Clinical Respiratory Medicine Flashcards

(231 cards)

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
Atopy
a (genetic) predisposition toward developing type I hypersensitivity reactions (excessive IgE production)
26
Hyperplasia
increased proliferation
27
Emphysema pathophysiology
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
28
Centriacinar emphysema
smoke particles get trapped in the airspaces of the bronchioles causing inflammation. neutrophils make elastase which destroys elastin
29
Panacinar emphysema
a-1 antitrypsin (a protein which destroys elastase) deficiency. leads to elastin destruction in bronchioles and alveoli
30
Periacinar (bullous) emphysema
alveoli expand to form large (>1cm) air spaces called bulla. rupture can leak air into the pleural cavity causing pneumothorax
31
Clinical definition of chronic bronchitis
a cough lasting for at least 3 consecutive months of the year for at least 2 consecutive years
32
Morphological changes of large airways in chronic bronchitis
- mucous gland hyperplasia - goblet cell hyperplasia - some inflammation and fibrosis
33
morphological changes of small airways in chronic bronchitis
- goblet cells appear | - inflammation and fibrosis (in long standing disease)
34
cause of obstruction in chronic bronchitis
airways obstructed by thick mucous and fibrosis
35
Causes of hypoxaemia in COPD
- 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
36
Hypoxic cor pulmonale
enlargement of the right ventricle of the heart. | because higher blood pressure is needed in the lungs due to vasoconstriction due to shunt
37
Asthma mechanism
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
38
Clinical definition of asthma
Chronic airflow obstruction causing WHEEZE which is VARIABLE and REVERSIBLE with asthma treatment
39
Symptoms of asthma
Wheeze Dry cough Dyspnoea (at rest) Chest tightness
40
Investigations used for diagnosis of asthma
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
41
Definition of COPD
``` airway obstruction (chronic bronchitis) and hyperinflation (emphysema). Constant and not fully reversible ```
42
Symptoms of COPD
``` Breathlessness on exertion chronic cough with sputum recurrent chest infections wheeze/ chest tightness weight loss ```
43
Investigations used for diagnosis of COPD
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
44
Management strategies for COPD
smoking cessation! vaccinations (increased risk of respiratory infection) long term oxygen therapy pulmonary rehabilitation (exercise, support, etc.) Inhaled therapy
45
characteristics of obstructive lung diseases
airflow limitation reduced peak expiratory flow rate reduced FEV1
46
pathogenesis
the development of a disease from the causes and origin to the end stages
47
Pulmonary embolism deffinition
a thrombus (blood clot) formed in the venous system that embolises to the pulmonary arteries
48
pulmonary embolism symptoms
pleuritic chest pain cough + haemoptysis dyspnoea MASSIVE PE: syncope cardiac arrest
49
pulmonary embolism investigations
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
50
Pulmonary embolism management
Immediate oxygen for resuscitation Anticoagulation: Heparin, Warfarin, DOACs Massive PE: Thrombolysis Pulmonary embolectomy
51
pulmonary infarction definition
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
52
pulmonary infarction management
100% oxygen (for initial resuscitation) mechanical ventilation ultimately depends on cause
53
pulmonary hypertension definition
elevated blood pressure (>25mmHg) in pulmonary arteries
54
causes of pulmonary hypertension
``` 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 ```
55
symptoms of pulmonary hypertension
exertional dyspnoea exertional presyncope/ syncope chest tightness
56
pulmonary hypertension investigations
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
57
management of pulmonary hypertension
``` Treatment of underlying condition Oxygen Anticoagulation Diuretics Lung/ Heart transplant Thromboendarterectomy (CTEPH) ``` PULMONARY VASODILATORS: CCBs Endothelin receptor antagonists Phosphodiesterase inhibitors Prostacyclin
58
theophyllines
IV/ oral bronchodilator used in asthma
59
venography
x-ray of the veins using an IV contrast. used to identify DVT and PE
60
Pleural effusion definition
an abnormal collection of fluid in the pleural space
61
Transudates
caused by an imbalance of hydrostatic forces influencing formation and absorption of pleural fluid usually bilateral pleural fluid protein <30g/l
62
Exudates
caused by an increase in the permeability of the pleural surface and/or local capillaries. usually unilateral pleural fluid protein >30g/l
63
Causes of transudates
left ventricular failure liver cirrhosis hypoalbuminaemia peritoneal dialysis hypothyroidism nephrotic syndrome mitral stenosis pulmonary embolism constrictive pericarditis ovarian hyperstimulation syndrome meig's syndrome
64
Causes of exudates
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......
65
Symptoms of pleural effusion
- 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...
66
Signs of pleural effusion
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 ```
67
when to investigate pleural effusion
clinical picture is usually characteristic for bilateral transudate. investigate if... -is unilateral unusual features fails to respond to appropriate treatment
68
Investigations for pleural effusion
1. CXR (confirms presence) 2. CT (differentiates malignant from benign) 3. Pleural aspiration 4. Pleural biopsy 5. Thoracoscopy
69
Management of pleural effusion
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
70
Malignant mesothelioma defnition
pleural malignanct caused by exposure to aasbestos (occurs 20-40yrs after exposure)
71
Malignant mesothelioma clinical presentations
breathlessness chest wall pain radiology = usually unilateral pleural thickening
72
Malignant mesothelioma treatment
pleuropneumonectomy (remova of entire lung and parietal pleura) if very fit otherwise, palliative treatment
73
pleural fibrosis
caused by inflammation, surgical trauma, pleural effusion, asbestos etc. pleura develops fibrous tissue and loses elastic properties which impairs lung function
74
pleural plaques
Benign plaques of the pleura caused by asbestos exposure. Can become calcified but rarely inhibit lung function. almost always asymptomatic
75
Empyema
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
76
appearance of tuberculous granuloma in TB
Rounded outline, Epithelioid and langhan's giant cells (transformed macrophages), Lymphocytes, plasma cell and fibroblasts, (Central caseous necrosis)
77
symptoms of primary TB
Usually asymptomatic, | Sometimes fever and malaise
78
Symptoms of post-primary TB
``` May be asymptomatic for months, Cough w/ sputum and haemoptysis, Pleuritic pain, Breathlessness, (Malaise, fever, weight loss, night sweats) ```
79
CXR of post-primary TB
Patchy, often bilateral shadowing in upper zones/ upper lower lobe, Cavitation if advanced, Calcification if chronic or healed
80
Anti-tuberculous drug therapy
For 2 months: Rifampicin, Isoniazid, Ethambutol, Pyrazinamide Then For 4 months: Rifampicin, Isoniazid
81
DOT
Directly Observed Therapy needed to make sure TB patients take medication as multi-drug resistant organisms pose a world issue
82
Public health duties of doctors managing TB
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.
83
Pathogenesis of primary TB
Inhaled mycobacteria implant in distal airspaces, No preceding exposure or immunity (usually in children), Usually no symptoms Can be cleared, become latent, or progress
84
Pathogenesis of post-primary TB
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
85
Fibrocaseous Tuberculosis
Large areas of fibrosis and caseous necrosis (cell death in which the dead tissue maintains a "cheese-like" appearance)
86
Miliary TB
TB that has disseminated throughout the body, characterised by minute tubercles
87
Caseating granuloma
A granuloma that shows caseous necrosis
88
Pharmacology of anti-tuberculous drugs
Rifampicin - inhibits mycobacterial RNA synthesis. Isonazid - inhibits mycobacterial cell wall synthesis. Ethambutol - inhibits mycobacterial cell wall synthesis Pyrazinamide - inhibits mycobacterial growth.
89
CFTCR
Cystic Fibrosis Transmembrane Conductance Regulator An active transport chloride channel found in many organs of the body
90
Mutations causing CF
There are ~30 mutations in the gene for CFTCR that cause cyctic fibrosis. Different mutations result in different phenotypes of the disease
91
Most common CFTCR gene mutation
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
92
Respiratory effects of CF
very thick secretions cause cillia collapse and excessive inflammation
93
Respiratory symptoms of CF
``` Progressive bronchiestasis (inflammation causing airway widening) Recurrent LRTIs Airflow obstruction - low FEV1 Cough w/ sputum production Haemoptysis - due to infection ```
94
GI effects of CF
digestive enzymes can't leave pancreas, bile can't leave liver inhibits digestion, fat soluble vitamins and minerals not absorbed
95
GI presentations of CF
Meconeum ileus/ DIOS Diarrhoea Malnutrition Diabetes
96
Possible complications of CF
``` Infertility, Osteoporosis, Diabetes Distal intestinal obstruction Hepatopathy ```
97
Reasons for infertility in CF
MALES: vas deferens don't develop in >95% FEMALES: fertile but malnutrition affects chances of conception
98
Reasons for osteoporosis in CF
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
Reasons for hepatopathy in CF
Bile produced is thick so blocks bile ducts. The surrounding liver becomes scarred, this fibrosis eventually spreads throughout the liver
100
Management of pancreatic insufficiency in CF
Enteric coated enzyme pellets High energy, high fat diet Fat soluble vitamin and mineral supplements
101
Management of chest infection in CF
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
Antenatal screening for CF
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
Neonatal screening for CF
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
Role of transplantation
Last resort treatment, Not a miracle cure Decision made by a multidisciplinary team
105
For a transplant a patient should have...
FEV1 of <30% hypoxia at rest, hypercapnia, worsening quality of life
106
For a transplant a patient must/ should NOT have...
``` Other organ failure/ dysfunction, Malignancty within 5 years, Drug, nicotine or alcohol dependency, Non-compliance, Low BMI ```
107
Symptoms of primary lung cancer
``` Chronic cough Haemoptysis Wheeze Chest pain Recurrent LRTIs Difficulty swallowing Hoarse voice Dyspnoea Weight loss ```
108
Signs of primary lung cancer
Finger clubbing, Lymphadenopathy, Hepatomegaly (liver enlargement) HPOA
109
Coin lesion
a mass <3cm in diameter seen on CXR
110
Causes of coin lesion on CXR
``` Primary lung cancer, Metastasis, Benign lung neoplasm, Infection (e.g. TB) Vascular haematoma (collection of blood) ```
111
4 Types of lung carcinoma
Small cell lung cancer, Adenocarcinoma, Squamous cell carcinoma, Large cell carcinoma
112
Spread of lung cancer within the thorax
Lymph node metastasis, Direct chest wall invasion Direct invasion of nerves Direct invasion of blood vessels (e.g. Superior vena cava)
113
Horner's syndrome | cause + symptoms
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
Superior Vena Cava Obstruction Symptoms
Dyspnoea Cough Swelling of face, neck and arms
115
Hypertrophic Pulmonary Osteoarthropathy (HPOA)
painful inflammation of the periosteum around ankles and wrists + finger clubbing
116
Common distant metastases of lung cancer
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
Investigations for staging of lung cancer
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
TNM staging
T = size and position of tumour N = lymph node metastases M = distant metastases
119
Staging for SCLC
Limited disease (LD) = contained in thorax Extensive disease (ED) = extrathoracic metastases
120
Principles for surgical treatment of lung cancer
Remove all of tumour + minimum amount of lung tissue = curative resection
121
Lung cancer surgeries
Wedge resection, Segmental resection, Lobectomy, Pneumonectomy
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Thoracotomy
An incision into the pleural space to gain access to the thoracic organs
123
Reasons for perioperative (after surgery) death | after lung cancer surgery
``` ARDS Bronchopneumonia MI Pneumothorax Intrathoracic bleeding ```
124
Non-fatal complication of lung cancer surgery
``` Post thoracotomy wound pain Empyema Bronchopleural fistula Wound infection Post-Op respiratory insufficiency ```
125
Radiotherapy side effects
Fibrosis - lung function tests essential, Fatigue, Dyspnoea + cough loss of chest and neck hair
126
Management of LD SCLC
Combination chemotherapy, Early thoracic radiotherapy, Prophylactic Cranial Irradiation (PCI)
127
Management of ED SCLC
4 cycles combination chemotherapy, PCI Palliative RT (if not fit for chemo) RT and steroids for brain mets
128
Programmed Cell Death Pathway (Nivolumab)
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
Tyrosine Kinase Inhibitors
Inhibit transduction cascades + shrink solid tumours. Well tolerated, tumour responses in many tumour types
130
Monoclonal antibodies
e.g. Herceptin Mab binds to cancer cell antigens, allows immune cells to recognise the cancer cells
131
Chimeric Antigen Receptor (CAR) T-cell therapy
T-cells are induced to produce CARs which can recognise cancer cells
132
Targeted drugs for adenocarcinoma with driver mutation
Approved drugs for 4 mutations/ rearrangements: - EGFR - ALK - ROS1 - BRAF
133
Bronchodilators for asthma management
B2 agonists Anti-muscarinics Theophylines (oral/IV) Magnesium
134
Anti-inflammatory asthma management
Inhaled corticosteroids - chronic Oral steroids - acute Leukotriene receptor antagonists (oral) - chronic Monoclonal antibodies - anti IgE - chronic
135
Types of inhalers
Pressurised Metered Dose Inhalers (pMDI) - can be with spacers Dry Powder Inhalers (DPI)
136
Benefit of inhalers
Direct delivery to target organ, Small dosage, Fast onset of effect, Minimal systemic exposure
137
Clinical management of acute, life threatening asthma
IV salbutamol IV theophylline IV/ nebulised magnesium IV hydrocortisone Intubate + ventilate
138
Non-pharmacological management of asthma
``` Exercise Smoking cessation Weight management Flu vaccinations Asthma action plans Inhaler technique Allergen avoidance Bronchial thermoplasty ```
139
consolidation
pus in alveoli
140
Symptoms of tonsillitis/ pharyngitis
``` Red, swollen tonsils, White/ yellow coating/patches Sore throat, Difficult/ painful swallowing, Lymphadenopathy, Sneezing, Runny nose, Cough, Fever ```
141
Symptoms of the common cold
``` Runny/ blocked nose, Sore throat, Cough, Sneezing, Fever, Malaise ```
142
Epstein Barr Virus (glandular fever/ mononucleosis) Symptoms
``` Sore throat, Lymphadenopathy, Fever, Fatigue, Malaise, Rash, Lack of appetite ```
143
Otitis Media Symptoms
``` Earache, Hearing problems, Ear discharge (if eardrum perforation), Pink, bulging eardrum, Fever ```
144
Sinusitis Symptoms
Facial pain, Nasal discharge, Blocked nose, Fever
145
Common bacteria causing URTIs
Streptococcus pyogenes
146
Common viruses causing URTIs
``` Rhinovirus, Adenovirus, Parainfluenza, Influenza, Epstein Barr Virus ```
147
Symptoms + Signs of Acute Bronchitis
``` Hacking cough + yellow/green sputum, Painful/ difficult breathing Sore throat, Headache, Runny/ blocked nose, Fatigue + Malaise ``` Wheeze Crackles
148
Symptoms of pneumonia
BRONCHOPNEUMONIA: Cough + purulent sputum LOBAR PNEUMONIA: Cough + rusty sputum, Haemoptysis, Rigors ``` GENERAL: Malaise, Fever, Chest pain (pleuritic), Dyspnoea ```
149
Signs of pneumonia
``` Pyrexia, tachypnoea, Central cyanosis, Dullness on percussion, Bronchial breath sounds, Inspiratory crackles, Increased vocal resonance ```
150
Bronchiectasis
A permanent dilation of bronchi causing a build-up of sputum
151
Symptoms and signs of bronchiectasis
``` *Chronic cough + sputum Wheeze, Dyspnoea, Flitting chest pains, Haemoptysis, Fatigue ``` Finger clubbing, Coarse inspiratory crackles
152
Lung abscess
A pus filled cavity that often follows pneumonia
153
Lung abscess symptoms and signs
``` Cough + purulent sputum Haemoptysis, Dyspnoea, Fever, Night sweats, Weight loss, Fatigue ``` Finger clubbing, Bronchial breath sounds, Localised dullness on percussion,
154
Pathogenesis of bronchopneumonia
Patchy inflammation + consolidation in bronchioles. Common in infants, elderly and immunocompromised patients. Most commonly caused by Staph. aureus and H. influenzae
155
Pathogenesis of lobar pneumonia
Inflammation + consolidation of alveoli in a whole lobe. Common in healthy adults Most commonly caused by strep. pneumoniae
156
Complications and consequences of LRTIs
``` Pleurisy, Pleural effusion, Empyema, Fibrosis, Lung abscess, Bronchiectasis, Septicaemia, Metastatic infection, ARDS ``` * Most resolve
157
Common organisms causing LRTIs
Strep. pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, Staph. aureus ``` ATYPICAL PATHOGENS: Mycoplasma, Chlamydia, Coxiella, Legionella ``` Viruses
158
Causes of recurrent Pneumonia
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
Differential spectrum of hospital acquired (nosocomial) vs. community acquired pneumonia
NOSOCOMIAL: Staph. aureus, Antibiotic resistant organisms COMMUNITY ACQUIRED: Strep. pneumoniae, Haemophilus influenzae, Viruses
160
Usual antimicrobial therapy of LRTIs
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
Specialist antimicrobial therapy of LRTIs
ASPIRATION PNEUMONIA: -metronidazole + amoxycillin (anaerobes) MRSA: - vancomycin - OR linezolid
162
Supportive therapy of LRTIs | in addition to antimicrobial therapy
Oxygen, IV fluids, Continuous Positive Airway Pressure (CPAP), Intubation + ventilation
163
Management of bronchiectasis
Chest physiotherapy, Prompt antibiotic treatment of infections, May need inhaled B2 agonists or corticosteroids
164
Management of lung abscess
Prolonged antibiotics, | Occasionally percutaneous drainage
165
Management of empyema
Chest drain, IV antibiotics (sometimes prolonged), Surgery (if above methods fail)
166
Common clinical symptoms of restrictive lung diseases
Dyspnoea, Cough, Chest pain
167
Diffuse Alveolar Damage Syndrome (DADS) definition
An acute interstitial syndrome characterised by: Widespread inflammation and fibrosis in the alveoli (Not an individual disease)
168
Causes of DADS
``` Major trauma, Infection, Chemical injury (toxic inhalation), Drugs, Radiation (sometimes idiopathic) ```
169
Sarcoidosis
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
Cause of sarcoidosis
idiopathic
171
Sarcoidosis investigations
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)
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Sarcoidosis management
No treatment - if mild and few symptoms Anti-inflammatories (NSAIDs) Topical steroids - for skin lesions Only some patients will progress, careful monitoring needed
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Idiopathic pulmonary fibrosis definition
Fibrotic scarring of lung tissue
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Idiopathic pulmonary fibrosis investigations
CXR: Basal/ posterior ground glass opacities, Honeycombing in later stages Pulmonary function tests: Forced vital capacity <80% of predicted normal Surgical biopsy: shows fibrosis
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Signs of interstitial lung disease
Crackles | Finger clubbing
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Chronic interstitial lung diseases
Idiopathic Pulmonary Fibrosis, Hypersensitivity Pneumonitis, Sarcoidosis ACUTE: DADS
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Management of Idiopathic Pulmonary Fibrosis
``` OAF (oral anti-fibrotic) Pirfenidone, Nintendinab (inhibits fibrotic process kinases), Palliative care, Transplant ```
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Hypersensitivity Pneumonitis definition
Granulomatous inflammation of alveoli caused by type III and IV hypersensitivity reactions
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Causes of Hypersensitivity Pneumonitis
``` Animal proteins, Fungi, Organisms in mouldy hay, Chemicals, Etc.... ``` *Occupational causes
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Hypersensitivity Pneumonitis investigations
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
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Hypersensitivity Pneumonitis management
Allergen avoidance, | Corticosteroids (e.g. prednisolone)
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Causes of restrictive lung disease
Most common: Interstitial lung disese (pulmonary fibrosis) ``` NON-LUNG CAUSES: Pleural effusion, Pneumothorax, Pleural thickening, Kyphoscoliosis, Rib fractures, Amyotrophic lateral sclerosis (muscular), Obesity, Pregnancy ```
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Lung Interstitium definition
The (potential) space between the alveolar epithelium and the capillary endothelium
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End-stage lung fibrosis/ Honeycomb lung
A shrunken, fibrotic, barely functioning lung caused by progressive fibrosis of lung tissue in interstitial lung diseases
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Symptoms of Honeycomb Lung
* Dyspnoea, * Dry cough, Haemoptysis, Wheeze, Chest pain
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People most likely to smoke
Permanently sick/ disabled, Unemployed and seeking work, Looking after home/ family
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Strategies to reduce smoking
``` 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
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Obstructive Sleep Apnoea Syndrome (OSAS)
Recurrent episodes of upper airway obstruction leading to apnoea (cessation of breathing) during sleep
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Presentations of sleep apnoea
``` Heavy snoring, Unrefreshing sleep, Daytime somnolence/ sleepiness, Poor daytime concentration, Oxygen desaturation (sometimes) ```
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Paediatric presentations of sleep apnoea
Failure to thrive, Neurocognitive defects/ ADHD, Systemic hypertension, Cor pulmonale
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Conditions associated with sleep apnoea
Hypertension, Increased risk of stroke, Increased risk of heat disease (maybe)
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Consequences of untreated sleep apnoea
Impaired quality of life, Marital disharmony, Increased risk of road traffic accident (RTA)
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Management of sleep apnoea
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
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Paediatric management of sleep apnoea
Adenotonsillectomy, CPAP, Weight loss, Avoid environmental tobacco smoke
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Other conditions causing excessive daytime sleepiness (not OSAS)
Narcolepsy, | Neuromuscular respiratory failure
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Neurological conditions associated with respiratory muscle weakness
Motor neurone disease (ALS) | Muscular dystrophy
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Symptoms of respiratory muscle weakness
Dyspnoea Recurrent chest infections Orthopnoea Morning headache Disturbed sleep *Worse during/ after sleep as accessory muscles paralysed and diaphragm weak*
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Signs of respiratory muscle weakness
``` Ankle oedema Paradoxical breathing ↑ pCO2 ↓ pO2 ↑ bicarbonate (Retained from kidneys to maintain pH) ```
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Investigations of respiratory muscle weakness
Lung function: ↓FEV1, ↓FVC , ↑FEV1/FVC ↓inspiratory and expiratory mouth pressures Assessment of hypoventilation: Overnight oximetry: desaturation Early morning arterial blood gases: ↑ pCO2, ↓ pO2
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Management of respiratory muscle weakness
Non-invasive ventilation (NIV), | Oxygen therapy
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Orthopnoea
Shortness of breath lying flat
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Epworth score
a subjective measure of sleepiness. | 8 situations are rated 0-3 according to how likely the patient is to doze
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Pressurised Metered Dose Inhalers (pMDI)
*Normal inhaler* Aerosol so low inspiratory flow needed Needs coordination Children must use spacers
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Dry Powder Inhalers (DPI)
Patient generates aerosol so high inspiratory flow needed | Less coordination required
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Inhaled therapy for COPD
1. SABA 2. + LAMA or LABA 3. + LAMA and LABA 4. + ICS
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Signs of asthma
Polyphonic wheezes | Hyperexpanded chest
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Signs of COPD
``` 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
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Causes of wheeze
``` Asthma COPD Acute bronchitis Cystic fibrosis Congestive heart failure Pulmonary neoplasia Bronchiectasis Tracheobronchomalacia ```
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Pulmonary Infarction Investigations
``` 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 ```
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Symptoms of pulmonary infarction
Haemoptysis Dyspnoea Pleuritic chest pain
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Supportive therapy in the treatment of LRTIs
Oxygen IV fluids CPAP Intubation + ventilation
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"Tracking" of pulmonary function
Reduced pulmonary development in early life leads to early decline of pulmonary function in adulthood
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PET/CT
PET and CT images are superimposed to give one, more accurate image Whole body PET/CT used to find metastases
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Factors influencing lung cancer management
Stage Type (from tissue diagnosis) ECOG Performance status
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Pulmonary neoplasia pathogenesis
Uncontrolled cell growth caused by mutations in the epithelial cells in the airways Carcinogens have a synergistic effect
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Performance status measurement for lung cancer
``` 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
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Chemotherapy side effects
``` Nausea + Vomiting Hair loss Bleeding/ clotting problems Loss of appetite Diarrhoea Constipation Fatigue ```
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Non-small cell lung cancer management
Surgery (usually inoperable) Radiotherapy Chemotherapy Chemoradiotherapy
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Stage III NSCLC Management
Radical Radiotherapy Chemoradiotherapy
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Stage IV NSCLC Management
Incurable Palliative RT = symptomatic benefit (esp bone pain from metastases) Palliative chemo = symptomatic benefit + survival advantage
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Palliative management of lung cancer
Symptom control, may include: - Chemotherapy - Radiotherapy - Opiates - Treatment of hypercalcaemia, hyponatraemia, dehydration etc. Decisions and planning
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Sarcoidosis symptoms
Dyspnoea Cough Skin lesions Arthalgia
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Idiopathic pulmonary fibrosis symptoms
Dyspnoea Cough Fatigue Weight loss
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Hypersensitivity pneumonitis symptoms
Chronic: Dyspnoea Cough Malaise ``` Acute Cough Fever Chills Myalgia *Can lead to respiratory failure ```
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Functional effects of restrictive lung disease
Diseases resulting in: - decreased lung volume - increased inspiratory effort - inadequate ventilation/ oxygenation
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Interstitial lung diseases
Diseases causing thickening of the interstitium resulting in progressive fibrosis of lung tissue. Normal lung tissue is gradually replaced by scar tissue
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Signs of TB
May be none ADVANCED DISEASE: Crackles Bronchial breathing Finger clubbing (rare unless very chronic)
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Side effects of rifampicin
Orange urine + tears OCP ineffective Hepatitis
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Side effects of isoniazid
Hepatitis | Peripheral neuropathy
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Side effects of pyrazinamide
gout
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Side effects of ethambutol
Optic neuropathy