Respiratory

Question 1

Helpful respiratory tests?

Answer 1

Lung function testing- spirometry, lung volumes, transfer factor- ability of O2 to cross alveolar membrane= decreased in emphysema, fibrosing alveolitis, anaemia, increased in pulm haemorrhage
Radiology- CT, plain XR, USS, bronchoscopy- indicated by radiology, haemoptysis, cough, wheeze, dyspnoea, undiagnosed infection, suspected aspiration of foreign body, therapeutic
Functional assessment; 6 minute walk, incremental shuttle walking test, cardio-resp exercise testing

Question 2

Normal intervals for PaO2, PaCO2, HCO3, pH? Type 1 and 2 resp failure values?

Answer 2

10.5-13.5
4.7-6
22-28
7.35-7.45
1= reduced PaO2 and normal/ low PaCO2
2= reduced PaO2 and increased PaCO2

Question 3

Alveolar-arterial gradient normal value? Raised in what? Hypoxaemia(reduced PaO2) due to what?

Answer 3

<2kPa
Alveolar membrane, interstitial diseases/ V/Q mismatch
Hypoventilation, reduced FiO2(or PATM)

Question 4

Response to hypoxia? High altitude pulm oedema and tx?

Answer 4

Pulm vasoconstriction and systemic vasodilation

1% at 4000m, 2-3 days after ascent, exaggerated hypoxic pulm vasoconstriction, tx= descent, O2, pulm vasodilators

Question 5

Functions of lungs and causes of disease? Single gene diseases? Issues with CF?

Answer 5

Gas exchange, acid-base balance, defence, hormones, heat exchange
Genes, environment, infection, cancer, AI disease, thromboembolism
CF, alpha-1 AT def, Kartagener’s syndrome, HHT, HPAH, pulm veno-occlusive disease, chronic gran disease
Abnormal ion transport, impaired mucociliary clearance, recurrent and chronic infections, impaired digestion, fertility issues, liver disease, diabetes

Question 6

Features of obstructive disease? Restrictive disease?

Answer 6

Narrowed airways- normal lung volume (FVC), long time to exhale(wheeze), FEV1/FVC<0.7, low FEV1, low peak flow, shallow spirometry graph e.g. asthma (variable) and COPD (fixed), CF, bronchiectasis

Low lung volumes, most breath out in 1st second, low FVC, normal/ high FEV1, FEV1/FVC>0.8, normal PEFR, tissue damage–> reduced lung volume e.g. interstitial lung diseases/ pulm fibrosis, sarcoidosis, neuromuscular disease

Question 7

Non-resp causes of SOB? Resp causes? Cause of low TLCO? High TLCO?

Answer 7

HD, anaemia, deconditioning, psychogenic
Asthma, pneumonia, PE, pneumothorax, hyperventiliation
Thickening alv-cap membrane, reduced volume

Increased cap blood volume, pulm haemorrhage

Question 8

Process of interstitial lung disease? Presentation x4? Split into what x2?

Answer 8

Disease of alveoli primarily–> scarring–> fibrosis
Dyspnoea, digits(clubbing,) dry cough, diffuse inspiratory crackles
Acute/ chronic
Acute= trauma, infection- TB, fungal, viral, drugs- nitrofurantoin and amiodarone, radiation, aspiration, gas inhalation, paraquat poisoning
Causes adult resp distress syndrome

Question 9

Chronic interstitial lung disease split into what? Process of idiopathic, shows what on CXR? Meds prescribed?

Answer 9

Idiopathic, pneumoconiosis, extrinsic allergic alveolitis/ hypersensitivity pneumonitis, sarcoidosis, connective tissue disease etc.

Unknown cause, gradual scarring–> pulm fibrosis–> resp failure–> cor pulmonale
Classic honeycombed due to fibrosis with inflammatory infiltrate
Pirfenidone- antifibrotic and anti-inflammatory, nintedanib= MAb targeting tyrosine kinase

Question 10

What is pneumoconiosis? examples?

Answer 10

Inhalation of something causes lung damage
Coal workers- coal taken up by macrophages, focal fibrous nodules due to scarring around bronchioles, veins and arteries–> coughing up black scarred tissue, Caplan’s syndrome- CWP with seropositive RA
Silicosis- inhaled stone/ sand from mining, silicon= toxic to macrophages, release enzymes–> alv destruction–> fibrosis, nodules of hard fibrous tissue form with empysema
Asbestosis–> slow progressing focal nodules at the lung bases, only after prolonged exposure

Question 11

What is extrinsic allergic alveolitis? Pres? e.g.?

Answer 11

Systemic reaction, inhaled dust–> allergic reaction and sensitisation, re-exposed–> type III(IgG) and immune complexes form–> inflammation, chronic–> fibrosis
Fever, weight loss, fatigue e.g. Farmer’s lung, pigeon fanciers lung etc. OLDs

Question 12

What is sarcoidosis?

Answer 12

Multisystem inflammatory disorder, mostly in lungs and mediastinal lymph nodes, non-caseating granulomas form due to CD-4 interactions–> type 4
Check serum ACE levels- secreted from nodules

Question 13

Types of occupational lung disorders?

Answer 13

Farmer’s lung- mouldy hay, pigeon fanciers lung- proteins in bird droppings, sugar workers, malt workers lung, cotton fibres, hot tub workers, prawn shellers lung etc.

Question 14

Occupational lung disorders can cause what conditions? Examples of hypersensitivity pneumonitis? Presents with what? Tx?

Answer 14

Bronchitis, fibrosis, carcinoma, asthma, hypersensitivity pneumonitis
Farmers lung, pigeon fanciers lung, winemakers lung, prawn shellers lung
Chronic cough and dyspnoea, fatigue

Avoid the antigen, corticosteroids for acute symptomatic relief

Question 15

Allergen triggers of asthma? Non-allergic? Exacerbating factors of asthma?

Answer 15

Dust, mites, pets, nuts, aspirin, drugs
Exercise, cold air, B-blockers, infection
Infection, trauma, allergens, pollution, smoking, stress, some medications

Question 16

S+S of asthma? Investigations?

Answer 16

Wheeze, SOBOE, chest tightness, unproductive cough with diurnal variation(worst in morning), hyperressonant percussion
Peak flow diary, spirometry FEV1/FVC<0.7, reversibility testing- given bronchodilator and peak flow is taken 20 mins later, FEV1 will improve>15% in patient in asthma

Question 17

Why is it bad if asthmatic has low CO2 (hypercapnia)? Tx?

Answer 17

Smooth muscle contraction and increased mucus–> asthma attack–> hyperventilation–> hypercapnia–> resp failure

Oxygen with nebulised SABA, 100mg hydrocortisone IV/ 40-50mg prednisolone PO, oxygen if sats<92%
PEF, sputum, FBC, U+E, CRP, blood cultures, ABG
If CO2 rises–> ITU/HDU

Question 18

Drug ladder for asthma?

Answer 18

SABA inhaler e.g. salbutamol for infrequent wheezy episodes
Add regular low dose inhaled corticosteroid
Add oral leukotriene receptor antagonist i.e. montelukast
Add LABA inhaler e.g. salmeterol, continue only if good response
Consider change–> maintenance and reliever therapy (MART) regime
Increased inhaled corticosteroid to a moderate dose
Consider increasing inhaled corticosteroid dose to high dose/ oral theophylline/ inhaled LAMA e.g. tiotropium
Refer to specialist

Question 19

How do SABAs work? Length of use? Inhaled corticosteroids e.g. beclomethasone used for what?

Answer 19

Adrenalin acts on smooth muscles–> dilatation of bronchioles and improves bronchoconstriction, used as reliever during acute exacerbations

Maintenance/ preventer and taken reguarly even when well

Question 20

How do LAMA work? How do leukotriene receptor antagonists work?

Answer 20

Block ACH receptors–> bronchodilation

e.g. montelukast- block effects of leukotrienes= inflammation, bronchoconstriction and mucus secretion

Question 21

How does theophylline work? MART?

Answer 21

Relaxing bronchial smooth muscle and reducing inflammation- narrow therapeutic window, toxic in excess- monitoring needed, 5 days after start and 3 days after each dose change

Combination inhaler= low dose inhaled corticosteroid and fast acting LABA, replaces all others- used as a preventer and a reliever when have symptoms

Question 22

What is pneumonia? Bacterial and viral causes? Types?

Answer 22

Inflammation and fluid collection in the lungs due to infection
Strep pneumoniae, staph aureus, legionella’s, jirovecci, virus= h.influenzae

Community acquired (CAP)= s.pneu, then h.influenzae, then mycoplasma pneu
Hospital acquired (HAP)- mostly gram -ve enteroa/ s.aureus
Aspiration- inhaled foreign object brings bacteria with e.g. people can't swallow properly

Question 23

People at risk of pneumonia?

Answer 23

Infants and elderly, COPD and other chronic, immunocompromised, nursing home residents, impaired swallowing, diabetics, CVD, congestive heart disease, alcoholics and IV drug users

Question 24

S+S of pneumonia? Investigations?

Answer 24

Pyrexia, cyanosis, tacypnoea, drop in bp, SPUTUM, confusion- esp elderly
Fever, rigors, fatigue, pleuritic chest pain, SOB, headache, cough with sputum

Gold standard= CXR- consolidation, listen to chest, determine organism= sputum sample and blood culture, urinary antigen test- legionellas, thoracentesis
Severity= CURB-65

Question 25

CURB-65 stands for?

Answer 25

Confusion, blood urea>7mmol/l, resp rate>30, BP<90/60, >65y/o= 1 point Score 1= treat as outpatient, 2= consider short stay hospital/ monitor closely as outpatient 3+= hospitalisation, consideration for ITU

Question 26

Tx for pneumonia?

Answer 26

Supportive and ABs, ABCDE approach- IV fluids, CPAP etc. analgesia- chest pain, AB- empirically immediately then guided after MC and S, thromboprophylaxis- risk of VTE

Question 27

ABs for pneumonia? For legionellas? May take how long for patient to fully recover from CAP?

Answer 27

Mild= oral amoxicillin, mod= oral amoxicillin and clarithromycin, severe= IV co-amoxiclav and clarithromycin Fluroquinolone (ciprofloxacin and clarithromycin) 6 months- residual symptoms

Question 28

Cause of mesothelioma? Symptoms? Investigations? Tx?

Answer 28

Asbestos Fever, weight loss, SOB, fatigue, persistent cough, clubbing CXR, CT Palliative, early= chemo/radiotherapy, surgery

Question 29

What is pneumothorax? 3 causes of pneumothorax?

Answer 29

Air in the pleural space- sudden onset, sharp, one sided pleuritic chest pain and SOB, worse when breathing in Truma- medical procedure, stab wounds, fractured ribs, medical procedure- biopsy, catheter Primary= damage to lungs with no underlying pathology- male, smoking, FH, CND Secondary= damage to lungs with underlying pathology

Question 30

Gold standard for pneumothorax diagnosis? Tx?

Answer 30

CXR: absent lung markings, collapsed lung, tracheal deviation towards pneumothorax Small spontaneous= heal on own, treat underlying cause, chest drain, surgery if bad

Question 31

What is tension pneumothorax? S+S? Tx?

Answer 31

Medical emergency- air in but not out--> increased resp rate Sudden onset SOB, pleural pain, reduced chest expansion, hyperresonant to percussion, reduced breath sounds Emergency needle thoracotomy- 2nd IC space mid clavicular line and drain out extra air

Question 32

What is pleural effusion? Fluids?

Answer 32

Build up of fluid in pleural space | Chyle, blood, serous pus

Question 33

What is transudate? Exudate?

Answer 33

Excessive production of pleural fluid/ resorption reduced e.g. heart failure, cirrhosis, nephrotic syndrome Damaged pleura e.g. PE, bacterial pneumonia, cancer, viral infection, pancreatitis

Question 34

S+S of pleural effusion? Investigations?

Answer 34

Decreased chest movement, reduced breath sounds, dull to percussion(all on affected side,) symptoms= SOB, cough, chest pain CXR: white fluid, CT, US, listen to chest: dull to percussion Thoracocentesis- what caused the pleural effusion?

Question 35

Tx for pleural effusion? Appearance and protein content of transudate? Exudate?

Answer 35

Aspirate/ chest drain, pleurodesis Clear<25g/L Cloudy>29g/L

Question 36

What value is pulm HTN? Causes split into what x4? What happens if pulm artery pressure is increased?

Answer 36

>25 mmHg Pre-capillary, capillary, post-capillary, chronic hypoxaemia R heart hypertrophy--> R HF--> ascites/ hepatomegaly

Question 37

Features of pre-capillary pulm HTN?

Answer 37

Multiple small PEs--> obliteration of vasc bed, L-->R shunts--> increased pulm blood flow and pressure Primary- familial?, two-hit hypothesis?

Question 38

E.g. of capillary pulm HTN? Features of post-capillary pulm HTN? Causes of chronic hypoxaemia?

Answer 38

Disease of pulm vascular bed e.g. emphysema, COPD Backlog of blood--> secondary pulm HTN, LV failure, MS--> CCH Living at high altitude, COPD

Question 39

High pressure leads to what? Haemorrhages? Presents? Tx?

Answer 39

Scarring--> reduced tCO--> dyspnoea, cyanosis--> haemorrhages--> haemoptysis--> narrowing of vessels--> fibrosis Fatigue, pre-syncope, tachycardia, raised JVP, altered heart sounds--> louder S2, peripheral oedema- sacral, ankle Treat cause, reduce risk of cor pulmonale Phosphodiesterase-5 inhibitors e.g. sildenafil, HF= diuretics, CCB= idiopathic, prostacyclin analogue- apoprostenol

Question 40

% of small cell and non small cell carcinoma of the bronchus/ pleura? Non small cell split into what 2 types? Cancers that metastasis to the lung?

Answer 40

10-15% 80-85%= squamous, adenocarcinoma Prostate, kidney, breast, bone, thyroid, ovary, colon

Question 41

Causes of lung cancer? S+S?

Answer 41

Smoking, metal dusts- chromium, asbestos, arsenic Cough, SOB, chest pain, haemoptysis, wt loss, anaemia, clubbing, supraclavicular/ axillary node enlargement

Question 42

Investigations for lung cancer?

Answer 42

CXR: hilar enlargement, peripheral opacity- visible lesion in lung field, pleural effusion- unilateral usually, collapse Staging CT scan of chest, pelvis and abdomen- stage, lymph node involvement and metastasis, contrast enhanced PET-CT= spread EBUS- tumour and US guided biopsy Histological diagnosis- check cell type, by bronchoscopy/ percutaneously

Question 43

Tx for stage 1/2 lung cancer? Stage 3/4? Complications?

Answer 43

Surgical excision and radical deep XR therapy Palliative chemo; chemo+ RT, care Panoasts tumour-->Horners syndrome, recurrent laryngeal nerve palsy, SVC obstruction, phrenic nerve palsy, metastasis, lambert eaton, SIADH, Cushing's

Question 44

Presentation of PE? RFs?

Answer 44

Sudden onset of SOB+ chest pain with past history of painful calves and recent long haul flight/ immobilisation, haemoptysis, pre-syncope, syncope, tachycardia, pyrecia, cyanosis, tachypnoea, HTN, raised JVP Recent immobilisation>3days, previous DVT/PE, pregnancy, thrombophilic syndromes- anti-phos, Factor V Leidens, malignancy, hormone therapy- HRT, COCP, smoking

Question 45

Well's score<2? 2-6? 6+? Other tests? Initial management?

Answer 45

PE unlikely Moderate possibility- do a D-dimer: -ve excludes PE, +ve= do imaging CTPA= gold standard O2, analgesia, anticoagulation- LMWH, start warfarin- long term/ DOAC e.g. rivaroxiban, embolectomy if large PE Haem unstable= alteplase RFs and cause gone- then stop Unknown cause/ prolonged risk, at least 6 months+ warfarin

Question 46

Features in a Well's score?

Answer 46

Clinical signs of PE/ DVT, PE most likely diagnosis, tachycardic, immobility>3 days, previous PE/DVT, haemoptysis, malignancy +/- treated in last 6 months

Question 47

What is COPD? 3 diseases under COPD? Type of resp failure?

Answer 47

Collection of lung diseases that cause irreversible obstruction to airflow out of the lungs Chronic bronchitis, emphysema, COAD Type 2- CO2 high, O2 low

Question 48

Causes of COPD?

Answer 48

Smoking= over 90% Some cases= alpha-1 anti-trypsin deficiency- pt= young, FH and liver disease A1ATD= lower acinar of the lungs are affected, those at top= COPD Other= CF, IV drug use- particularly cocaine, industrial exposure--> irritants e.g. mining

Question 49

Pathophysiology of emphysema? Chronic bronchitis?

Answer 49

Alveoli become large and lose their elasticity- they therefore cannot recoil and so expel all of the air out, smoking= releases inflammatory factors- break down collagen and elastic in the airways Airways--> inflamed due to irritants--> increased mucus production, smoking= increase in mucus gland number, irritants damage cilia, cannot remove mucus--> chronic cough and mucus/ phlegm production

Question 50

S+S of COPD? Investigations?

Answer 50

``` Signs= barrel shaped chest, ankle swelling, sputum, chronic cough, wheeze, cyanosis- blue lips and skin Symptoms= tired and lack of energy, low mood, SOB ``` Gold standard= spirometry- FEV1/FVC<70% CXR= shows hyperinflation of lungs, flattened diaphragm, barrel-shaped chest, DLCO

Question 51

Tx of COPD?

Answer 51

Aimed at improving symptoms and slowing down the progression- target sats- 88-92% Acute= O2, nebuliser SABA- salbutamol, inhaled steroids, treat the cause(infection= ABs) Long-term= smoking cessation, LAMA/LABA= tiotropium/ salmeterol, pulmonary rehab, inhaled corticosteroids, LTOT if criteria met, pneumococcal plus annual influenza vaccine

Question 52

In COPD leads to what eventually?

Answer 52

Normal respiratory--> hypoxic drive Raised CO2--> hypercapnia--> acid-base disorders, increases H+ which lowers pH, stimulates central chemoreceptors(medulla oblongata) and directly stimulates peripheral chemoreceptors- carotid bodies and aortic arch Chemoreceptors= less responsive to O2 levels, develop tolerance to chronically elevated arterial CO2 Target pulse oximetry= 88-92%

Question 53

A1AT deficiency causes what % of emphysema? A1AT regulates what activity? What builds up in the liver causing cirrhosis? What does this destroy leading to emphysema? Always consider in who and what? What in the lungs are affected?

Answer 53

2%= inherited Elastase activity In the liver Alveoli Young patients with COPD and deranged LFTs The lower acinar of the lungs, those at the top= COPD

Question 54

Features of chronic bronchitis?

Answer 54

``` Clinical diagnosis= daily productive cough for 3 months/ more in at least 2 consecutive years Overweight and cyanotic Elevated haemoglobin Peripheral oedema Wheezing ```

Question 55

Features of emphysema?

Answer 55

Permanent enlargement and destruction of airspaces distal to the terminal bronchiole Older and thin Severe dyspnoea Quiet chest X-ray= hyperinflation, flattened diaphragms

Question 56

Drug ladder for COPD?

Answer 56

SABA-->LABA--> LABA+ corticosteroid--> LABA+ corticosteroid+ LAMA

Question 57

Adverse effects of Beta agonists? Of corticosteroids?

Answer 57

Tremor, palpitations, hypokalaemia- low K+, muscle cramps Osteoporosis and subsequent fractures, take bisphosphonates and vit D analogue, increase infection risk, weight gain

Question 58

What is bronchiectasis? Causes? Investigations?

Answer 58

Irreversible dilation of the bronchioles, build up of mucus, increase chance of infection, scarred, loss of cilia End point/ complication of lots of lung diseases e.g. COPD, CF, infection HRCT, sputum culture: look for infectious agents in the airways so can treat with the right antibiotic

Question 59

Tx of bronchiectasis?

Answer 59

Symptom management, non pharmacological= stop smoking, vaccinations, pharmacological= ABs, bronchodilators, steroids

Question 60

Presentation of bronchiectasis?

Answer 60

Chronic cough, foul-smelling sputum, flecked blood sometimes, inflam and fibrosis in adjacent tissue

Question 61

What does cystic fibrosis cause a defect in? Presents where? Affects what? S+S?

Answer 61

CFTR channel protein- Cl---> thick mucus clogging ducts Childhood Airways, pancreas, GI tract etc Signs= steatorrhoea, children with failure to thrive, finger clubbing, rectal prolapse, symptoms= heavy mucus production and cough

Question 62

Investigations for cystic fibrosis?

Answer 62

90%= diagnosed before age of 8, sweat (NaCl test)- parents taste salt when kissing baby, Cl- pumped out onto skin instead of into lumen Genetic testing- F508= most common Faecal elastase in newborns- marker of pancreatic damage caused by CF

Question 63

PP of cystic fibrosis? Tx?

Answer 63

CTFR= Cl- and water cannot move into lumen, Na+ also into cells and draws water in and makes mucus more thick and sticky ``` LE= about 50, non-pharm= physio, high calorie diets Pharm= ABs prevent infections, anti-mucinolytics- carbocyctiene, enzymes and PPI, insulin, bisphosphonates Surgery= lung surgery if bad ```

Question 64

When can and can't people stand with CXR? Process of viewing?

Answer 64

PA= can, AP= can't Diaphram--> mediastinal- heart, hilarity common for lymphadenopathy, pleura, through rib spaces- compare sites, apex of lungs- 'Bermuda's triangle,' back at hilum, then below hemidiaphragm, then shoulders

Question 65

2 Qs for CXR? If pathology obscures RH border what lobe? Doesn't obscure? What is consolidation?

Answer 65

Is abnormality dense/ Lucent? Mass effect/ volume loss? Right middle lobe, right lower lobe Solid mass e.g. blood, pus, tumour No volume loss= collapse

Question 66

ABCDE signs of heart failure of XR?

Answer 66

Alveolar oedema, Kerly B lines- leak into interstitial space, Cardiomegaly>50% thoracic cage, upper lobe venous distension, Effusions- both costophrenic angles

Question 67

Signs of left upper lobe collapse?

Answer 67

Forwards, blurred left lung appearance, can be malignant

Question 68

Type 1 resp failure caused by what? Type 2?

Answer 68

Limitation of ventilation, perfusion/ diffusion e.g. COPD, pneumonia, pulm fibrosis, asthma, pneumothorax, ARDs Alv hypventilation, CO2--> alv not removed e.g. drug overdose, muscle disorders, severe asthma, MG, ARDs, increased airway resistance- COPD/ asthma, reduced breathing effort- effort/ brainstem lesion/ obesity Neuromuscular problem- GB syndrome, MND

Question 69

Tx of resp failure? FEV1, FEV1/FVC ratio and peak flow in obstructive and restrictive disease?

Answer 69

ABC, oxygen, cause, continuous positive airway pressure- CPAP= type 1, non-invasive ventilation- NIV- type 2 Reduced FEV1, ratio and peak flow e.g. COPD, asthma, CF, increased airway resistance Reduced FVC, FEV1, normal ratio and PEFR e.g. pulm fibrosis, asbestosis, silicosis, decreased airways compliance (volumes)

Question 70

What is inspiratory reserve volume? Minute volume? Expiratory reserve volume? Residual volume?

Answer 70

Additional volume that can be forcibly inhaled following a normal inspiration Volume of air inhaled and exhaled per minute Additional volume can be forcibly exhaled following normal expiration Volume remaining after maximal expiration

Question 71

What is vital capacity?Functional residual capacity? Inspiratory capacity? Total lung capacity? Tidal volume?

Answer 71

Maximal volume forcibly exhaled after maximal inspiration Volume air remaining at end of normal expiration Volume can be inspired following normal, quite expiration, equal to TV+ IRV Volume of air in lungs at end of maximal inspiration Volume moved in and out of resp tract during each ventilatory cycle

Question 72

What is FEV1? FVC? Forced expiratory flow(FEF25-75)? Peak expiratory flow?

Answer 72

Volume of air that is forcibly exhaled in one second Volume can be maximally forcefully exhaled Average forced expiratory flow during the mid portion of FVC Peak flow rate during expiration

Question 73

What is TB caused by? Spread by what? Affects where in the lungs? What is it also? S+S?

Answer 73

Mycobacterium tuberculosis- aerobic, non-motile rod shaped Airborne droplets Apex of lungs Notifiable disease with long latency period Signs= cough up blood, inidividual= look unwell, symptoms= fever, night sweats, chills, chest pain

Question 74

Diagnosis of TB?

Answer 74

Gold standard= sputum test x3 Ziehl-Nielsen stain Mantoux skin test- intradermal infection antigen, cell mediated response recorded at 48-72 hours, strong= active TB, false +ves with previous exposure/ BCG, false -ves= immunosuppression CXR= enlarged lymph nodes, hole/ coin shape in CT= Gohn complex CT scan Lumbar puncture and CSF examination- all cases biliary TB Bronchoscopy if no sputum Histology= caveating granuloma

Question 75

3 types of TB?

Answer 75

Healthy= never infected Active- bacteria multiplying in lungs Latent- bacteria not dividing, asymptomatic, reactivated by depressed immune system

Question 76

Tx for TB? What given to reduce risk of isoniazid-induced peripheral neuropathy? If affecting CNS how long tx?

Answer 76

6 months RIPE= rifampicin, isoniazid, pyramidine, ethambutol Pyroxidine 12 months

Question 77

What give meds under supervision in TB? In what patients experience multi drug resistance--> isoniazid and rifampicin?

Answer 77

Direct observed therapy= DOTs | HIV patients, extensively drug resistance TB

Question 78

SEs of rifampicin? Isoniazid? Pyramidine? Ethambutol?

Answer 78

Red body fluids- urine, sweat, tears Peripheral neuropathy Hepatitis 'Eye'- Visual problems

Question 79

Prevention in TB?

Answer 79

CXR of contacts of case, Mantoux test | Vaccination with BCG- neonatal in high risk groups= FH, ethnic minority, high incidence areas

Question 80

Bacilli + macrophages in TB form what? Subpleural lesion produced? Ghon complex consists of what? Primary lesion can also occur where? Bacilli taken where?

Answer 80

Granuloma Ghon focus- central area of caseation surrounded by epitheloid cells and Langhan's giants cells, small nodule in mid zone on CXR Caseous lesions in lymph nodes and primary ghon focus In GI tract- ileocaecal region, Lymph nodes --> secondary lesions

Question 81

In most people with TB what 2 things heal and calcify? Dissemination of primary infection happens occasionally to cause what? Flow of TB types?

Answer 81

Primary focus and lymph nodes, can contain bacilli can be reactivated if IS depressed Miliary TB Primary TB--> progressive primary TB--> post primary TB (reactivation/ reinfection)

Question 82

Types of extra-plum TB? RFs for TB?

Answer 82

Hilar lymphadenopathy, bone pain/ swelling, abdominal, genito-urinary, CNS- meningitis+ CNS palsy, tuberculoma Sub-Saharan Africa, HIV--> immunosuppression, IVDU, homeless, alcoholic, prisons

Question 83

Rhinovirus causes what? Adenovirus? RSV? Parainfluenza virus?

Answer 83

Common cold- sinusitis and bronchitis Pharyngitis and bronchitis Bronchiolitis in kids and pneumonia in immunocompromised Croup- swelling in windpipe, ''Barking cough", stridor, hoarse voice, fever and runny nose

Question 84

Presentation of pharyngitis? Diff diagnosis?

Answer 84

Usually viral, also s.aureus Young w/sore throat, tender neck glands, large tonsils w/exudate Glandular fever, EBV, acute HIV infection

Question 85

Presentation of sinusitis? Acute epiglottitis? Caused by what? Why incidence increased?

Answer 85

Pain in L ear w/10 day cold, history of rhinitis, uses steroid nasal spray Sore throat and pain when swallowing(odynophagia), febrile and high pitched wheeze when breathing in--> H/influenzae B, due to Hip vaccine

Question 86

Presentation of whooping cough? Caused by? See what therefore? Comps? Most do what but lasts how long?

Answer 86

Young mother w/cough w/occasional vomit and sub conjunctival haemorrhage(red eyes) Bordetella pertussis- increased lymphocytes in blood and TH17--> chronic inflammation and cough Pneumonia, encephalopathy, subconjunctival haemorrhage Recover well, months

Question 87

Some whooping cough pts develop what? Tx?

Answer 87

Esp babies<2 months old= pneumonia +/- subsequent bronchiectasis, fits and brain damage Clarithromycin dose PO, pregnant= erythromycin Not macrolides= cotrimoxazole, exclude from school etc until treated for 5d

Question 88

Presentation of croup-acute laryngo-tracheobronchiolitis? Due to what virus?

Answer 88

3 yo w/barking cough, inspiratory stridor and is cyanosed- parainfluenza virus

Question 89

Presentation of bronchiolitis? Due to what virus?

Answer 89

3m child w/severe resp distress (sats=88%, wheeze, child premature@7m)- respiratory syncytial virus(RSV)--> inflammation of bronchioles and mucus production

Question 90

3 examples of immune mediated lung disease? What does pulm vasculitis describe? Lung vasculitis most commonly seen with what?

Answer 90

Pulm vasculitis, Goodpastures syndrome and Wegener's granulomatosis Destruction of blood vessel disorders Primary idiopathic, small vessel/ ANCA-ass vasculitis, granulomatosis with polyangitis, microscopic polyangitis, Chur-Strauss syndrome Medium vessels- classic PN Large vessel- Takayasu Primary IC- mediated vasculitis= Goodpasture's disease Secondary vasculitis

Question 91

What is Goodpastures syndrome? What is pulmonary-renal syndrome? Caused by what? Epidemiology?

Answer 91

Ab to type IV collagens after some viral infections Acute GN + lung symptoms (haemoptysis/ diffuse pulm haemorrhage)- by anti-glomerular basement membrane antibodies--> kidney's basement membrane and alveolar membrane, may be ANCA +ve Individuals>16 years

Question 92

S+S of Goodpasture's? Investigation and diagnosis? Differential?

Answer 92

Starts as upper resp tract symptoms, followed by cough, intermittent haemoptysis, tiredness, eventual anaemia, massive bleeding CXR= infiltrates due to pulm haemorrhage, often in lower zones, kidney biopsy: crescentic GN Idiopathic pulm haemosiderosis- no anti-basement membrane ABs and kidneys less involved, children under 7, cough and anaemia and pulm bleeding, ass--> cow's milk

Question 93

Tx for Goodpasture's?

Answer 93

Some may spontaneously improve, others--> renal failure Treat shock, vigorous immunosuppressive tx e.g. corticosteroids and plasmapheresis- remove blood and clean to remove antibodies before inserting back in

Question 94

What is Wegener's granulomatosis?

Answer 94

Unknown aetiology, necrotising granulomatous inflammation and vasculitis of small and medium vessels One of primary systemic vasculitides in which small arteries= predominantly affected Lesions involving upper resp tract, lungs and kidneys

Question 95

S+S of WG?

Answer 95

Start with severe rhinorrhoea and nasal mucosal ulceration- 'saddle-nose' deformity Followed by cough, haemoptysis and pleuritic pain Renal disease--> rapidly progressive GN with crescent formation, proteinuria/ haematuria May also be skin purpura/ nodules, peripheral neuropathy, arthritis/ arthralgia/ ocular involvement

Question 96

Investigation and diagnosis of WG? Differential?

Answer 96

Bloods= cytoplasmic ANCA directed against PR3, raised ESR/CRP CXR= nodular masses/ pneumonic filtrates with cavitation- clear migratory pattern Differential: midline granuloma (affects nose and sinuses) Churg-Strauss syndrome- small arteries, male 40s, 3= rhinitis, asthma, eosinophilia and systemic vasculitis, high eosinophil and ANCA positive Microscopic vasculitis polyangitis- haemoptysis, ANCA positive, lungs and kidneys

Question 97

Tx of WG?

Answer 97

Depends on extent of disease, severe= tx with corticosteroids e.g. cyclophosphamide/ rituximab Azathioprine and methotrexate used as maintenance