Respiratory Flashcards

1
Q

CHRONIC OBSTRUCTIVE PULMONARY DISEASE

What features show it is more likely a patient has COPD than Asthma?

A

1) Onset >35
2) Smoking/pollution related
3) Chronic Dyspnoea
4) Sputum production

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2
Q

What is Chronic Bronchitis?

A
  • Cough and sputum production for 3+ months in 2 consecutive years
  • Permanent narrowing of the airways
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3
Q

What are the causes of Chronic bronchitis?

A
  • mucous gland hypertrophy and hyperplasia

- bronchial wall inflammation and mucosal oedema

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4
Q

How would a patient appear if they had Chronic Bronchitis?

A

’ Blue Bloaters’

  • Overnight
  • Peripheral Oedema
  • Cyanosed
  • Low PaO2 and high PaCO2
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5
Q

why should we be careful when giving O2 therapy to someone with Chronic bronchitis?

A

They rely on their hypoxic drive to breath as their respiratory centres are insensitive to CO2. If we take their hypoxic drive away by giving O2 this could be fatal to the patient

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6
Q

What is Emphysema?

A

Dilation and destruction of alveolar walls distal to terminal bronchioles

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7
Q

What does dilation and destruction of alveolar walls lead to?

A

1) Decreased elastic recoil (keeps airways open during expiration)
2) Increased air trapping = increased dead space

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8
Q

How does a patient with Emphysema appear?

A

‘Pink Puffer’

  • thin
  • hyperinflated chest
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9
Q

How is Respiration driven?

A

an increase in PaCO2

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10
Q

Pathology of Cigarette smoke and what it causes

A

1) - Mucous gland hypertrophy
- increase in immune cells (neutrophils, macrophages, lymphocytes)
- release of inflammatory mediators (elastases, proteases, IL-1, TNF-8)

2) This increase in inflammation breaks down the lung parenchyma

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11
Q

CHRONIC OBSTRUCTIVE PULMONARY DISEASE

Signs and Symptoms?

A

symptoms

1) Chronic productive cough
2) Wheeze
3) Dyspnoea

signs

1) Breathless
2) Tachypnoea
3) Prolonged expiration
4) hyperinflated chest
5) Decreased lung expansion
6) Use of accessory muscles
7) wheeze

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12
Q

CHRONIC OBSTRUCTIVE PULMONARY DISEASE

Diagnosis?

A

1) FEV1/FVC= <0.7

2) INCREASED TLC and RV

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13
Q

CHRONIC OBSTRUCTIVE PULMONARY DISEASE

What can be seen on bloods, CXR and ABG

A

bloods= increased packed cell volume

CXR= hyperinflated lungs and flat diaphragm

ABG= decreased PaO2

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14
Q

CHRONIC OBSTRUCTIVE PULMONARY DISEASE

Stages of COPD?

A

stage 1= <80% FEV1 - predicted
stage 2= 50-79% FEV1
stage 3= 30-49% FEV1
stage 4= <30% or <50% FEV1 if respiratory failure

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15
Q

CHRONIC OBSTRUCTIVE PULMONARY DISEASE

What must all diagnosed patients receive

A

Steroid Trial:

Oral prednisolone for 2 weeks and if FEV1 rises by >15% COPD is steroid responsive

therefore they may benefit from long term inhaled corticosteroids

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16
Q

CHRONIC OBSTRUCTIVE PULMONARY DISEASE

Treatment?

A
  • cessation of smoking and BMI control
  • SAB2A and LAB2A if persists
  • short acting antimuscarinic (ipratropium) may be enough for mild
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17
Q

CHRONIC OBSTRUCTIVE PULMONARY DISEASE

treatment of severe?

A

1) LAB2A
2) Corticosteroids
3) Long term oxygen therapy

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18
Q

CHRONIC OBSTRUCTIVE PULMONARY DISEASE

What is an acute exacerbation?

A
respiratory failure/ 
2/3 of:
1) Worsening dyspnoea
2) Worsening wheeze
3) Increased coughing
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19
Q

CHRONIC OBSTRUCTIVE PULMONARY DISEASE

treatment of an acute exacerbation?

A

Low conc 02 through venturi mask (SaO2 88-92%)

Abx if infective

  • salbutamol
  • prednisolone
  • ipratropium
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20
Q

ASTHMA

Characteristics?

A

1) bronchial muscle contraction - triggered by stimuli
2) Mucosal swelling and inflammation - mast degranulation = mediator and histamine release
3) Increased mucous production

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21
Q

ASTHMA

Classifications?

A

Eosinophilic- Extrinsic (atopic) - allergens proven by +ve skin prick reactions

& Intrinsic

Non- eosinophilic

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22
Q

ASTHMA

Aetiology?

A
  • Individuals who readily develop IgE against common allergens
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23
Q

ASTHMA

Genetic Cause?

A

IL-4 clusters on chromosome 5. this produces IL-3,4,5 &13

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24
Q

ASTHMA

Environmental cause?

A

childhood exposure to allergens (hygiene hypothesis)

if you grow up in a clean area your risk is increased

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25
ASTHMA Pathology of the inflammation?
- Mast cells, eosinophils, T-lymphocytes and dendritic cells increased in bronchial wall 1) T- cells release IL-3,4,5 &13 2) IL-4 &13 produce IgE instead of B-cells/ antibodies 3) IgE attaches to mast cell= degranulation when inhaled allergens are encountered 4) Inflammatory mediator and histamine released
26
ASTHMA Pathological changes to the airway
- Bronchial Smooth muscle undergoes hypertrophy and hyperplasia - airway wall thickened by deposition of collagen below the basement membrane - metaplasia of respiratory epithelium
27
ASTHMA How many people suffer in the U.K?
5-8%(more in developed countries (hygiene hypothesis)
28
ASTHMA Precipitants?
- fumes - exercise - viral infections - cold air - Beta blockers - NSAIDS - smoking - stress
29
ASTHMA Clinical features?
1) Wheeze 2) Dyspnoea 3) Tight chest 4) tachypnoea these all vary diurnally (daily)
30
ASTHMA what jobs may increase your chance of developing or worsening asthma?
- animal handlers - food processors - paint sprayers
31
ASTHMA Diagnosis?
2 week peak flow diary - 3 each morning and 3 each night- best score
32
ASTHMA Non medical treatment?
- stop smoking - avoid allergens - avoid beta blockers/ NSAIDs
33
ASTHMA | Step by step treatment? can move up and down the steps accordingly
1) Short acting beta 2 agonist (salbutamol- BASELINE) 2) Inhaled corticosteroids (ICS) 3) Add LTRA 4) Add long acting beta2 agonist + - LTRA 5) Increased dose of ICS, SAB2A, LAB2A +- LTRA 6) Trial addition of theophylline / muscarinic receptor antagonist - Refer to asthma clinic and specialist may recommend PO prednisolone
34
ASTHMA What is an LTRA?
leukotriene receptor agonist
35
ASTHMA Features of an acute attack?
1) Pulse <110bpm 2) Respiratory rate >25 3) Cant complete sentences 4) PEF 35-50% predicted
36
ASTHMA When may an attack be life threatening / fatal?
- cyanosis - silent chest - bradycardic - PEF <33% predicted
37
ASTHMA Treatment of an acute attack?
- nebulised salbutamol and ipratropium - prednisolone - O2 through venturi (24%)
38
ASTHMA When can someone be discharged after a severe attack?
- PEF >75% - Diurnal variation <25% - Stable for 24 hrs + - once discharged give PO prednisolone to be taken OD
39
LUNG CANCER What are 95% of all lung tumours?
Bronchial Carcinoma's
40
LUNG CANCER Risk Factors?
- smoking - asbestos - radiation (radon) - arsenic
41
LUNG CANCER Types?
Small cell and non-small cell
42
LUNG CANCER Subtypes of Non-small cell?
Squamous Adenocarcinoma Large Cell Small Cell
43
LUNG CANCER What does Squamous Lung Cancer present as?
It presents AS an obstructive lesion leading to infection
44
LUNG CANCER What is Adenocarcinoma associated with?
asbestos and non smokers. occurs peripherally
45
LUNG CANCER WHat is LArge Cell?
poorly differentiated tumour that metastasizes early
46
LUNG CANCER What is small cell?
it arises from endocrine cells and secretes polypeptide hormones also metastases early so a poor prognosis
47
LUNG CANCER Epidemiology?
`19% of all cancers. 27% of all cancer deaths. poor prognosis
48
LUNG CANCER Local Effects?
- cough - dyspnoea - haemoptysis - chest pain - slowly resolving/ recurrent pneumonia - weight loss/ anorexia
49
LUNG CANCER Invasive Effects?
1) Arm pain (brachial plexus) 2) Facial plethora 3) Horner's Syndrome (stellate ganglion) 4) Hoarseness (Left recurrent laryngeal) 5) Pleural effusion (pleura)
50
LUNG CANCER Common sites for Mets?
- bone - brain - liver - pleura - lymph nodes
51
LUNG CANCER Commonly secreted hormones from the tumour and their effects?
``` ACTH = Cushing's PTH = Hypercalcaemia ADH = SIADH ```
52
LUNG CANCER | 3 steps to an Investigation?
1) Confirm diagnosis 2) Assess spread 3) Stage the tumour
53
LUNG CANCER Investigations?
1st = CXR then CT of chest to stage it, then PET scan to check for Mets
54
LUNG CANCER Staging?
``` primary tumour (T0-T4) regional nodes (N0-N3) distant mets (M0-M1) ``` ``` T0 T1 T2 T3 T4 N0 N1 N2 N3 M0 M1 ```
55
LUNG CANCER Describe the 4 numbered stages
Stage 1= T1/T2, N0, MO Stage 2= T1, T2, N1 OR T3 Stage 3= T3, N1, M0 OR T1-T3, N2 Stage 4= T1-T4, N0-N3, M1 (instant stage 4 if distant metastases)
56
LUNG CANCER Treatment of non-small T1/T2
Curative surgery or curative radiotherapy
57
LUNG CANCER What occurs before any surgery occurs?
WHO Performance status: ECG&PFTs to assess if they are fit enough to actually have the surgery and recover
58
LUNG CANCER What happens post op?
radio/chemo therapy
59
LUNG CANCER How is radiotherapy given?
3x every day for 12 days.
60
LUNG CANCER Treatment of Stage 3/4?
palliative radio/chemo
61
LUNG CANCER WHat is palliative radiotherapy good for?
local symptoms such as bone pain and haemoptysis
62
LUNG CANCER What is palliative chemo good for
Systemic symptoms and maintaining quality of life right up until death
63
LUNG CANCER Side effects of Chemo?
- alopecia - nausea + vomiting - Peripheral neuropathies - Bone marrow suppression
64
LUNG CANCER Side effects of Radiotherapy?
- Fatigue - Anorexia - cough - oesophagitis
65
treatment for small cell LUNG CANCER?
palliative chemo/ radio
66
PNEUMONIA Which groups are at risk?
- old people - IVDU - alcoholics - diabetics - immunocompromised (AIDs)
67
PNEUMONIA Aetiology? (typical and hospital acquired)
TYPICAL: - S.aureus - H.influenzae - S.pneumoniae - Klebsiella pneumoniae HOSPITAL: S.aureus -ve enterobacteria
68
PNEUMONIA Epidemiology and what is the mortality rate in hospital?
5-11 per 1000 people 21% mortality
69
PNEUMONIA Symptoms?
1) fever 2) Sweats 3) pleuritic pain 4) Purulent cough 5) weakness 6) Dyspnoea
70
PNEUMONIA Signs?
1) Confusion 2) Tachycardia 3) Tachypnoea 4) Lung consolidation features e.g. ( crackles, dull percussion and bronchial breathing)
71
PNEUMONIA Tests?
CXR- to see for consolidation (follow up to check for cancer/complications) Bloods ( increased WCC and CRP) Sputum test for MC&S Green swab for flu
72
PNEUMONIA How is the severity determined?
CURB-65 1 point each for: - confusion - urea >7mmol/L - resp rate >30 - Age >65 - BP <90 systolic/ <60 diastolic
73
PNEUMONIA For the CURB-65 what do the different scores represent?
``` 0-1= home treatment 2= hospital treatment 3-5= severe/ ITU/ Mortality is 15-40% ```
74
PNEUMONIA Type 1 respiratory failure is common after pneumonia. what is the cycle of draining an infected pleural effusion
pneumonia causes a pleural effusion, exudate produced and this needs to be drained signs of infection = if exudate is yellow, smelly, acidic
75
PNEUMONIA Treatment of Mild, moderate and severe?
mild= PO amoxicillin moderate= PO amoxicillin + PO clarithromycin severe= IV cefuroxime and IV clarithromycin
76
PNEUMONIA Who is eligible for Vaccine?
- age over 65 - people with chronic conditions (heart and lung e.g.) - Diabetes Mellitus - Immunosuppressed (AIDS) - People on Chemo
77
TUBERCULOSIS | Epidemiology?
- in UK African and indian immigrants are common - Biggest killer of a single infectious disease in the world. 2 million deaths a year - biggest cause of death for people with HIV
78
TUBERCULOSIS Cause?
mycobacterium tuberculosis =primary tuberculosis that is spread by aerosols
79
TUBERCULOSIS Pathophysiology?
1) Bacteria ingested by macrophages become granulomas which are the primary focus (these are recognised by exudation and neutrophil infiltration) 2) Also occurs in mediastinal lymph node (primary complex) 3) Typical Granulomatous LEsions form 4) They are calcified/ walled off = bacteria remains latent?
80
TUBERCULOSIS What is Dissemination and where is it likely to spread after dissemination?
When the bacteria fails to stay contained Spreads into lungs, CNS, Bone, abdomen , Commonly= lymphadenopathy
81
TUBERCULOSIS What is Dissemination to the lungs and CNS called?
lung: Miliary TB | CNS= TB meningitis
82
TUBERCULOSIS Most people present with post-primary TB, what symptoms may they have?
- weight loss - night sweats Pulmonary: - Over 3 week cough - Haemoptysis - Dyspnoea - chest pain Takes 4-8 weeks to develop
83
TUBERCULOSIS Complications?
1) Pleural effusion 2) Pericardial effusion 3) Lung collapse 4) Lung consolidation (becomes solid)
84
TUBERCULOSIS Investigations?
1st CXR = see cavitating lesion in upper lobes + loss of volume Sputum test by coughing or broncho-alveolar lavage
85
TUBERCULOSIS What is the name of the sputum test and what culture medium is used?
Zeihl-Neeson Test with a Lowenstein Jenson culture medium
86
TUBERCULOSIS Latent TB tests?
1) Mantoux test | 2) Interferon- Gamma testing
87
TUBERCULOSIS Treatment of latent TB?
Isoniazid for 6 months
88
TUBERCULOSIS Treatment of Non Drug resistant TB?
First 2 months: 1) Rifampicin 2) Isoniazid 3) Pyrazinamide 4) Ethambutol then another 4 months with: 1) Rifampicin 2) Isoniazid
89
TUBERCULOSIS Side effects of Rifampicin?
pink urine, low platelets, induces CYP450, Flu symptoms
90
TUBERCULOSIS Side effects of Isoniazid?
neuropathy, low WCC, inhibits CYP450
91
TUBERCULOSIS Side effects of Pyrazinamide?
rash and arthralgia
92
TUBERCULOSIS Side effects of Ethambutol
Optic Neuritis
93
PULMONARY EMBOLISM Pathophysiology?
1) Embolism obstructs ventricular outflow tract 2) Increased in pulmonary vascular resistance 3) Right heart failure 4) Lung tissue is ventilated but not perfused - impaired gas exchange
94
PULMONARY EMBOLISM Risk factors?
1) Recent flight 2) Recent surgery / immobilization 3) Recent fracture 4) Pregnant or the pill 5) Cancer 6) Heart failure
95
PULMONARY EMBOLISM Features?
Small-medium: Tachycardia, tachypnoea, pleuritic chest pain, breathlessness, syncope Large: SAME but also cyanosis, pale and sweaty and distended/ increased JVP
96
PULMONARY EMBOLISM What is the Name of the pre test probability test?
wells score
97
PULMONARY EMBOLISM | Diagnostic tests?
cxr- normal or decreased vascular markings ECG- inverted T IN v1-v4, tachycardia, RBBB ABG- type 1 respiratory failure
98
PULMONARY EMBOLISM Gold standard imaging?
CTPA= CT pulmonary angiography
99
PULMONARY EMBOLISM | what is given to people of low risk and high risk of PE?
low risk = d-dimer high risk = LMWH (low molecular weight heparin)
100
PULMONARY EMBOLISM Treatment of small?
1st - D-dimer test if that is positive do a CTPA if that is positive give warfarin/ NOAC
101
PULMONARY EMBOLISM Treatment of medium? and what should be given if they're compromised?
LMWH + O2, morphine and fluids if they're compromised
102
PULMONARY EMBOLISM Treatment of large?
Thrombolysis (alteplase)
103
PULMONARY EMBOLISM How long is treatment?
Normally 3 months, 6 months if idiopathic maybe lifelong if they're recurrent
104
RESPIRATORY FAILURE How is type 1 defined?
PaO2<8kPa
105
RESPIRATORY FAILURE How is type 2 defined?
PaO2<8kPa | PaCO2>6kPa
106
RESPIRATORY FAILURE Cause of Type 1?
Ventilation- perfusion mismatch may be due to Asthma, COPD, Pulmonary oedema, Pneumonia, Pulmonary Fibrosis
107
RESPIRATORY FAILURE Cause of Type 2?
Alveolar Hypoventilation 1) Pulmonary (Fibrosis, COPD, Asthma) 2) Reduced respiratory flow (trauma, opiates) 3) Neuromuscular (Myasthenia Gravis, Guillan Barre) 4) Thoracic wall disease (kyphoscoliosis)
108
RESPIRATORY FAILURE Investigations? (ABG already done)
CXR, FBC, U+E, Spirometry, CRP
109
RESPIRATORY FAILURE Treatment of type 1?
treat underlying cause + high saturated O2 through venturi 35-60%
110
RESPIRATORY FAILURE Treatment of type 2?
treat hypoxia first as patient can rely on the respiratory drive to breathe if they have hypoxia 24% O2 through venture then ABG every 20 mins to check if its working, Titrate O2 up slowly
111
RESPIRATORY FAILURE There are two types of severe treatment. Name them
Type 1: Continuous Positive Airways Pressure (CPAP) Type 2: Bilevel Positive Airways Pressure (BiPAP)
112
URT INFECTIONS Causes of Sinusitis?
Bacteria: H influenzae, S pneumoniae Virus: Rhinovirus, Coronavirus
113
URT INFECTIONS Symptoms of Sinusitis?
Headache, frontal pain, Nasal discharge
114
URT INFECTIONS Pharyngitis causes?
S.aureus, H.influenzae, S,pyogenes, S.pneumoniae virus: EBV and Adenoviruses
115
What is EBV?
Epstein-Barr Virus
116
URT INFECTIONS Criteria for Pharyngitis?
1) Tonsillar exudate 2) No cough 3) Fever
117
URT INFECTIONS What is Croup?
Laryngo tracheobronchitis
118
URT INFECTIONS What is Laryngo Tracheobronchitis caused by and how is it treated?
Parainfluenza viruses and steroids with O2 therapy
119
INFLUENZA WHat are the two proteins found on the influenza virus?
Haemagglutinin (H) | Neuraminidase (N)
120
What is the function of Haemagglutinin?
Sticking onto the host respiratory cell/ epithelium
121
what is the function of Neuraminidase?
Lysis of host cell so the virus can be released
122
Why is Influenza A worse than B?
it has less robust genetics so mutates much more frequently
123
What is Antigenic Drift?
Small mutations so only small changes made to the virus so small infection
124
What is Antigenic Shift?
Complete change in the proteins H&N so it is unrecognisable to the immune system = infection
125
INFLUENZA How is it transmitted?
Aerosols and droplets
126
INFLUENZA Symptoms?
1) Myalgia 2) Fever 3) Tired 4) Headache 5) Sore throat 6) Dry cough
127
INFLUENZA Diagnosed?
by green swab
128
INFLUENZA Treatment?
Paracetamol, bed rest and fluids
129
INFLUENZA When does Antigenic Drift happen a lot?
Seasonally e.g. every year new vaccine needs to be made
130
INFLUENZA What would cause a viral pandemic?
when Antigenic Shift occurs
131
What is Alpha- 1 antitrypsin?
Alpha1 - antitrypsin is a protease inhibitor inactivated by cigarette smoke.
132
BRONCHIECTASIS What is it?
• Chronic infection of the bronchi and bronchioles
133
BRONCHIECTASIS What is bronchiectasis a result of, and give 5 causes for this.
A result of chronic inflammation ``` CAUSES genetic conditions (CF, immotile cilia), childhood infections (Pertussis), chronic lung infections (TB), idiopathic immunodeficiency. ```
134
BRONCHIECTASIS Give 4 symptoms and 2 signs a person with bronchiectasis may have.
``` Chronic purulent cough, dyspnoea, wheeze, recurrent chest infections, haemoptysis. ``` Signs are clubbing and crackles.
135
BRONCHIECTASIS What is gold standard investigation and what would spirometry likely show?
CT chest is gold standard (CXR can be used too). obstructive
136
BRONCHIECTASIS Give 3 organisms commonly causing acute exacerbations
S aureus, H influenzae, P aeruginosa
137
BRONCHIECTASIS Give 3 non-pharmacological and 3 pharmacological rx.
Non-drug: flu + pneumococcal vaccines physiotherapy stop smoking. Drugs: mucolytics, Abx, SABAs.
138
HYPERSENSITIVITY PNEUMONITIS What is it?
Inhalation of allergens (fungal spores or avian proteins) provokes a hypersensitivity reaction
139
HYPERSENSITIVITY PNEUMONITIS Causes?
- Farmers lung - malt workers lung - mushroom workers lung - cheese washers lung - wine makers lung
140
HYPERSENSITIVITY PNEUMONITIS Acute phase?
alveoli are infiltrated with acute inflammatory cells
141
HYPERSENSITIVITY PNEUMONITIS Chronic exposure?
- granuloma formation | - obliterative bronchiolitis
142
HYPERSENSITIVITY PNEUMONITIS treatment of acute and chronic?
Acute • Remove allergen and give O2 • Oral prednisolone Chronic • Avoid exposure – facemask • Long-term steroids often achieve CXR and physiological improvement • Compensation may be payable
143
HYPERSENSITIVITY PNEUMONITIS Investigations? Acute and chronic
Acute • Bloods – FBC , raised ESR, ABGs • CXR – upper-zone consolidation • Lung function tests Chronic • Blood tests • CXR – upper zone fibrosis; honeycomb lung
144
HYPERSENSITIVITY PNEUMONITIS Acute clinical presentation?
``` • 4-6h post exposure o Fevers o Rigors o Myalgia o Dry cough o Dyspnoea o Crackles (no wheeze) ```
145
HYPERSENSITIVITY PNEUMONITIS Chronic clinical presentation?
``` • Chronic o Increasing dyspnoea o Weight loss o Exertional dyspnoea o Type I respiratory failure o Cor pulmonale ```
146
CYSTIC FIBROSIS Epidemiology?
1/20 caucasians carry, 1/2000 affected.
147
CYSTIC FIBROSIS | Where is the genetic problem?
Deletion mutation in a gene on chromosome 7 that encodes the CF transmembrane conductance regulator (CFTR) protein
148
CYSTIC FIBROSIS Pathophysiology of the gene defect?
Mutations affect the cystic fibrosis transmembrane conductance regulator (CFTR). Lead to impaired Cl- and H2O transport across cell membranes leading to viscosity of secretions.
149
CYSTIC FIBROSIS Give 4 places CFTR is found
Lungs, pancreas, GIT, reproductive tract.
150
CYSTIC FIBROSIS Common presenting features?
Recurrent respiratory infections small intestine obstruction in the young failure to thrive cough haemoptysis wheeze Bilateral coarse crackles
151
CYSTIC FIBROSIS Give 2 pancreatic symptoms and one reproductive.
Pancreatic: DM and steatorrhoea. Reproductive: infertility
152
CYSTIC FIBROSIS Investigations?
Sweat test – sweat sodium and chloride >60mmol/L; chloride > sodium Genetics – screen for known common CF mutations – family screening + counselling Faecal elastase – screens for pancreatic dysfunction
153
CYSTIC FIBROSIS Treatment?
``` Chest • Regular physiotherapy o Postural drainage o Active cycle breathing techniques o Forced expiratory techniques • Abx for acute infective exacerbations • Bronchodilators ``` ``` GI • Pancreatic enzyme replacement • Fat soluble vitamin supplements • Ursodeoxycholic acid – for impaired liver function • Cirrhosis = liver transplant ``` ``` Other • Treat CF-related diabetes • Screen for/treat osteoporosis • Treat arthritis, sinusitis, vasculitis • Fertility and genetic counselling ```
154
SARCIODOSIS What is it?
A multisystem granulomatous disorder of unknown cause.
155
SARCIODOSIS What group are affected more frequently and more severely?
afro-caribbeans
156
SARCIODOSIS What is the most common way it presents?
Symptomless found incidentally on a CXR with bilateral hilar lymphadenopathy, ± fibrosis and pulmonary infiltrates (latter 2 less common early on).
157
SARCIODOSIS Give 2 lung symptoms, 1 skin, 2 eye, 1 bone, 1 cardiac.
Lung: Dyspnoea, dry cough. Skin: Erythema nodosum. Eye: Uveitis, conjunctivitis. Bone: Polyarthralgia. Heart: Bundle branch block.
158
SARCIODOSIS What is the diagnostic test and what is found? What are 2 other blood tests you would look for? What will lung function tests show?
Biopsy is diagnostic: non-caseating granuloma. Look for increased ACE and hypercalcaemia (due to granulomas). Lung function tests can show a restrictive defect.
159
SARCIODOSIS When is treatment indicated and what is given?
Parenchymal lung disease on CXR, ocular, cardiac or neurologcal involvement, or hypercalcaemia. Treated with prednisolone.
160
SARCIODOSIS Prognosis?
60% resolve in 2 years
161
3 holistic lung tests?
6 minute walking test. Incremental shuttle walking test. Cardio-respiratory exercise testing.
162
What is Mesothelioma?
Tumour of mesothelial cells that usually occur in the pleura, caused by asbestos exposure
163
Mesothelioma clinical presentation, investigation and treatment?
- chest pain - dyspnoea - weight loss CXR/CT Chemo
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PLEURAL EFFUSIONS What is it?
excessive fluid in pleural space
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PLEURAL EFFUSIONS How is Transudates and exudates defined?
Transudates : <25g/L protein Exudates : >35g/L
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PLEURAL EFFUSIONS what do you call blood in the pleura? what do you call pus in the pleura?
Haemothorax Empyema
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PLEURAL EFFUSIONS Cause of Transudates?
1) Increase venous pressure e.g.g HF 2) Hypalbuminaemia 3) Hypothyroidism
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PLEURAL EFFUSIONS Cause of exudates?
1) TRauma 2) Cancer 3) Infection (TB, Pneumonia, SLE)
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PLEURAL EFFUSIONS Signs and symptoms?
``` Breathless Reduced breath sounds Dull percussion Reduced chest wall movement Tracheal deviation ```
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PLEURAL EFFUSIONS Diagnostic tests?
1st CXR- dense shadows with blunt angles 2nd- aspiration of fluid, send for cytology, bacteriology, protein, glucose, pH
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PLEURAL EFFUSIONS treatment?
Transudates- treat cause Exudates = Drain Drain if symptomatic and surgery if persistent
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PNEUMOTHORAX What is it?
Air in pleural space = collapsed lung
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What is a Tension Pneumothorax?
pleural tear acts as a one way valve so air can go in but not out
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How does a tension pneumothorax cause a cardiac arrest?
Unilateral increase in pleural pressure = increased respiratory distress = shock and cardiac arrest
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Treatment of tension pneumothorax?
1st - needle decompression at 2nd intercostal space at midclavicular line
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PNEUMOTHORAX Difference between tension and normal?
Tracheal deviation away from side of pneumothorax in tension
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PNEUMOTHORAX Aetiology?
- COPD - asthma - Pneumonia - TB
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PNEUMOTHORAX How may a spontaneous one occur?
thin young man - rupture of sub-pleural bulla
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PNEUMOTHORAX Clinical features?
1) Pleuritic chest pai 2) dyspnoea 3) Decreased breath sounds 4) Hyper- resonant percussion 5) Reduced expansion
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PNEUMOTHORAX Diagnostics?
CXR - pleural linings, no lung markings, shifted mediastinum
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PNEUMOTHORAX Treatment?
1st - Aspirate 2nd - chest drain primary = >2cm + breathless = Aspirate secondary = >2cm + breathless + over 50 = intercostal drain
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PULMONARY HYPERTENSION What is it?
- Pulmonary arterial pressure of over 25mmHg at rest and secondary RV failure
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PULMONARY HYPERTENSION What is the normal mean pulmonary arterial pressure and mean arterial pressure? (MPAP and MAP)
MPAP = 10-14mmHg MAP= 90mmHg
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PULMONARY HYPERTENSION Aetiology?
Occurs due to increase in pulmonary vascular resistance or increase in pulmonary blood flow
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PULMONARY HYPERTENSION causes?
Drugs = methotrexate, amiodarone HIV, portal HTN, autoimmune rheumatic e.g. RA Heart - valvular heart disease, systolic/diastolic failure Lung- COPD, fibrosis
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PULMONARY HYPERTENSION Symptoms?
initial - Exertional dyspnoea and fatigue Proegresses to : RV failure, cor pulmonale = increased JVP, Hepatomegaly, peripheral oedema
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PULMONARY HYPERTENSION Signs?
Loud pulmonary 2nd sound, RV heave
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PULMONARY HYPERTENSION Diagnostic tests?
CXR- enlarged proximal pulmonary arteries ECG- RVH, P pulmonale - peaked p waves
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PULMONARY HYPERTENSION Treatment?
1st oxygen warfarin diuretics = oedema oral CCBs = pulmonary vasodilators
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What drugs will reduce pulmonary resistance?
Sildenafil
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PULMONARY HYPERTENSION Worst case scenario treatment?
Lung and heart transplant - unlikely
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Name some lung consolidation features
Bronchial breathing, dull percussions, crackles
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BRONCHIECTASIS What does the inflammation lead to?
* Abnormal and permanent dilation of these airways * Leads to impaired clearance of bronchial secretions * Secondary bacterial infection * May be localised to a lobe or generalized
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Complications of TB (other organs)
Meningitis Addison's Hepatitis