that happens because of a lung condition. Pushing against high pressure in your pulmonary artery can cause your right ventricle to fail.

If suspected to ECG and Echo

107
Q

How is COPD managed?

A
108
Q

What is the combination inhaled therapy used for COPD?

A

ICS + SAMA + LABA + LAMA

Can also use a methylxanthine (theophylline) and a carbocisteine

109
Q

Name a SAMA.

What is the mechanism of action of SAMAs?

What is the onset of action of a SAMA?
How long do they last?

A

Ipratropium Bromide

110
Q

Name a LAMA

What is the mechanism of action of LAMAs?

How long do they last?

A

Tiotropium

111
Q

What are the side effects of SAMAs and LAMAs?

A
112
Q

What is important to remember about methylxanthines?

A

They have a narrow therapeutic range - need monitoring!

Metabolised by CP450 - therefore affected by many drugs because of this.

113
Q

Which antibiotic can be given for streptococcus pneumonia?

A

Amoxicillin
Clarithromycin
Doxycycline

114
Q

Which antibiotic can be given for Staph aureus?

A

Vancomycin for MRSA
Flucloxacillin

115
Q

How are acute exacerbations of COPD managed?

A
116
Q
A

5

117
Q

What is apnoea?

What are the two types of apnoea?

A

Apnoea = cessation of breathing during sleep

  • Obstructive Sleep Apnoea
  • Central Sleep Apnoea - less common = absence of ventilatory drive caused by brain stem injury
118
Q

What causes obstructive sleep apnoea?

A

Recurrent episodes of upper airway collapse during sleep

119
Q

What are the symptoms of sleep apnoea?

A

Snoring, apnoea episodes (stopping breathing >10 seconds), excessive daytime sleepiness

120
Q

What is sleepiness measured by?

A

Epworth Sleepiness Score

121
Q

What are the RF for obstructive sleep apnoea?

A
122
Q

What are the Sx of sleep apnoea?

A
123
Q

How is sleep apnoea managed?

A
124
Q

What are red flag Sx related to sleep apnoea?

A
125
Q

What does smoking cause?

A
  • Contains carcinogens -> genetic mutations -> lung cancer, mesothelioma
  • CO causes carboxyhaemoglobin
  • Impairs ciliary function - decreased muco-ciliary escalator = inc respiratory infections

Causes hyperplasia of goblet cells - inc mucus production

126
Q

Why does smoking cause dependence and withdrawal?

A
127
Q

What drugs can be given for smoking cessation?

A

Nictotine replacement therapy

Bupropion (Zyban) - AD

Vareniciline (Champix) - partial agonist of ACh receptor - most effective Tx

128
Q

Cessation of smoking for 5 years gains a P what?

A

Reduced risk of LC (although not the same as a non-smoker)

An extra 6-10 years of life

129
Q

Which is the commonest occupational lung disease?

A

Asthma

130
Q

What types of pneumoconiosis are there? (Caused by mineral dust)

A

Coal Worker’s Lung
Asbestosis
Silicosis

131
Q

What is the difference between occupational asthma and work-exacerbated asthma?

A

Occupational asthma = develops for the first time when an individual is exposed to an irritant or sensitiser at work.

Work-exacerbated asthma = pre-existing asthma made worse at work

132
Q

What things can cause occupational asthma?

A
133
Q

How can you tell if it is occupational asthma?

A
134
Q

How is occupational asthma managed?

A
135
Q

What is pneumoconiosis?

A

Lung fibrosis from inhaling inorganic particles or mineral dust at work

136
Q

What is the pathophysiology of pneumoconiosis?

A

Inert particles get lodged in airways – conc needed for disease depends on dust (high conc coal, lower conc silica/asbestos). Macrophages fill with dust ➡️ inflammation ➡️ fibrosis.

137
Q

What does coal-workers pneumoconiosis cause?

A

Progressive massive fibrosis

Carbon accumulation ➡️ activation of alveolar macrophages ➡️ progressive fibrosis & restrictive lung disease.

This causes breathlessness, cough and weight loss. Can cause death.

138
Q

Which workers are at risk of developing silicosis?

A
139
Q

How does silicosis appear on CXR?

A

Restrictive lung + fibrosis
Eggshell calcification of hilar lymph nodes

140
Q

What is silicosis a RF for?

A

Developing mycobacterium TB and lung cancer

141
Q

How are pneumoconioses managed?

A
142
Q

What types of asbestos-related lung disease are there?

A

Benign – no symptoms – doesn’t progress – cannot become malignant. Calcified pleural plaques (only asbestos causes); benign pleural effusion & benign pleural thickening

Asbestosis = only asbestosis if there is fibrosis of the lungs (different from other asbestos related lung diseases) – restrictive lung disease. Identical presentation to IPF – bi-basal, fine crackles, 33% clubbing

Malignant = mesothelioma or LC. LC risk = x7 if non-smoker, x93 if smoker.
Mesothelioma = malignancy of pleura & peritoneum.

143
Q

What are the two types of asbestos fibres?

A

2 types – amphibole (blue) & serpentine (white - less toxic). Amphibole causes mesothelioma & asbestosis.

144
Q

How does asbestosis present?

A

Same as IPF

Bi-basal fine crackles
1/3 will have clubbing

145
Q

What is mesothelioma?
How does it present?

A

Mesothelioma = malignancy of pleura and peritoneum

Sx = persistent chest pain, breathlessness, weight loss, unilateral pleural effusion (exudate).

146
Q

Which occupations carry a risk of asbestos exposure?

A
147
Q

What do these CT scans show?

A
148
Q

Which of these conditions does not usually cause any Sx?
1 - asbestosis
2 - progressive massive fibrosis
3 - mesothelioma
4 - silicosis
5 - pleural plaques

A

Pleural plaques

149
Q

What is the medical term for bleeding from the nose?

A

Epistaxis

150
Q

What is the impact of nitrous oxide on health?

A
151
Q

How does cold dry air affect the airways?

A

Can cause bronchoconstriction - possibly due to loss of water from the airways

152
Q

How does hot humid air affect the airways?

A

Cause bronchoconstriction secondary to vagal mechanisms

153
Q

How do thunderstorms affect respiratory health?

A

Inc conc of pollen debris and O3 => allergic exacerbation of asthma

154
Q

What is the commonest inherited genetic condition in the UK?
What type of inheritance does this have?

A

CF

Inheritance - autosomal recessive

155
Q

Which protein is altered in CF?

A

Cystic Fibrosis Transmembrane Regulator Protein (CFTR)
- on Chromosome 7 (7q31)

Approx - 1700 different mutations can occur! (because problem can occur at any stage of transcription, translocation or processing etc). Means that there are different ° of impairment to the P depending on which mutation has occurred.

156
Q

What does the CFTR protein do?

A

Controls Cl- channels in epithelial cells - defects can prevent transport of Cl out of cells. These channels also are meant to inhibit Na reabsorption and regulate HCO3.

If there is a defect - Cl & Na (with water) builds up inside the cell. This means that mucus becomes very dry and thick - high viscosity -> impairment of mucociliary escalator and decreased clearance.

Causes obstruction, infection, inflammation, inc URTIs and lung damage.

157
Q

What organs are affected by CF?

A
158
Q

What are the respiratory tract symptoms of CF?

A
159
Q

Which organisms are often found in respiratory infections with CF?

A
160
Q

What are the different classes of CF?

A

Class 1 = no CTFR made
Class 2 = misfolding of CTFR occurs
Class 3 = CTFR but poor function
Class 4 = CTFR ion channel is faulty – impaired Cl conductance.
Class 5 = reduced amount of CTFR protein

Classes 4&5 have less severe clinical disease than 1-3

161
Q

How does CF impact on the GI tract?

A

Pancreas = sticky secretions ➡️ blockage of ducts ➡️ failure to deliver digestive enzymes ➡️ destruction of the pancreas
➡️ decreased lipases = dec absorption of fat in SI = steatorrhoea, lack of ADEK, lack of insulin (causing DM),

Intestine = sticky secretions due to lack of water content ➡️ obstruction (meconium ileus equivalent)

Can get liver cirrhosis

162
Q

How can CF impacts on the GI tract be managed?

A

Endocrine insufficiency – can give insulin

Exocrine insufficiency – can give enzyme replacement therapy (amylase, lipase and proteases = Creon), multivitamins and enteral support where needed

163
Q

What other ways can CF impact the patient?

A

Can cause increased sweating (used as a diagnostic test)

Reproductive problems & sub fertility - vas deferens can fail to canalise, azoospermia.

Big psychological and social impact on P and family

164
Q

How does CF present in newborns?

A

Meconium ileus
Failure to thrive
Recurrent respiratory infections

165
Q

How is CF diagnosed?

A

If CFTR is not working - chloride can build up in sweat = high chlorine levels on a sweat test

166
Q

How is CF screened?

A
167
Q

How is CF managed?

A

Prompt Abx for respiratory infections
Intense chest physio
Nebulised DNAase - degrades the high concentration of DNA in secretions = decreased viscosity
Mucolytic drugs
Bronchodilators
LTOT

168
Q

What is the life expectancy of someone with CF?

A

About 50

169
Q

What factors can affect an individual’s pulmonary function test (PFT)?

A
170
Q
A
171
Q

What are the contraindications to dynamic lung function testing?

A
172
Q

When is peak expiratory flow reduced?

A

In obstructive airway disease (asthma, COPD and BET)

May also be reduced by diseases of the chest wall (NMD and kyphoscoliosis) or diseases affecting the upper airways (tracheal tumour, thyroid goitre)

173
Q

What does spirometry measure?

A

The FEV1 (forced expiratory vol in 1s) and the FVC (forced vital capacity)

174
Q

What is the normal range for spirometry?

A

80% if FVC should be exhaled in first second (FEV1) - therefore normal FEV1 = 0.75-0.85 (80%).

FEV1 and FVC peak in 30s - decline by 30ml/yr after this :(

175
Q

How does spirometry determine if there is obstructive or restrictive disease?

A

Obstructive - FEV1 is reduced - may take up to 15s to expel all the air. FEV1 is reduced more than FVC - so FEV1/FVC <0.7

Restrictive - FVC is decreased (less compliance) and FEV1 is reduced as less vol to expel but not to the same extent. So FEV1/FVC is either normal or increased.

176
Q

What are flow-volume loops used to differentiate?

A

Between extra thoracic and intra-thoracic obstruction

177
Q

In restrictive disorders, is TLC reduced or increased?

A

Reduced

178
Q

In obstructive disorders, is TLC reduced or increased?

A

Increased

179
Q

What does TLCO/DLCO measure?

A

The diffusing capacity - is an estimate of how much CO diffuses across the alveolar-capillary membrane

180
Q

When is TLCO decreased?

A

Ventilation / perfusion mismatch
Impeded blood flow (e.g. PE)
Reduced alveolar SA (emphysema)
Impeded transport of O2 across the membrane (e.g. interstitial lung disease)
Respiratory muscle weakness => restriction

181
Q

When is TLCO increased?

A

When there is increased pulmonary blood vol - e.g. high cardiac output, polycythaemia and pulmonary haemorrhage

182
Q

What does KCO measure?

A

The transfer of CO in ventilated alveoli (disregards unventilated alveoli)

183
Q
A

4 - Decreased TLCO and KCO

184
Q
A

2 - Increased FEV1 / FVC

185
Q

How can you differentiate between asthma and COPD on lung function tests?

A

FEV1/FVC is below 0.7 for both BUT
Asthma - TLCO and KCO will be increased, COPD = these will be decreased a lot!

186
Q
A
187
Q

Which diseases cause restriction of the lungs?

A
188
Q

What type of respiratory disease is seen in these graphs?

A
189
Q

What type of respiratory disease is seen in these graphs?

A
190
Q

How can KCO be used to distinguish between intrathoracic and extra thoracic conditions?

A

KCO - measures the CO transferred in ventilated alveoli.

TLCO and KCO will both be reduced by intrathoracic conditions, however KCO will not be diminished by extra thoracic conditions.

Therefore - if TLCO and KCO are reduced = intrathoracic
If only TLCO reduced and KCO is normal = extrathoracic

191
Q

What things can cause restrictive lung disease?

A

Parenchymal Lung Disease (pulmonary fibrosis, sarcoidosis, pneumoconiosis)

Pleural disease
Obesity
Chest Wall Disease

192
Q

How is the FEV1/FVC ratio affected by restrictive lung disease?

A

It is either normal or increased.

193
Q

Why does most DPLD (diffuse Parenchymal Lung Disease) occur?

A

Is an injury to the tissue of the lungs (alveoli, interstitium) ➡️ inflammation and fibrosis. Cytokines are released in injury - stimulate fibroblasts which cause permanent fibrosis of the lung.

194
Q

What factors can cause damage to the lungs in DPLD?

A
195
Q

What are the Sx of DPLD?

A
196
Q

What are the clinical signs of DPLD?

A
197
Q
A

MLA Revision (9 decks)

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