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Phase 2a Flashcards > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Helpful respiratory tests?

A

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

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2
Q

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

A

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

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3
Q

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

A

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

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4
Q

Response to hypoxia? High altitude pulm oedema and tx?

A

Pulm vasoconstriction and systemic vasodilation

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

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5
Q

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

A

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

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6
Q

Features of obstructive disease? Restrictive disease?

A

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

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7
Q

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

A

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

Increased cap blood volume, pulm haemorrhage

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8
Q

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

A

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

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9
Q

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

A

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

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10
Q

What is pneumoconiosis? examples?

A

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

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11
Q

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

A

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

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12
Q

What is sarcoidosis?

A

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

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13
Q

Types of occupational lung disorders?

A

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.

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14
Q

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

A

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

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15
Q

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

A

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

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16
Q

S+S of asthma? Investigations?

A

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

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17
Q

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

A

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

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18
Q

Drug ladder for asthma?

A

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

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19
Q

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

A

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

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20
Q

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

A

Block ACH receptors–> bronchodilation

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

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21
Q

How does theophylline work? MART?

A

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

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22
Q

What is pneumonia? Bacterial and viral causes? Types?

A

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
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23
Q

People at risk of pneumonia?

A

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

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24
Q

S+S of pneumonia? Investigations?

A

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

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25
Q

CURB-65 stands for?

A

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

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26
Q

Tx for pneumonia?

A

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

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27
Q

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

A

Mild= oral amoxicillin, mod= oral amoxicillin and clarithromycin, severe= IV co-amoxiclav and clarithromycin

Fluroquinolone (ciprofloxacin and clarithromycin)

6 months- residual symptoms

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28
Q

Cause of mesothelioma? Symptoms? Investigations? Tx?

A

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

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29
Q

What is pneumothorax? 3 causes of pneumothorax?

A

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

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30
Q

Gold standard for pneumothorax diagnosis? Tx?

A

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

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31
Q

What is tension pneumothorax? S+S? Tx?

A

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

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32
Q

What is pleural effusion? Fluids?

A

Build up of fluid in pleural space

Chyle, blood, serous pus

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33
Q

What is transudate? Exudate?

A

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

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34
Q

S+S of pleural effusion? Investigations?

A

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?

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35
Q

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

A

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

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36
Q

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

A

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

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37
Q

Features of pre-capillary pulm HTN?

A

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

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38
Q

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

A

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

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39
Q

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

A

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

40
Q

% 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?

A

10-15%
80-85%= squamous, adenocarcinoma

Prostate, kidney, breast, bone, thyroid, ovary, colon

41
Q

Causes of lung cancer? S+S?

A

Smoking, metal dusts- chromium, asbestos, arsenic

Cough, SOB, chest pain, haemoptysis, wt loss, anaemia, clubbing, supraclavicular/ axillary node enlargement

42
Q

Investigations for lung cancer?

A

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

43
Q

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

A

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

44
Q

Presentation of PE? RFs?

A

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

45
Q

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

A

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

46
Q

Features in a Well’s score?

A

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

47
Q

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

A

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

48
Q

Causes of COPD?

A

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

49
Q

Pathophysiology of emphysema? Chronic bronchitis?

A

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

50
Q

S+S of COPD? Investigations?

A 
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

51
Q

Tx of COPD?

A

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

52
Q

In COPD leads to what eventually?

A

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%

53
Q

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?

A

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

54
Q

Features of chronic bronchitis?

A 
Clinical diagnosis= daily productive cough for 3 months/ more in at least 2 consecutive years 
Overweight and cyanotic
Elevated haemoglobin
Peripheral oedema
Wheezing
55
Q

Features of emphysema?

A

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

56
Q

Drug ladder for COPD?

A

SABA–>LABA–> LABA+ corticosteroid–> LABA+ corticosteroid+ LAMA

57
Q

Adverse effects of Beta agonists? Of corticosteroids?

A

Tremor, palpitations, hypokalaemia- low K+, muscle cramps

Osteoporosis and subsequent fractures, take bisphosphonates and vit D analogue, increase infection risk, weight gain

58
Q

What is bronchiectasis? Causes? Investigations?

A

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

59
Q

Tx of bronchiectasis?

A

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

60
Q

Presentation of bronchiectasis?

A

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

61
Q

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

A

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

62
Q

Investigations for cystic fibrosis?

A

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

63
Q

PP of cystic fibrosis? Tx?

A

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
64
Q

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

A

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

65
Q

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

A

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

66
Q

ABCDE signs of heart failure of XR?

A

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

67
Q

Signs of left upper lobe collapse?

A

Forwards, blurred left lung appearance, can be malignant

68
Q

Type 1 resp failure caused by what? Type 2?

A

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

69
Q

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

A

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)

70
Q

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

A

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

71
Q

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

A

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

72
Q

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

A

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

73
Q

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

A

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

74
Q

Diagnosis of TB?

A

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

75
Q

3 types of TB?

A

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

76
Q

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

A

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

77
Q

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

A

Direct observed therapy= DOTs

HIV patients, extensively drug resistance TB

78
Q

SEs of rifampicin? Isoniazid? Pyramidine? Ethambutol?

A

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

79
Q

Prevention in TB?

A

CXR of contacts of case, Mantoux test

Vaccination with BCG- neonatal in high risk groups= FH, ethnic minority, high incidence areas

80
Q

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

A

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

81
Q

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

A

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)

82
Q

Types of extra-plum TB? RFs for TB?

A

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

83
Q

Rhinovirus causes what? Adenovirus? RSV? Parainfluenza virus?

A

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

84
Q

Presentation of pharyngitis? Diff diagnosis?

A

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

85
Q

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

A

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

86
Q

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

A

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

87
Q

Some whooping cough pts develop what? Tx?

A

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

88
Q

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

A

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

89
Q

Presentation of bronchiolitis? Due to what virus?

A

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

90
Q

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

A

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

91
Q

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

A

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

92
Q

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

A

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

93
Q

Tx for Goodpasture’s?

A

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

94
Q

What is Wegener’s granulomatosis?

A

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

95
Q

S+S of WG?

A

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

96
Q

Investigation and diagnosis of WG? Differential?

A

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

97
Q

Tx of WG?

A

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

Phase 2a Flashcards (14 decks)

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