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Phase 2 mine > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What is Kussmal’s breathing?

A

Found in DKA or other acidoses where breaths are fast or normal rate but maximal inspirations and expirations are taken

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2
Q

What is Agonal breathing?

A

Not normal gasping for air apnoea in between sign of brainstem reflex and brain hypoxia

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3
Q

What can cause cough and dyspnoea?

A

Obstructive lung disease, restrictive lung disease, pulmonary vascular abnormalitiy infections and maligancy

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4
Q

What are the areas you can get cancer in the lung?

A

The bronchioles bonchogenic or alveolar

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5
Q

What are the types of bronchiole cancer?

A

central small cell or squamous or peripheral adenocarcinoma and large cell

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6
Q

Is primary lung cancer more or less common than secondary lung cancer?

A

secondary is more common

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7
Q

what cancers commonly metastasise to the lung?

A

Breast, colon and renal cell carcinoma

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8
Q

Where can metastases in the lungs be?

A

lung parenchyma, pleura, endobronchial mucosa and lymphatics

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9
Q

What are the main categories of lung disease?

A

infection, cancer and

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10
Q

What is important to know about SOB?

A

Onset timing variation severity exacerbating relieving associated symptoms.

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11
Q

What are lung finction tests?

A

Spirometry, lung volumes transfer factor mouth pressures

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12
Q

What radiology can be used in lungs?

A

Plain X-ray, CT scanning ultrasound CMR MRPA ventilation/perfusion scans

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13
Q

What is type 1 respiratory filure?

A

Low pO2 with lowr or normal co2

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14
Q

What is type 2 respiratory failure?

A

Low pO2 and high pa CO2

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15
Q

What can cause a large arteriolar alveolar gradient?

A

V/Q mismatch, Diffusion limitation, shunt right to lefft

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16
Q

What causes high altitude pulmonary oedema physiologically?

A

pulmonary vasoconstrction.

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17
Q

What can cause lung disease?

A

Genes environment, infection, cancer autoimmune disease, thromboembolism

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18
Q

What is transfer factor?

A

diffusing capacity, looking at uptake of CO during a breath hold then look at expired concentrations.

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19
Q

What does arterial alveolar gradient show?

A

MEasure of efficuency of transfer of the oxygen from lveolus to the arteroile

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20
Q

Why is arteriol alveolar important?

A

shows lung function and can show a problem where things look normal

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21
Q

What can cause respirartory failure?

A

Low oxygen delivery, airways obstruction, gas exchange/diffusion limitation, ventilation/perfusion mismatching, alveolar hypoventilation

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22
Q

What can cause type 1 respiratory failure?

A

Pneumonia pulmonary embolism

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23
Q

What can cause type 2 respiratory failure?

A

Emphysema Neuromuscular disease

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24
Q

What types of failure cause type 2 failure?

A

Airways obstruction, alveolar hypoventilation

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25
Q

What ca cause acidaemia?

A

increase in acidic compounds, increased CO2 production and loss of HCO3

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26
Q

What happens to breathing at night time?

A

the tongue falls back and soft tissue relaxes which can cause obstruction to the airways

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27
Q

What is obstructive sleep apnoea?

A

From large amounts of soft tissue, from adenoids or obesity,

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28
Q

What are characteristics of obstructive sleep apnoea?

A

Continual respiratroy effort, rising and falling spO2, often steady response nasal flow is interrupted

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29
Q

What is treatment for Type 1 respiratory failure

A

CPAP

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30
Q

What is BiPAP?

A

Different pressure on inspiration and expiration good for type 2 faulre

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31
Q

What is s symptom of hypercapnia?

A

Headache

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32
Q

Where does asthma affect?

A

Constriction and growth of muscle hypertrophy, inflammation of airway wall, leukocytes thick sticky mucus,

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33
Q

What are the types of asthma?

A

allergi asthma and non-allergic asthma (esinophillic TH2/non-eosinophillic low TH2)
eosinophilic then atopic fungal commer aeroallergens ocupation pets exposures or non-atopic
non eosinophilic asma subgroups are unknown

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34
Q

What is allergic asthma?

A

eosinophils entering the lungs as part of an allergic reaction causing inflammation.

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35
Q

What is atopy?

A

tendancy to produce a response to air allogens dust pollen etc 25% positive only half of those have disease IgE mediated reactions to common aeroallergens

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36
Q

What is asthma COPD?

A

can get COPD without smoking with asthma and can have symptoms overlap

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37
Q

How to tell if its asthma presenting complaint?

A

presenting complain episodic wheeze, cough breathlessness variation brittle disease type 1 chronic sever type 2 sudden dips provoking factors worse in morning than evening perimenstrural asthma laughter

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38
Q

How to gauge severity of disease?

A

level of treatment required to control, A&E attendances admissons ITU care attendanced for GP for courses of antibiotics and steroids.
day to day control reent noctrunal waking usual symptoms in a day does it get in way of ADLs, exacerbations

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39
Q

What is the history of complaint needs to be asked?

A

Timing of events, age of onset fluctiations in how bad it is, after choking, chlorine exposure

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40
Q

What to ask about associated problems/

A

Eczema hayfever, nasal disease, other food allergies drug allergies reflux disease

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41
Q

Why is PMH important in asthma?

A

can present ast vasculitius tmours or other dseases

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42
Q

What are important about asthma drug history?

A

What are they supposed to smoke, what do the actually take, beta blockers, things can make asthma work or cause it

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43
Q

Family history what do you need for asthma?

A

do they smoke? famiy situaion mental health assiciations.

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44
Q

What assesses occupational history?

A

dust aerosol fumes or allergens? does it get better on holiday?

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45
Q

How is asthma differentiated from COPD?

A

chronic decline but can coexist

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46
Q

What is the character o asthma wheeze?

A

not crackles polyphonic exiratory

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47
Q

what tests to do for asthma?

A

Blood counts eosinophl.3 of above test for atopy skin prick tests, chest XRayy to check other things. Lung function testing expect obstruction but more in FEV1 more than FVC variable peak flow, challenge test to see if can induce it FeNO exhaled nitric oxide marker of eosinophilic asthma

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48
Q

Who’s most at risk of death from asthma?

A

more the 3 classes of drugs ITU in past recent admission or frequent attender near fatal disease brittle disease

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49
Q

What are differential diagnosis for asthma?

A

Bronchiolitis, bronchiectasis, CF PE CEA CFA hyperventilation bronchial obstruction vocal cord dysfunction, aspiration CCF COPD

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50
Q

What drugs are available for asthma?

A

bronchodilators(symptomatic only), anti-inflammatory, new biological drugs

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51
Q

Why are oral steroids bad?

A

systemic side effects: diabetes cataracts osteoporosis hypertension skin thinning easy bruising growth retardation osteonecrosis of femoral head adrenal suppression

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52
Q

What is the way to take steroids in asthma?

A

aerosol to reduce side effects

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53
Q

How to treat acute asthma?

A

oxygen, 40-60%, salbutamol nebulisa and prednisolone consider magnesim or aminophylline watch arrhythmias hypokalaemia tension pneumothorx chest xray if suspected

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54
Q

How to classify asthma attack?

A

uncontrolled or moderate PEFR>50% RR<25 pulse<110 normal speach
or severe where PEFR33-50% RR>25 HR>110 cant talk in whole sentences
Life threatening saO292% less or paO2 less than 8 normal paCO2 caltered consciousness near fatal same as before but with raised CO2

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55
Q

What is the burden of asthma?

A

Highe most common disease 5.4m in the uk with is significant death rates 1400

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56
Q

What protects upper airways from infections?

A

commensal bacteria but not so many, swallowing reflex neurological and anatomical factors mucocilliary escalator,innate and adaptive system

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57
Q

What can make you at risk of respiratory tract infections?

A

Swallowing altered lung physiology, colonisation of upper airway immune dysfunction co-morbidities

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58
Q

What is bronchial breathing?

A

Suggests consolidation in the lung usually pneumonia

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59
Q

How to tell you have pneumonia?

A

inflammation in the lungs, usually mean bacteria itis is virus or non infectious process. sob chest pain coughing and fever
Fever sweats rigors, cough, sputum sometiems no though, SOB, pleuritic chest pain, systemic features like weakness malaise extrapulmonary neurological or gastro with certain organisms rash for some
signs raised HR Low BP raised resp fever dehydration, signs of lung consolidation on percussion auscultation

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60
Q

Who is at risk of pneumonia?

A

Infants and elderly COPD other lung disease immunocompromised nursing home residnents impared swallow, diabetes congestive heart disease, alcoholics and IV drug users

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61
Q

what is pathogenesis of pneumonia?

A

enter the lung, macrophage phagocytoses them, sometiems get overwhelmed gets inflammatory signals for neutrophils lung fills with puss, the resolution phase will all inflammatory cells are removed and or in severe disease can get excessive inflamation and lead to lung damage

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62
Q

what investigations for pneumonia?

A

CXR FBC neutrophil biochem renal imparment hydration CRP assess severity, pulse oximitry assess severity and if required arterial blood gas definie respiratory failure microbiological tests

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63
Q

What to screen in pneumonia?

A

HIV

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64
Q

How to assess the severity of pneumonia?

A

BUFFALO/Sepsis six and CURB65 confusion urea resp rate bloodbressure low age over 65 predicts mortality 0=0.7% score 4/5 40% mortality

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65
Q

What are the two mechanisms of antibiotic treatment?

A

nuclear missile will work for now expensive side effects promotes resistance, or sniper might miss but better profile saved options for later

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66
Q

How are hard to culture bacteria tested for?

A

urinary antigens so dont have to culture

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67
Q

What to do to treat with antimicrobials in pneumonia?

A

Amoxicillin in community or clarithromycin and doxy, if its moderae 2 types more severe at least two use co-amoxiclav/

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68
Q

How long to treat with antimicrobial in severe infection?

A

5 days don’t extend unnecessarily

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69
Q

What is treatment for leigonella?

A

fluoroquinolones

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70
Q

What is necrotising pneumonia?

A

Causes destruction of lungs need different antimicrobials

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71
Q

what is an empyema?

A

Pleural effusion that is infected

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72
Q

what is a parapneumonic effusion?

A

Fluid on the lung as a result of failure to clear an infection

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73
Q

what is treatment for parapenuonic effusion?

A

sampling for pH glucose and stains culture and then thorachiocenesis to drain it

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74
Q

how can infections cause abscess in lung?

A

embolisation of bacterial infected tissue that travels to the young.

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75
Q

What is Lemierres disease?

A

Lung infection from throat infection

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76
Q

How to treat hospital-aquired pneumonia?

A

General principle start broad and then focus treatment when have some results. often need more specialised antibiotics as they are often worse hospital bacteria

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77
Q

What to consider in immunocompromised?

A

Fungal viral many different types. so much more complicated

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78
Q

What most often cause upper resp tract infection?

A

Virauses rhinibirus influenza A coronaviruses then predispose to bacterial infections

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79
Q

What is the use of tamiflu and others?

A

Not much might reduce duration better as preventive

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80
Q

What often cause phsrryngitis?

A

Viral 70-80% rhinovirus adenovirus, Glandular fevere epstine Barr virus Acute HIV infection
Bacterial group A strep beta haemolytic associated with rheumatic fevere scarlet fever PSGN other strep cocci Neisseria gonorrhoea and lemierres disease or diptherira

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81
Q

Corynebacterium diptheriae has what feature?

A

pseudomembranous layer on the throat, think abut in children who are unvaccinated

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82
Q

What is sinusitis?

A

usually viral but somtime bacterial and can caus inflammation and blocking exit so cant drain.

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83
Q

What is complication of sinusitis?

A

brain abbesses

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84
Q

What is acute epiglottitis?

A

be careful not to touch it and block airways adults have it and often get it in immunocompromised now children protected from it with vaccination

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85
Q

Which cytokines are involved with eosiphilic asthma?

A

IL5 IL13 IL4

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86
Q

What are the biological drugs used for in asthma?

A

As IL inhibitors to stop inflammation

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87
Q

What are the bronchodilater classes?

A

Beta agonists leukotriene receptor antagonists theophyllines and anticholinergics

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88
Q

What are the anti inflammatory drugs used in asthma?

A

Steroids

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89
Q

What is omalizumab?

A

anti-IgE for atopic allergics

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90
Q

What is mepolizumab?

A

anti IL-5 drugs

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91
Q

What is dupilumab?

A

Anti IL-13

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92
Q

What is important with asthma ongoing treatment?

A

Keep checking as thigns can go downhill

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93
Q

What to do to distcharge after an asthma attack?

A

Educate to prevent readmissions, achieve >75% peak flow prednisolone for 7-14 days never decreaseuntil better. step up treatment asthma sction pla nurse led followup and early review at GP practice

94
Q

How to measure damage with interstitial lung disease?

A

chest Xrays are good and FVC FEV1 gas transfer as CO is not absorbed as well FVC is usually reduced and reduced transfer and hypoxia onexertion

95
Q

What type of disease is interstitial lung disease?

A

most are restrictive

96
Q

What is the physiological change in ILD?

A

thickening of the membrane in alveoli

97
Q

What is ILD?

A

Umbrella term for aetiologies of pathology.

98
Q

What are the classifications of ILD?

A

Idiopathic, autoimmune hypersensitivity pneumonitis sarcoidosis and others

99
Q

What can ILD be grouped into?

A

Ones tha call pulmonary fibrosis and those that don’t

100
Q

What is IPF?

A

idiopathic pulmonary fibrosis which is rapid and progressive fibrosis without a known cause 2-5 survival from diagnosis. lung scarring more common in men usual interstitial pneumonia histology pattern unknown cause at this time

101
Q

What is pathogenesis of IPF?

A

Fibroblasts repair damaged tisssue and make myofibrolasts and eposit collagen and then die and they proliferate and cause thickening of the tissues causes honeombing of the lungs

102
Q

What key features of IPF?

A

Collections of fibroblasts thickening of alveolar intersitium honeycoming of alveoli, affecte periphery and base of lungs spatial heterogenity

103
Q

What is treatment for IPF?

A

not immune supression Pirfenidone affecte TGFbeta reduced fibroblast activity 3 tablets 3 a day main side effects photosensitivity GI upset, only slows decline, Nintebanib GI upset it works on tyrosine kinase inhibition to affect fibrosis and angiogeneses

104
Q

What is efficacy of IPF treatment?

A

it reduces progression doesnt stop just gives longer time to live

105
Q

What is hypersensitivity pneumonitis (extrinsic allergy alveolitis)?

A

Inflammation plays significant tole may fibrose and scar and can look like IPF in chronic form type 3 hypersinsitvy reaction immune complex reaction

106
Q

What is pathogenisis of hypersensitivity pneumonitis?

A

IgG antibodies roduced against an antigen in the lung and sensitisation, they are deposited in the lung and not degraded leading to symptoms.

107
Q

What is clinical history needed for in hypersensitivity pneumonitis?

A

pets mould occupation

108
Q

What is way to loo at it?

A

Lymphocytes in the lung decected wth bronchiolalveolar lavage to test for deposits.

109
Q

What is treatment for hypersensitivity pneumonitis?

A

Identify cause and avoid it, steroids can help in acute/subacute disease. Progression may still occur in those after it is removed and causes chronic can look lik IPF

110
Q

What is connective tissue interstital lung diseases?

A

lung diesase related to systemic inflammatory diseases

111
Q

Which type of systemic sclerosis is more associated with lung disease?

A

diffuse cutaneous

112
Q

What can treat scleroderma for lung disease?

A

Cyclophosphamide and moycophenate can improve FVC and nintedanib can stop fibrosis if its present

113
Q

What is drug induseced ILD?

A

gets fibrosis from certain drugs like nitrofurantoin, treatment is don’t take it agian

114
Q

What drugs can cause ILD?

A

Nitrofurantoin, methotrexate, aniodarone, Bleomycin novel checkpoint inhbitors

115
Q

What is the palliative treatment with ILD?

A

opioids for breathlessness and pain anxiolytics for anxiety, supplementary oxygen therapy.

116
Q

What is survival rate for 5 years?

A

5-10%

117
Q

What is main cause for lung cancer?

A

Smoking, occupational, asbestosis radon nickel chromate arsenic uranium and lung fibrosis

118
Q

What are symptoms of lung cancer?

A

Cough and recurrent chest infections, haemoptysisn SOB, B symtoms from metastasis, extra pulmonary changes due to cancer

119
Q

What are some paraneoplastic changes for lung diseae?

A

secretion of PTH, SIADH secretion of ACTCH and other hormones, hypertropnic pulmonary osteoarthropathy, myasthenic syndrome eaton lambert, finger clubbing migratory thrombophlebitis non-infective endocarditsi DIC

120
Q

What ar most primary lung cancers?

A

carcinoma 90% them squamus cell adenocarcinoma large cell undifferentiated carcinoma small cell carcinoid tumours

121
Q

What can cause lung cancer?

A

severe dysplasia in p53 leads to carcinoma progression

122
Q

What is small cell carcinoma?

A

High grade tumour spreads rapidly chemo is primary treatment cure rates low often has spread at presentation

123
Q

What is non small cell cancers?

A

variable epithelia neoplasm with smoking association may have metastisised more often surgery and radiation and newer treatments can work

124
Q

What are the new treatments for non small cell lung carcinoma?

A

checkpoint molecular markers can be identified and then used to treat

125
Q

What is carcinoid tumour?

A

uniform patern of cells neuroendocrine tuour they are malignant but are not very agressive compared to small cell

126
Q

How is lung cancer usually investigated?

A

Bronchoscopy with biopsys of tissue and nodes

127
Q

What cancer can be in the lung that isnt carcinoma?

A

Lymphoma, usually less agressive can also have hogkins lymphoma in lung

128
Q

What are non malignant causes of lung tumorus?

A

TB and other infections, lymph nodes, Benign neoplasia

129
Q

What is hamartoma?

A

benign neoplasia growth of normal tissue but in haphazard pattern,

130
Q

What is pleural neoplasia?

A

main two are pleural fibroma and malignant mesothelioma

131
Q

What is a pleural fibroma?

A

Most are benign cause discomfort and can release hormones,

132
Q

What cancer does asbestos cause?

A

mesothelioma,

133
Q

What diseases is asbestos linked with?

A

Plaques persitent pleural effusion pleural fibrosis, ung cancer asbestosis diffuse interstitial fibrosis and mesothelioma

134
Q

What is the cause of cancer with asbestotos?

A

Chronic inflammation leading to dysplasia

135
Q

What is the behaviour of mesothelioma?

A

Goes through chest walls and lung tissues highly invasive can invade heart oesophagus and other tissues can metastasise

136
Q

What is treatment for early mesothelioma?

A

plurectomy

137
Q

What is treatment for mesothelioma?

A

surgery chemo radio but not got a good prognosis at all

138
Q

What is legal aspect of lung cancer?

A

If it’s work related it needs referring to coroner to see if blame can be attributed

139
Q

What are complications of non cancer objects?

A

acute obstructions can lead to distal collapse and over expansion

140
Q

What is pathogensis of asthma?

A

Bronchial obstruction with distal overinflationor atelectasis, mucus plugging of bronchi, bronchial inflammation, seromucinouse gland hypertrophy, bronchial wall smooth muscel hypertrophy thickening of bronchial basement membrane

141
Q

What can cause chronic obsruction?

A

chronic brocnchitis or emphysema asthma and bronchiectasis

142
Q

What is bronchiectasis?

A

Permanent dilatation of bronchi and bronchioles, due to obstruction or severe inflammation usually lower lobes pooling of secretions and prne to infections

143
Q

What are the symptoms of bronchiectsiais?

A

Chronic cough wiht expectoratin of large quantities of foul-smelling sputume sometimes with blood

144
Q

What are the complications of bronchiectasis?

A

pneumonia, fungal colonsiation emphysema septicaemia meningits metastatic abscesses and can get amyloid formation and wiht time cor Pulmaonale

145
Q

What is chronic bronchitis/

A

Chronic productive cough mucus hypersecretion often from tobacco, usually affects middle aged could have pollution and prone to recurrent infections

146
Q

What happens in chronic broncitis progression?

A

Hypercapnia, hypoxaemia cyanosis right heart faulure

147
Q

What is emphysema?

A

enlargement of alveolar airspaces with destruction of elastin walls frequent association with bronchitis usually caused by smoking

148
Q

does emphysema cause cancer?

A

No not in itself

149
Q

What can cause emphysema ?

A

Smoking alpha1 antitrypsin defieciency, coal dust cadmium

150
Q

What is ARDS?

A

acute intersitial injury often fro trauma shcok infections gas inhalation narcotic abuse

151
Q

What is the pathlogy of ARDS?

A

diffuse alveolar damage with alveolar tissue getting inflammed and not transfering gas effectively anymore

152
Q

What is radiation pneumonitis?

A

side effect of radiotherapy simiar to ILD

153
Q

What are pneumoconiosis?

A

from inhaled dust like organic material or chemical progressive fibrosis

154
Q

What is coal workers pneumoconisosis?

A

anthracosis blackenign macules agregated of macrophages nodularity leading to breathlessnes then can become progressive massive fibrosis emphysema

155
Q

What ILD can asbestos do?

A

Cause diffuse pulmonary fibrosis (asbestosis)

156
Q

What is sarcoidosis?

A

Granulomatous disease non necrotising granulomas

157
Q

what is rheumatoid problems in lungs?

A

Diffuse fibrosis can have inflammation,

158
Q

What is diffuse malignancy?

A

Diffuse infiltration of cancer causing inflammation and fibrosis

159
Q

What are most common drugs used in lung disease?

A

corticosteroids and beta agonists

160
Q

What are the two forms of inhaled drugs?

A

Nebulisers aerosiol or dry powder formulation

161
Q

Where do most drugs need to go?

A

To the respiratory region as there are less filtration and mucous

162
Q

What size of particles get to alveolar region?

A

much smaller partices

163
Q

Why are lungs good for dugs?

A

Large area robust fewere systemic effects,

164
Q

What are delivery systems for inhaled drutgs?

A

Pressurised metered dose inhalers spacer devices or dry powder inhalers, nebulisers

165
Q

Why might yo use a nebuliser?

A

high dose and no need for technique of breathin

166
Q

What are the two ways to do bronchodilation?

A

adrenergic sympathetic or anti-cholinergic parasympathetic to block bronchoconstriciton

167
Q

What are the beta 2 adrenoceptors?

A

SABA LABA ultra-LABA short long estra long often with steroid inhalers

168
Q

How do anticholinergic bronchodilators work?

A

blocking muscarinic receptors in the lungs to stop activation of the muscle

169
Q

What are the muscarnic receptor antagonists?

A

Ipatropium bromide tiotropium bromide are mimics of atropine

170
Q

How do anti-inflammatory steroids work?

A

they reduce numbers of eosinophils, they supress production of chemotactic mediators reduce adhesion molecule expression and inhibit inflammatory cell survival in the airway downregulates inflammatory genes

171
Q

What is corticosteroid resitance?

A

often linked to non-eosinphillic type asthma COPD are resistant becuause doesnt have disease modifying affects

172
Q

Why are steroids and beta 2 agonists used in conjunction?

A

Steroids cause more receptor expression so potentiate beta agonists and the LABA increase translocation of Gene regulation from cytoplasm causing greaer efficacy of steroid action

173
Q

What is advantage of therapeutic antibodies?

A

long half life subcutaneous can be done by patient, work much better in certain things

174
Q

What is treatments for bronchiectasis?

A

Mucoulytic treat hypersecretion, beta agonists

175
Q

What is pneumothorax?

A

Presence of air into pleural space. air has entered frm hole in lung or chest wall injury can lead to collapse

176
Q

What is a tension pneumothorax?

A

one way valve causing positive pressure in the lung every time you breath in, high pressure in pleural space causes displacement of mediastinum. medical emergency,

177
Q

What is primary spontaneous pneumothorax?

A

Rupture of apical pleural bleb no underlying disease male taller smokers 20-40y/o

178
Q

What is secondar spontaneous pneumothroax?

A

caused by underlyin disease with asthma ILD CF lung cancer cystic lung disease COPD marfan’s birt-hogg dube, infection PCP TB catamenial pneumothorax

179
Q

What are other causes of pneumothroax?

A

penetrating chest wall injury, puncture from rib rupture bronchus or oesophagus, iatrogenic from pacemakers CT lung biopsy central line insertion mechanical ventilation pleural aspiration

180
Q

What is presentation of pneumothorax?

A

Acute sudden onset, breathlessness, pleuritic chest pain, life threatening respiratory failure cardiac arrest
tachypnoea, hypoxia unilateral chest wall expansion reduced breath sounds hyper resonant percussion, deviated trachea, distended neck veins surgical emphysema, cardiovascular compromise

181
Q

How to manage pneumothorax?

A

If less than 2 cm and well let go home and wait for it to settle over time. safety net though.
if larger aspirate up to 1.5 litres, chest drain or surgery for peristent and recurrent ones

182
Q

What is surgical emphysema?

A

Air under the skin from a tension pneumothorax need big chest drain

183
Q

What is pleural effusion?

A

Collection of fluid in the pleural space

184
Q

What is transudate effusion?

A

pleural protein low increased hydrostatic pressure or reduced osmotic pressure in microvascuature, heart failure cirrhotic licer disease renal failure hypoalbuminaemia myxodema ascites peritoneal. Meig’s syndrome right sided effusion ovarian fibroma ascities

185
Q

What are exudate effusions?

A

High protein. increase in capilliary prermeability and impared resorption. pneumonia cancer TB autoimmune conditions PE benign asbetos related effusion pancreatitis subdiaphragmatic collections post cardia surgery dreslers syndrome drug induces amiodarone Beta blockers methotrexate, henytoin

186
Q

What are signs and symptoms of pleural effusion?

A

Breathlessness cough pain fever additional relating to underlyinc cause, reduced chest wall expansion quiet breath soudns stoney dull percussion reduced tactile vocal fremitus mediastinal shift from affected side

187
Q

What is investigation for pleural effusion?

A

pleural aspiration, should be straw coloured.

188
Q

What is chylothorax?

A

milky pleural aspirate from blockage of lymph or thoraxic duct issue

189
Q

What to look at in pleural aspiration?

A

Macroscopic appearance clour, pH protein level LDH lucose amylase culture and TB cytology

190
Q

Where des chest drain go?

A

triangle under armpit lateral edge of latisimus dorsi, lateral edge of pectoris major, 5th intercostal space

191
Q

What is haemothorax?

A

Blood in pleural cavity use haematocrit to check

192
Q

What is cause of ahemothroax ?

A

Trauma post-operative, bleeding disorders, lung cancer, PE aortic rupture, thoracic endometriosis,

193
Q

How to treat haemothorax?

A

Drain with large bore, treat underlying causse stop bleeding

194
Q

What is hydropneumothorax?

A

usually iatrogenic air and fluid in pleural cavity

195
Q

What is pleural thickening?

A

can look like effusion thickening of the pleura either laer often related to asbestos exposure, can happen follwing infection epyeme chest trauma or haemothorax,

196
Q

What is pneumomediastinum?

A

air in mediatinum from lungs trachea oseophaus peritoneal cavity can track to neck and face oesophageal rupture

197
Q

What is importantt test for in TB?

A

HIV

198
Q

Where is TB very common?

A

Eastern europe and sub saharan africa.

199
Q

How is TB spread?

A

Droplets in the air coughed by someone. or in contamitate cows milk which presents with GI illeocecal disease

200
Q

What is the pathogenesis of TB?

A

macrophages engulf but can’t destroy, form granuloma to lock them away to die and often happens in apexis of the lungs. This usually allowed them to stop the infection from spreading

201
Q

What happens in TB with weakened immune system?

A

Granuloma fails and get dead TB and dead immune cell and get cavitating granuloma and inflammation of surrounding tissue ghon focus

202
Q

What is the presetation of TB?

A

Weight loss low grade fever anorexia night sweats and malaise, pulmonary cough for 3 weeks or more chest pain, breathlessness haemoptysis can be associatew with other lung conditions lymh node swelling discharge bone pain joing pain ascited abdominal lymph nodes ileal malabsorption Genito-urinary TB epididymitis frequency dysuria and haematuria

203
Q

WHat are the effectd of TB in the lung?

A

can erode into pleura and cause effusion, can erode into bronchus and causes pericardial effusion collapse of lung and consolidation

204
Q

Where can Tb infect?

A

GI lymph node, Pleurall Bone and joind CNS

205
Q

What is the name fo rTB all over body?

A

Miliary TB

206
Q

What happens in latent TB?

A

Body keeps it at bay but then can reactivate,

207
Q

How to diagnose active TB?

A

Definitive microbiology ,icroscopy AFB PCR culture suputum urine CFS pleural fluid lymoh node, non specific prolongued inflammatory respnse anaemia, low albumin hypergammaglobulinaemia hypercalcaemia thrombocytosis suggestive histopathologie of caseating granuloma with ZN

208
Q

How to diagnose laten TB?

A

use inderect measurements immune response to organism, mantoux tuberculin skin test, not sensitve for immunosuressed only moderately specific can also test blood, interferron gamma release assay

209
Q

Wha is treatment of active TB?

A

at least 4 for at least 6 months, rifampicin isoniazid, pyrazinamide ethambutol last two for first 2 months only

210
Q

What are problems with TB drugs?

A

side effects? Rifanpicine does red urine hepatitis drug interactions i

211
Q

Why is TB treatment so long?

A

most killed but go dormant and can relapse over time

212
Q

What is drug resistant TB?

A

multi and mono drug resistance aroudn 5 % drug resistance in UKvery high in Russia and China

213
Q

What is the most cost effective COPD treatment?

A

Flu vaccine and smoking cessation

214
Q

What is needed for COPD?

A

Obstrutive spirometry, Post bronchodilatorFEV1 RVC ratio low FEV1 is low

215
Q

What mechanisms underlie COPD?

A

Small airways disease airway inflammation aurway fibrosis luminal plugs and increased ariways resistance, Parenchymal destruction loss of elastic recoil

216
Q

What changes on flow volume curve for COPD?

A

high lung volume tidal breathing

217
Q

Clinical feature of COPD?

A

Cor pulmale, barrel chest from hyperinflation, breathless wheeze

218
Q

Who is pink puffer?

A

weight loss breathles emphysematous mainties sp O2

219
Q

What is a blue bloadter

A

cought phlegma cor pulmonale cyanosed

220
Q

Risk factor for COPD?

A

Cigarette smoke occupational dust and chemicals, environmental tobaccos smoke indoor and outdoor air pollution Genes, infections in utero condition

221
Q

How to mark dyspnoea?

A

1-5 SOB on marked exertion, 2 SOB on hills 3 slow or stop on flat, exercise tolerance 100m on flat 5 housebound/SOB on minor tasks

222
Q

What is involved withquality of life scores?

A

it is good for monitoring that patient’s progression

223
Q

What factors affect COPD decline?

A

Lung disease breathlessness, excercise limitation depression anxiety muscle wasting disability and personality and environment vicious cycle

224
Q

What are other COPD like diseases/

A

Any cause of SOB, heart railrue PE, pneumonia lung cancer asthma bronchiectasis

225
Q

What are differences in COPD and asthma/

A

Aasthma has variability and response to bronchodilator, spiraomitary may be normal diurnal variation

226
Q

What is pathological differentiation between asthma and COPD?

A

both inflammation asthma thickening basmente menbrane but get fibrosis in COPD asthma eosinophysls and COPD more neutrophyls

227
Q

What are comorbidities with COPD?

A

cancer depression anxiety, infections, and others

228
Q

What are options for COPD?

A

Rehabilitation exercise trainign programs for increasing tolerance. SABA and LAABAs and anticholiergics inhaled steroids are the main things

229
Q

What are treatment aims for COPD?

A

Reduce symptoms, inprove excercise tollerance improve health status reduces exacerbations, reduce mortaliti

230
Q

What happens in COPD exacerbation?

A

Negaticve QOL, impact on symptoms and lung function, increased economic costs,

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