Clinical Respiratory Medicine Flashcards

1
Q

embryonic stage of devlelopment

A

trachea and main bronchi appear

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2
Q

pseudoglandular stage of development

A

all conducting airways form

epithelial cells differentiate

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3
Q

canalicular stage of development

A

respiratory airways form
blood-gas barrier thins
surfactant appears

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4
Q

saccular stage of development

A

saccules (terminal sacs) appear

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5
Q

alveolar stage of development

A

saccules form alveoli

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6
Q

lung development into childhood

A

alveoli continue to multiply

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7
Q

stages of lung morphogenesis

A
  1. Embryonic
  2. Pseudo-glandular
  3. Canalicular
  4. Saccular
  5. Alveolar
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8
Q

stage of lung development at which extra-uterine life is possible

A

late canalicular / early saccular

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9
Q

Tracheo-bronchomalacia pathophysiology

A

Cartilage in airways doesn’t form properly in early development.

leads to “floppy” airways that are only held open by muscle

usually resolves naturally without treatment

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10
Q

Symptoms of tracheo-bronchomalacia

A

Barking cough
Dyspnoea on exertion
Recurrent /early croup
Frequent infections

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11
Q

Congenital Pulmonary Airway Malformation (CPAM)

aka Pulmonary adenomatoid malformation

A

overgrowth of terminal bronchioles creates areas of cystic tissue that cannot function normally

may resolve spontaneously in utero.
most cases are asymptomatic.
sometimes other areas of the lung are compressed (causing difficulty breathing) or other organs are compressed.

surgery may be required

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12
Q

Infant respiratory distress syndrome/ Surfactant Deficiency Disorder/ Hyaline Membrane Disease

A

surfactant deficiency

treated with surfactant replacement

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13
Q

fetal origins of COPD

A

in utero nicotine exposure
fetal infection
poor maternal nutrition
Low birth weight/ prematurity

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14
Q

pediatric origins of COPD

A

infection
growth
environmental pollutants

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15
Q

Remodelling

definition + examples

A

The alteration of structure following external influence

e.g lung hypoplasia caused by pre-natal nicotine exposure.
chronic inflammation in asthma causing airway narrowing

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16
Q

Specific features to be included in the clinical history of asthma

A
childhood asthma
inhalers taken (+ doses)
occupation (past and present)
smoking - pack year history
eczema
hayfever
atopic disease in family
pets
phycosocial aspects - stress
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17
Q

Specific features to be included in the clinical history of COPD

A
childhood asthma
inhalers taken (+ doses)
occupation (past and present)
smoking - pack year history
past respiratory diseases
Ischaemic heart diease
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18
Q

assessing the severity of acute COPD

A

Uses FEV1/FVC

> 80% = mild
50 - 79% = moderate
30 - 49% = severe
<30% = very severe

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19
Q

assessing the severity of acute severe asthma

A
can be: moderate, severe, life threatening or near fatal.
objectively measured using:-
- ability to speak
- heart rate
- respiratory rate
- peak expiratory flow
- O2 saturation and PaO2

near fatal = raised PaCO2

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20
Q

nebulisers

A

used if a patient cannot use an inhaler

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21
Q

proven aetiological factors of asthma

A

Atopy - tendency for IgE response to allergens
Smoking
maternal smoking during pregnancy
occupational factors - spray paint, rodent urinary protein, grains, crustacean

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22
Q

putative aetiological factors for asthma

A
obesity
diet
reduced exposure to microbes
pollution
cleaning sprays
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23
Q

The British Thoracic Society’s “Stepwise” approach to management of asthma

A

There are different steps for different intensities of treatment
Patients should try to be on the lowest step on which they can maintain control of their asthma

This reduces cost and adverse effects

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24
Q

Epidemiology

A

The incidence, distribution and determinants of disease in a population

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25
Q

Atopy

A

a (genetic) predisposition toward developing type I hypersensitivity reactions (excessive IgE production)

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26
Q

Hyperplasia

A

increased proliferation

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27
Q

Emphysema pathophysiology

A

increase in size of air spaces (hyperinflation) due to destruction of elastin causing dilatation and destruction of alveolar cell walls

Airways collapse due to pressure in chest cavity on expiration, no elastin to hold them open

Air becomes trapped

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28
Q

Centriacinar emphysema

A

smoke particles get trapped in the airspaces of the bronchioles causing inflammation.

neutrophils make elastase which destroys elastin

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29
Q

Panacinar emphysema

A

a-1 antitrypsin (a protein which destroys elastase) deficiency.

leads to elastin destruction in bronchioles and alveoli

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30
Q

Periacinar (bullous) emphysema

A

alveoli expand to form large (>1cm) air spaces called bulla.

rupture can leak air into the pleural cavity causing pneumothorax

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31
Q

Clinical definition of chronic bronchitis

A

a cough lasting for at least 3 consecutive months of the year for at least 2 consecutive years

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32
Q

Morphological changes of large airways in chronic bronchitis

A
  • mucous gland hyperplasia
  • goblet cell hyperplasia
  • some inflammation and fibrosis
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33
Q

morphological changes of small airways in chronic bronchitis

A
  • goblet cells appear

- inflammation and fibrosis (in long standing disease)

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34
Q

cause of obstruction in chronic bronchitis

A

airways obstructed by thick mucous and fibrosis

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35
Q

Causes of hypoxaemia in COPD

A
  • Airway obstruction
  • loss of alveolar surface area for gas exchange
  • reduced respiratory drive (central chemoreceptors get used to high [H+] in CSF

These all cause low ventilation

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36
Q

Hypoxic cor pulmonale

A

enlargement of the right ventricle of the heart.

because higher blood pressure is needed in the lungs due to vasoconstriction due to shunt

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37
Q

Asthma mechanism

A

Type I hypersensitivity in the airways.

IgE is produced in response to stress, chemicals cold, etc…
IgE triggers mast cell degranulation which causes:-
1. Bronchial smooth muscle contraction (immediate response)
2. Chronic inflammation of airways

This narrows the airways

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38
Q

Clinical definition of asthma

A

Chronic airflow obstruction causing WHEEZE which is VARIABLE and REVERSIBLE with asthma treatment

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39
Q

Symptoms of asthma

A

Wheeze
Dry cough
Dyspnoea (at rest)
Chest tightness

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40
Q

Investigations used for diagnosis of asthma

A

Spirometry: Low FEV1/FVC
Peak-flow monitoring: Variable obstruction
reversibility with bronchodilator/ oral corticosteroids
Skin prick test: proves atopy
Bronchial provocation: response to lower loses of bronchial constrictors (methacholine etc.)
Fractional exhaled NO: ↑ due to inflammation in airways
CXR: Hyperinflation
FBC: Eosinophillia = atopy

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41
Q

Definition of COPD

A
airway obstruction (chronic bronchitis) and hyperinflation (emphysema).
Constant and not fully reversible
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42
Q

Symptoms of COPD

A
Breathlessness on exertion
chronic cough with sputum
recurrent chest infections
wheeze/ chest tightness
weight loss
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43
Q

Investigations used for diagnosis of COPD

A

Spirometry: low FEV1/FVC = fixed airflow obstruction
Reversibility: Minimal w/ bronchodilators and oral corticosteroids
CXR: Hyperinflated lungs, compressed diaphragm and heart
Full pulmonary function testing: ↑RV, ↑TLC and RV/TLC> 30% = emphysema
Blood gases: ↓PaO2, ↑PaCO2

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44
Q

Management strategies for COPD

A

smoking cessation!
vaccinations (increased risk of respiratory infection)
long term oxygen therapy
pulmonary rehabilitation (exercise, support, etc.)
Inhaled therapy

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45
Q

characteristics of obstructive lung diseases

A

airflow limitation
reduced peak expiratory flow rate
reduced FEV1

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46
Q

pathogenesis

A

the development of a disease from the causes and origin to the end stages

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47
Q

Pulmonary embolism deffinition

A

a thrombus (blood clot) formed in the venous system that embolises to the pulmonary arteries

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48
Q

pulmonary embolism symptoms

A

pleuritic chest pain
cough + haemoptysis
dyspnoea

MASSIVE PE:
syncope
cardiac arrest

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49
Q

pulmonary embolism investigations

A

Pre-test probability: Wells/ Geneva score
V/Q scan: Low perfusion
CT pulmonary angiogram: Shows occlusion of pulmonary artery
D-dimer: High
ECG: Tachycardia
Blood Gases: ↓PCO2 + Hypoxia

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50
Q

Pulmonary embolism management

A

Immediate oxygen for resuscitation

Anticoagulation:
Heparin, Warfarin, DOACs

Massive PE: Thrombolysis Pulmonary embolectomy

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51
Q

pulmonary infarction definition

A

local necrosis of lung tissue caused by obstruction of arterial blood (usually due to PE)

most common in people with underlying lung disease (e.g. COPD) as well tissue is well oxygenated from multiple sources

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52
Q

pulmonary infarction management

A

100% oxygen (for initial resuscitation)
mechanical ventilation

ultimately depends on cause

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53
Q

pulmonary hypertension definition

A

elevated blood pressure (>25mmHg) in pulmonary arteries

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54
Q

causes of pulmonary hypertension

A
Idiopathic
Secondary to chronic respiratory disease
Secondary to left heart disease
Artery Occlusion (Chronic thromboembolic PH /CTEPH)
Collagen vascular disease
Portal hypertension
Congenital HD (L -> R shunt)
HIV
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55
Q

symptoms of pulmonary hypertension

A

exertional dyspnoea
exertional presyncope/ syncope
chest tightness

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56
Q

pulmonary hypertension investigations

A

Doppler echo: Estimates pulmonary artery systolic pressure
V/Q scan: CTEPH
CT(PA)/ CXR: Enlarged pulmonary arteries
Right heart catheterisation: Direct measurement of pulmonary artery pressure

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57
Q

management of pulmonary hypertension

A
Treatment of underlying condition
Oxygen
Anticoagulation
Diuretics
Lung/ Heart transplant
Thromboendarterectomy (CTEPH)

PULMONARY VASODILATORS: CCBs
Endothelin receptor antagonists
Phosphodiesterase inhibitors
Prostacyclin

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58
Q

theophyllines

A

IV/ oral bronchodilator used in asthma

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59
Q

venography

A

x-ray of the veins using an IV contrast. used to identify DVT and PE

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60
Q

Pleural effusion definition

A

an abnormal collection of fluid in the pleural space

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61
Q

Transudates

A

caused by an imbalance of hydrostatic forces influencing formation and absorption of pleural fluid

usually bilateral
pleural fluid protein <30g/l

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62
Q

Exudates

A

caused by an increase in the permeability of the pleural surface and/or local capillaries.

usually unilateral
pleural fluid protein >30g/l

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63
Q

Causes of transudates

A

left ventricular failure
liver cirrhosis
hypoalbuminaemia
peritoneal dialysis

hypothyroidism
nephrotic syndrome
mitral stenosis
pulmonary embolism

constrictive pericarditis
ovarian hyperstimulation syndrome
meig’s syndrome

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64
Q

Causes of exudates

A

malignancy
parapneumonic

pulmonary embolism/ infarction
rheumatoid arthritis
autoimmune diseases
benign asbestos effusion
pancreatitis
post myocardial infarction

yellow nail syndrome
Drugs: amiodarome, nitrofuratoin, phenytoin, methotrexate, carbamazapine……

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65
Q

Symptoms of pleural effusion

A
  • asyptomatic (if small and accumulates slowly)
  • increasing breathlessness
  • pleuritic chest pain ( improves if inflammatory, worsens w/ malignancy)
  • dull ache
  • dry couch
  • weight loss, malaise, fevers, night sweats…
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66
Q

Signs of pleural effusion

A

On affected side of chest:

  • decreased expansion
  • stony dullness to percussion
  • bronchial breathing sounds
  • decreased vocal resonance
clubbing
increased JVP
trachea moved away from large effusion
cervical lymphadenopathy
peripheral oedema
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67
Q

when to investigate pleural effusion

A

clinical picture is usually characteristic for bilateral transudate. investigate if…
-is unilateral
unusual features
fails to respond to appropriate treatment

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68
Q

Investigations for pleural effusion

A
  1. CXR (confirms presence)
  2. CT (differentiates malignant from benign)
  3. Pleural aspiration
  4. Pleural biopsy
  5. Thoracoscopy
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69
Q

Management of pleural effusion

A

Treatment of cause

Pleurodhesis (drain)
Chemical pleurodhesis (e.g. talc slurry)
Surgical pleurodhesis  (performed at time of thoracoscopy)

Palliative (e.g. if due to malignancy) = repeated pleural aspiration

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70
Q

Malignant mesothelioma defnition

A

pleural malignanct caused by exposure to aasbestos (occurs 20-40yrs after exposure)

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71
Q

Malignant mesothelioma clinical presentations

A

breathlessness
chest wall pain

radiology = usually unilateral pleural thickening

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72
Q

Malignant mesothelioma treatment

A

pleuropneumonectomy (remova of entire lung and parietal pleura) if very fit

otherwise, palliative treatment

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73
Q

pleural fibrosis

A

caused by inflammation, surgical trauma, pleural effusion, asbestos etc.

pleura develops fibrous tissue and loses elastic properties which impairs lung function

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74
Q

pleural plaques

A

Benign plaques of the pleura caused by asbestos exposure. Can become calcified but rarely inhibit lung function.
almost always asymptomatic

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75
Q

Empyema

A

collection of pus in the pleural cavity which can eventually form fibrous scar tissue and inhibit lung function.

caused by pneumonia, trauma, surgery…

Symptoms: chest pain, fever, NO cough.
Diagnosed by pleural aspiration

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76
Q

appearance of tuberculous granuloma in TB

A

Rounded outline,
Epithelioid and langhan’s giant cells (transformed macrophages),
Lymphocytes, plasma cell and fibroblasts,
(Central caseous necrosis)

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77
Q

symptoms of primary TB

A

Usually asymptomatic,

Sometimes fever and malaise

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78
Q

Symptoms of post-primary TB

A
May be asymptomatic for months,
Cough w/ sputum and haemoptysis,
Pleuritic pain,
Breathlessness,
(Malaise, fever, weight loss, night sweats)
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79
Q

CXR of post-primary TB

A

Patchy, often bilateral shadowing in upper zones/ upper lower lobe,
Cavitation if advanced,
Calcification if chronic or healed

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80
Q

Anti-tuberculous drug therapy

A

For 2 months: Rifampicin, Isoniazid, Ethambutol, Pyrazinamide

Then For 4 months: Rifampicin, Isoniazid

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81
Q

DOT

A

Directly Observed Therapy

needed to make sure TB patients take medication as multi-drug resistant organisms pose a world issue

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82
Q

Public health duties of doctors managing TB

A

Legal requirement to report all cases to public health,
Should ensure patients take drugs,
TB contact tracing: must screen close household contacts and, if they are infected, casual contacts.
HIV screening in patients from areas with high HIV prevalence.

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83
Q

Pathogenesis of primary TB

A

Inhaled mycobacteria implant in distal airspaces,
No preceding exposure or immunity (usually in children),
Usually no symptoms

Can be cleared, become latent, or progress

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84
Q

Pathogenesis of post-primary TB

A

Caused by reactivation of latent mycobacteria or new re-infection from an outside source.

May progress to:

  • TB caseous pneumonia (when lesions coalesce)
  • Miliary TB
  • Fibrocaseous TB
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85
Q

Fibrocaseous Tuberculosis

A

Large areas of fibrosis and caseous necrosis (cell death in which the dead tissue maintains a “cheese-like” appearance)

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86
Q

Miliary TB

A

TB that has disseminated throughout the body, characterised by minute tubercles

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87
Q

Caseating granuloma

A

A granuloma that shows caseous necrosis

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88
Q

Pharmacology of anti-tuberculous drugs

A

Rifampicin - inhibits mycobacterial RNA synthesis.
Isonazid - inhibits mycobacterial cell wall synthesis.
Ethambutol - inhibits mycobacterial cell wall synthesis
Pyrazinamide - inhibits mycobacterial growth.

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89
Q

CFTCR

A

Cystic Fibrosis Transmembrane Conductance Regulator

An active transport chloride channel found in many organs of the body

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90
Q

Mutations causing CF

A

There are ~30 mutations in the gene for CFTCR that cause cyctic fibrosis. Different mutations result in different phenotypes of the disease

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91
Q

Most common CFTCR gene mutation

A

Delta F508 - responsible for 2/3 cases worldwide.

A deletion of 3 nucleotides resulting in the loss of phenylalanine, producing a CFTCR protein with abnormal folding

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92
Q

Respiratory effects of CF

A

very thick secretions cause cillia collapse and excessive inflammation

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93
Q

Respiratory symptoms of CF

A
Progressive bronchiestasis (inflammation causing airway widening)
Recurrent LRTIs
Airflow obstruction - low FEV1
Cough w/ sputum production
Haemoptysis - due to infection
94
Q

GI effects of CF

A

digestive enzymes can’t leave pancreas, bile can’t leave liver

inhibits digestion, fat soluble vitamins and minerals not absorbed

95
Q

GI presentations of CF

A

Meconeum ileus/ DIOS
Diarrhoea
Malnutrition
Diabetes

96
Q

Possible complications of CF

A
Infertility,
Osteoporosis,
Diabetes 
Distal intestinal obstruction
Hepatopathy
97
Q

Reasons for infertility in CF

A

MALES:
vas deferens don’t develop in >95%

FEMALES:
fertile but malnutrition affects chances of conception

98
Q

Reasons for osteoporosis in CF

A

Vitamin D needed for bone development, but is a fat soluble vitamin so not absorbed as bile ducts are blocked. (bile needed to break down fat to be absorbed)

99
Q

Reasons for hepatopathy in CF

A

Bile produced is thick so blocks bile ducts. The surrounding liver becomes scarred, this fibrosis eventually spreads throughout the liver

100
Q

Management of pancreatic insufficiency in CF

A

Enteric coated enzyme pellets
High energy, high fat diet
Fat soluble vitamin and mineral supplements

101
Q

Management of chest infection in CF

A

Segregation of patients to prevent cross-infection
Prophylactic antibiotics
Annual influenza vaccination
Mucolytics (thin sputum)
Anti-inflammatory drugs (ibuprofen, azithromycin, prednisolone)
Physiotherapy - breathing techniques
- airway clearance devices

102
Q

Antenatal screening for CF

A

Chorionic Villous Sampling (CVS)

  • performed when parents have CF gene or foetus has echogenic (bright on ultrasound) bowel
  • 1% risk to baby
  • performed at ~11 weeks
103
Q

Neonatal screening for CF

A

Newborn blood spot (guthrie test) at 5 days
-measures immunoreactive trypsinogen (a pancreatic enzyme precursor found in neonates w/ CF)

If positive…

  1. mutation analysis
  2. sweat test
104
Q

Role of transplantation

A

Last resort treatment,
Not a miracle cure

Decision made by a multidisciplinary team

105
Q

For a transplant a patient should have…

A

FEV1 of <30%
hypoxia at rest,
hypercapnia,
worsening quality of life

106
Q

For a transplant a patient must/ should NOT have…

A
Other organ failure/ dysfunction,
Malignancty within 5 years,
Drug, nicotine or alcohol dependency,
Non-compliance,
Low BMI
107
Q

Symptoms of primary lung cancer

A
Chronic cough
Haemoptysis
Wheeze
Chest pain
Recurrent LRTIs
Difficulty swallowing
Hoarse voice
Dyspnoea
Weight loss
108
Q

Signs of primary lung cancer

A

Finger clubbing,
Lymphadenopathy,
Hepatomegaly (liver enlargement)
HPOA

109
Q

Coin lesion

A

a mass <3cm in diameter seen on CXR

110
Q

Causes of coin lesion on CXR

A
Primary lung cancer,
Metastasis,
Benign lung neoplasm,
Infection (e.g. TB)
Vascular haematoma (collection of blood)
111
Q

4 Types of lung carcinoma

A

Small cell lung cancer,

Adenocarcinoma,
Squamous cell carcinoma,
Large cell carcinoma

112
Q

Spread of lung cancer within the thorax

A

Lymph node metastasis,
Direct chest wall invasion
Direct invasion of nerves
Direct invasion of blood vessels (e.g. Superior vena cava)

113
Q

Horner’s syndrome

cause + symptoms

A

Caused by direct invasion of the sympathetic chain.

Causes a constricted pupil, droopy eyelid and decreased sweating on the same side as the invasion.

114
Q

Superior Vena Cava Obstruction Symptoms

A

Dyspnoea
Cough
Swelling of face, neck and arms

115
Q

Hypertrophic Pulmonary Osteoarthropathy (HPOA)

A

painful inflammation of the periosteum around ankles and wrists + finger clubbing

116
Q

Common distant metastases of lung cancer

A

Bone,
Brain,
Liver,
Adrenal glands

  • Lungs are the only organ that receives the entire body’s blood flow, so metastases to and from them are common
117
Q

Investigations for staging of lung cancer

A

Clinical history/ examination
(ECOG) Performance status
Pulmonary function

CXR
CT/PET

Bronchoscopy
Image guided biopsy
Mediastinoscopy/otomy
Surgical excision biopsy
Sputum cytology (rarely done)
118
Q

TNM staging

A

T = size and position of tumour

N = lymph node metastases

M = distant metastases

119
Q

Staging for SCLC

A

Limited disease (LD) = contained in thorax

Extensive disease (ED) = extrathoracic metastases

120
Q

Principles for surgical treatment of lung cancer

A

Remove all of tumour + minimum amount of lung tissue = curative resection

121
Q

Lung cancer surgeries

A

Wedge resection,
Segmental resection,
Lobectomy,
Pneumonectomy

122
Q

Thoracotomy

A

An incision into the pleural space to gain access to the thoracic organs

123
Q

Reasons for perioperative (after surgery) death

after lung cancer surgery

A
ARDS
Bronchopneumonia
MI
Pneumothorax
Intrathoracic bleeding
124
Q

Non-fatal complication of lung cancer surgery

A
Post thoracotomy wound pain
Empyema
Bronchopleural fistula
Wound infection
Post-Op respiratory insufficiency
125
Q

Radiotherapy side effects

A

Fibrosis - lung function tests essential,
Fatigue,
Dyspnoea + cough
loss of chest and neck hair

126
Q

Management of LD SCLC

A

Combination chemotherapy,
Early thoracic radiotherapy,
Prophylactic Cranial Irradiation (PCI)

127
Q

Management of ED SCLC

A

4 cycles combination chemotherapy,
PCI
Palliative RT (if not fit for chemo)

RT and steroids for brain mets

128
Q

Programmed Cell Death Pathway (Nivolumab)

A

Nivolumab blocks the binding of PDL1 (on cancer cells) to PD1 (on T-cells).
This precents T-cell inactivation

Increases 1yr survival from 24% to 42%

129
Q

Tyrosine Kinase Inhibitors

A

Inhibit transduction cascades + shrink solid tumours.

Well tolerated, tumour responses in many tumour types

130
Q

Monoclonal antibodies

A

e.g. Herceptin

Mab binds to cancer cell antigens, allows immune cells to recognise the cancer cells

131
Q

Chimeric Antigen Receptor (CAR) T-cell therapy

A

T-cells are induced to produce CARs which can recognise cancer cells

132
Q

Targeted drugs for adenocarcinoma with driver mutation

A

Approved drugs for 4 mutations/ rearrangements:

  • EGFR
  • ALK
  • ROS1
  • BRAF
133
Q

Bronchodilators for asthma management

A

B2 agonists
Anti-muscarinics
Theophylines (oral/IV)
Magnesium

134
Q

Anti-inflammatory asthma management

A

Inhaled corticosteroids - chronic
Oral steroids - acute
Leukotriene receptor antagonists (oral) - chronic
Monoclonal antibodies - anti IgE - chronic

135
Q

Types of inhalers

A

Pressurised Metered Dose Inhalers (pMDI) - can be with spacers

Dry Powder Inhalers (DPI)

136
Q

Benefit of inhalers

A

Direct delivery to target organ,
Small dosage,
Fast onset of effect,
Minimal systemic exposure

137
Q

Clinical management of acute, life threatening asthma

A

IV salbutamol
IV theophylline
IV/ nebulised magnesium
IV hydrocortisone

Intubate + ventilate

138
Q

Non-pharmacological management of asthma

A
Exercise
Smoking cessation
Weight management
Flu vaccinations
Asthma action plans
Inhaler technique
Allergen avoidance
Bronchial thermoplasty
139
Q

consolidation

A

pus in alveoli

140
Q

Symptoms of tonsillitis/ pharyngitis

A
Red, swollen tonsils,
White/ yellow coating/patches
Sore throat,
Difficult/ painful swallowing,
Lymphadenopathy,
Sneezing,
Runny nose,
Cough,
Fever
141
Q

Symptoms of the common cold

A
Runny/ blocked nose,
Sore throat,
Cough,
Sneezing,
Fever,
Malaise
142
Q

Epstein Barr Virus (glandular fever/ mononucleosis) Symptoms

A
Sore throat,
Lymphadenopathy,
Fever,
Fatigue,
Malaise,
Rash,
Lack of appetite
143
Q

Otitis Media Symptoms

A
Earache,
Hearing problems,
Ear discharge (if eardrum perforation),
Pink, bulging eardrum,
Fever
144
Q

Sinusitis Symptoms

A

Facial pain,
Nasal discharge,
Blocked nose,
Fever

145
Q

Common bacteria causing URTIs

A

Streptococcus pyogenes

146
Q

Common viruses causing URTIs

A
Rhinovirus,
Adenovirus,
Parainfluenza,
Influenza,
Epstein Barr Virus
147
Q

Symptoms + Signs of Acute Bronchitis

A
Hacking cough + yellow/green sputum,
Painful/ difficult breathing
Sore throat,
Headache,
Runny/ blocked nose,
Fatigue + Malaise

Wheeze
Crackles

148
Q

Symptoms of pneumonia

A

BRONCHOPNEUMONIA:
Cough + purulent sputum

LOBAR PNEUMONIA:
Cough + rusty sputum,
Haemoptysis,
Rigors

GENERAL:
Malaise,
Fever,
Chest pain (pleuritic),
Dyspnoea
149
Q

Signs of pneumonia

A
Pyrexia,
tachypnoea,
Central cyanosis,
Dullness on percussion,
Bronchial breath sounds,
Inspiratory crackles,
Increased vocal resonance
150
Q

Bronchiectasis

A

A permanent dilation of bronchi causing a build-up of sputum

151
Q

Symptoms and signs of bronchiectasis

A
*Chronic cough + sputum
Wheeze,
Dyspnoea,
Flitting chest pains,
Haemoptysis,
Fatigue

Finger clubbing,
Coarse inspiratory crackles

152
Q

Lung abscess

A

A pus filled cavity that often follows pneumonia

153
Q

Lung abscess symptoms and signs

A
Cough + purulent sputum
Haemoptysis,
Dyspnoea,
Fever,
Night sweats,
Weight loss,
Fatigue

Finger clubbing,
Bronchial breath sounds,
Localised dullness on percussion,

154
Q

Pathogenesis of bronchopneumonia

A

Patchy inflammation + consolidation in bronchioles.

Common in infants, elderly and immunocompromised patients.

Most commonly caused by Staph. aureus and H. influenzae

155
Q

Pathogenesis of lobar pneumonia

A

Inflammation + consolidation of alveoli in a whole lobe.

Common in healthy adults

Most commonly caused by strep. pneumoniae

156
Q

Complications and consequences of LRTIs

A
Pleurisy, 
Pleural effusion,
Empyema,
Fibrosis,
Lung abscess,
Bronchiectasis,
Septicaemia,
Metastatic infection,
ARDS
  • Most resolve
157
Q

Common organisms causing LRTIs

A

Strep. pneumoniae,
Haemophilus influenzae,
Moraxella catarrhalis,
Staph. aureus

ATYPICAL PATHOGENS:
Mycoplasma,
Chlamydia,
Coxiella,
Legionella

Viruses

158
Q

Causes of recurrent Pneumonia

A

Local bronchial obstruction (tumour, foreign body etc),
Generalised lung disease (e.g. COPD, CF)
Non-respiratory disease (e.g. HIV)
Local pulmonary damage (e.g. bronchiectasis)

159
Q

Differential spectrum of hospital acquired (nosocomial) vs. community acquired pneumonia

A

NOSOCOMIAL:
Staph. aureus,
Antibiotic resistant organisms

COMMUNITY ACQUIRED:
Strep. pneumoniae,
Haemophilus influenzae,
Viruses

160
Q

Usual antimicrobial therapy of LRTIs

A

LOW RISK, TREATED IN COMMUNITY:
-amoxycillin or clarithromycin/ doxycyclin

HOSPITAL TREATMENT REQUIRED:
-amoxycillin or levofloxacin (penicillin allergy) AND clarithromycin

HIGH RISK OF DEATH, ITU:
-co-amoxiclav or levofloxacin (penicillin allergy) AND clarithromycin

161
Q

Specialist antimicrobial therapy of LRTIs

A

ASPIRATION PNEUMONIA:
-metronidazole + amoxycillin (anaerobes)

MRSA:

  • vancomycin
  • OR linezolid
162
Q

Supportive therapy of LRTIs

in addition to antimicrobial therapy

A

Oxygen,
IV fluids,
Continuous Positive Airway Pressure (CPAP),
Intubation + ventilation

163
Q

Management of bronchiectasis

A

Chest physiotherapy,
Prompt antibiotic treatment of infections,

May need inhaled B2 agonists or corticosteroids

164
Q

Management of lung abscess

A

Prolonged antibiotics,

Occasionally percutaneous drainage

165
Q

Management of empyema

A

Chest drain,
IV antibiotics (sometimes prolonged),
Surgery (if above methods fail)

166
Q

Common clinical symptoms of restrictive lung diseases

A

Dyspnoea,
Cough,
Chest pain

167
Q

Diffuse Alveolar Damage Syndrome (DADS) definition

A

An acute interstitial syndrome characterised by:
Widespread inflammation and fibrosis in the alveoli

(Not an individual disease)

168
Q

Causes of DADS

A
Major trauma,
Infection,
Chemical injury (toxic inhalation),
Drugs,
Radiation
(sometimes idiopathic)
169
Q

Sarcoidosis

A

A multi-system granulomatous disease
(non-caseating granulomas form in many organs)
Most commonly affects lymph nodes and lungs

also called “Granulomatous lung disease”

170
Q

Cause of sarcoidosis

A

idiopathic

171
Q

Sarcoidosis investigations

A

CXR: Hilar lymphadenopathy + fibrosis, Honeycombing in later stages

Bronchoscopy: Hilar lymphadenopathy

Pulmonary function tests: Forced vital capacity <80% of predicted normal

Biopsy: Non-caseating granulomas (can be from any affected area)

172
Q

Sarcoidosis management

A

No treatment - if mild and few symptoms
Anti-inflammatories (NSAIDs)
Topical steroids - for skin lesions

Only some patients will progress, careful monitoring needed

173
Q

Idiopathic pulmonary fibrosis definition

A

Fibrotic scarring of lung tissue

174
Q

Idiopathic pulmonary fibrosis investigations

A

CXR: Basal/ posterior ground glass opacities, Honeycombing in later stages

Pulmonary function tests: Forced vital capacity <80% of predicted normal

Surgical biopsy: shows fibrosis

175
Q

Signs of interstitial lung disease

A

Crackles

Finger clubbing

176
Q

Chronic interstitial lung diseases

A

Idiopathic Pulmonary Fibrosis,
Hypersensitivity Pneumonitis,
Sarcoidosis

ACUTE: DADS

177
Q

Management of Idiopathic Pulmonary Fibrosis

A
OAF (oral anti-fibrotic)
Pirfenidone,
Nintendinab (inhibits fibrotic process kinases),
Palliative care,
Transplant
178
Q

Hypersensitivity Pneumonitis definition

A

Granulomatous inflammation of alveoli caused by type III and IV hypersensitivity reactions

179
Q

Causes of Hypersensitivity Pneumonitis

A
Animal proteins,
Fungi,
Organisms in mouldy hay,
Chemicals,
Etc....

*Occupational causes

180
Q

Hypersensitivity Pneumonitis investigations

A

CXR: Poorly defined small opacities. Honeycombing in later stages

Pulmonary function tests: Forced vital capacity <80% of predicted normal

Bloods: ↑IgG

Bronchoscopy + Biopsy: Centriacinar granulomas

181
Q

Hypersensitivity Pneumonitis management

A

Allergen avoidance,

Corticosteroids (e.g. prednisolone)

182
Q

Causes of restrictive lung disease

A

Most common: Interstitial lung disese (pulmonary fibrosis)

NON-LUNG CAUSES:
Pleural effusion,
Pneumothorax,
Pleural thickening,
Kyphoscoliosis,
Rib fractures,
Amyotrophic lateral sclerosis (muscular),
Obesity,
Pregnancy
183
Q

Lung Interstitium definition

A

The (potential) space between the alveolar epithelium and the capillary endothelium

184
Q

End-stage lung fibrosis/ Honeycomb lung

A

A shrunken, fibrotic, barely functioning lung caused by progressive fibrosis of lung tissue in interstitial lung diseases

185
Q

Symptoms of Honeycomb Lung

A
  • Dyspnoea,
  • Dry cough,

Haemoptysis,
Wheeze,
Chest pain

186
Q

People most likely to smoke

A

Permanently sick/ disabled,
Unemployed and seeking work,
Looking after home/ family

187
Q

Strategies to reduce smoking

A
Standardised packaging,
Ban in public places and workplaces,
Smoking advisory service
Taxation
Laws forbidding vending machines, proxy purchases etc.

*5000 people in UK employed in tobacco industry

188
Q

Obstructive Sleep Apnoea Syndrome (OSAS)

A

Recurrent episodes of upper airway obstruction leading to apnoea (cessation of breathing) during sleep

189
Q

Presentations of sleep apnoea

A
Heavy snoring,
Unrefreshing sleep,
Daytime somnolence/ sleepiness,
Poor daytime concentration,
Oxygen desaturation (sometimes)
190
Q

Paediatric presentations of sleep apnoea

A

Failure to thrive,
Neurocognitive defects/ ADHD,
Systemic hypertension,
Cor pulmonale

191
Q

Conditions associated with sleep apnoea

A

Hypertension,
Increased risk of stroke,
Increased risk of heat disease (maybe)

192
Q

Consequences of untreated sleep apnoea

A

Impaired quality of life,
Marital disharmony,
Increased risk of road traffic accident (RTA)

193
Q

Management of sleep apnoea

A

Identify exacerbating factors
(weight reduction, alcohol avoidance, treatment of endocrine disorders - e.g. hypothyroidism)

Continuous Positive Airway pressure (CPAP),
Mandibular repositioning splint

*Advise not to drive and inform DVLA until treated

194
Q

Paediatric management of sleep apnoea

A

Adenotonsillectomy,
CPAP,
Weight loss,
Avoid environmental tobacco smoke

195
Q

Other conditions causing excessive daytime sleepiness (not OSAS)

A

Narcolepsy,

Neuromuscular respiratory failure

196
Q

Neurological conditions associated with respiratory muscle weakness

A

Motor neurone disease (ALS)

Muscular dystrophy

197
Q

Symptoms of respiratory muscle weakness

A

Dyspnoea Recurrent chest infections Orthopnoea Morning headache Disturbed sleep

Worse during/ after sleep as accessory muscles paralysed and diaphragm weak

198
Q

Signs of respiratory muscle weakness

A
Ankle oedema
Paradoxical breathing
↑ pCO2
↓ pO2
↑ bicarbonate (Retained from kidneys to    maintain pH)
199
Q

Investigations of respiratory muscle weakness

A

Lung function: ↓FEV1, ↓FVC , ↑FEV1/FVC
↓inspiratory and expiratory mouth pressures

Assessment of hypoventilation:
Overnight oximetry: desaturation
Early morning arterial blood gases: ↑ pCO2, ↓ pO2

200
Q

Management of respiratory muscle weakness

A

Non-invasive ventilation (NIV),

Oxygen therapy

201
Q

Orthopnoea

A

Shortness of breath lying flat

202
Q

Epworth score

A

a subjective measure of sleepiness.

8 situations are rated 0-3 according to how likely the patient is to doze

203
Q

Pressurised Metered Dose Inhalers (pMDI)

A

Normal inhaler
Aerosol so low inspiratory flow needed
Needs coordination
Children must use spacers

204
Q

Dry Powder Inhalers (DPI)

A

Patient generates aerosol so high inspiratory flow needed

Less coordination required

205
Q

Inhaled therapy for COPD

A
  1. SABA
    • LAMA or LABA
    • LAMA and LABA
    • ICS
206
Q

Signs of asthma

A

Polyphonic wheezes

Hyperexpanded chest

207
Q

Signs of COPD

A
CO2 flap
Hyperexpanded (barrel) chest
Paradoxical movement of ribs and abdomen
Reduced chest expansion
Laryngeal descent
↓ dullness to percussion
↓ breath sounds

Signs of respiratory failure:
Tachypnoea, Cyanosis, Use of accessory muscles, Pursed lip breathing, Peripheral oedema

208
Q

Causes of wheeze

A
Asthma
COPD
Acute bronchitis
Cystic fibrosis
Congestive heart failure
Pulmonary neoplasia
Bronchiectasis
Tracheobronchomalacia
209
Q

Pulmonary Infarction Investigations

A
FBC: ↑WBC, ↑ESR
Blood gasses: ↓PO2, ↑PCO2
D-dimer: ↑ if PE
CXR/CT: wedge shaped opacity
CT PA: Shows occlusion
V/Q scan: Low perfusion
210
Q

Symptoms of pulmonary infarction

A

Haemoptysis
Dyspnoea
Pleuritic chest pain

211
Q

Supportive therapy in the treatment of LRTIs

A

Oxygen
IV fluids
CPAP
Intubation + ventilation

212
Q

“Tracking” of pulmonary function

A

Reduced pulmonary development in early life leads to early decline of pulmonary function in adulthood

213
Q

PET/CT

A

PET and CT images are superimposed to give one, more accurate image
Whole body PET/CT used to find metastases

214
Q

Factors influencing lung cancer management

A

Stage
Type (from tissue diagnosis)
ECOG Performance status

215
Q

Pulmonary neoplasia pathogenesis

A

Uncontrolled cell growth caused by mutations in the epithelial cells in the airways
Carcinogens have a synergistic effect

216
Q

Performance status measurement for lung cancer

A
0 = asymptomatic
1 = symptomatic, able to do light work
2 = has to rest but for <50% of the day
3 = has to rest > 50% of the day
4 = bedbound

Used to decide therapeutic options

217
Q

Chemotherapy side effects

A
Nausea + Vomiting
Hair loss
Bleeding/ clotting problems
Loss of appetite
Diarrhoea
Constipation
Fatigue
218
Q

Non-small cell lung cancer management

A

Surgery (usually inoperable)
Radiotherapy
Chemotherapy
Chemoradiotherapy

219
Q

Stage III NSCLC Management

A

Radical Radiotherapy

Chemoradiotherapy

220
Q

Stage IV NSCLC Management

A

Incurable

Palliative RT = symptomatic benefit (esp bone pain from metastases)

Palliative chemo = symptomatic benefit + survival advantage

221
Q

Palliative management of lung cancer

A

Symptom control, may include:

  • Chemotherapy
  • Radiotherapy
  • Opiates
  • Treatment of hypercalcaemia, hyponatraemia, dehydration etc.

Decisions and planning

222
Q

Sarcoidosis symptoms

A

Dyspnoea
Cough
Skin lesions
Arthalgia

223
Q

Idiopathic pulmonary fibrosis symptoms

A

Dyspnoea
Cough
Fatigue
Weight loss

224
Q

Hypersensitivity pneumonitis symptoms

A

Chronic:
Dyspnoea
Cough
Malaise

Acute
Cough
Fever
Chills
Myalgia
*Can lead to respiratory failure
225
Q

Functional effects of restrictive lung disease

A

Diseases resulting in:

  • decreased lung volume
  • increased inspiratory effort
  • inadequate ventilation/ oxygenation
226
Q

Interstitial lung diseases

A

Diseases causing thickening of the interstitium resulting in progressive fibrosis of lung tissue.

Normal lung tissue is gradually replaced by scar tissue

227
Q

Signs of TB

A

May be none

ADVANCED DISEASE:
Crackles
Bronchial breathing
Finger clubbing (rare unless very chronic)

228
Q

Side effects of rifampicin

A

Orange urine + tears
OCP ineffective
Hepatitis

229
Q

Side effects of isoniazid

A

Hepatitis

Peripheral neuropathy

230
Q

Side effects of pyrazinamide

A

gout

231
Q

Side effects of ethambutol

A

Optic neuropathy