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Phase 2A > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What is spirometry?

A

assesses lung function by measuring expiration volume after max inhale

differentiates between obstructive and restrictive lung disease

Includes FEV1, FVC, and % (normal 0.7)

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2
Q

What is FEV1? Normal values?

A

Forced expiratory volume in 1’s

Volume exhaled in 1st second after deep inspiration and forced expiration

80% or greater than predicted is normal

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3
Q

What is FVC? Normal values?

A

Forced Vital Capacity

Total volume of air that patient can forcibly exhale in one breath

  • *80% or greater** than predicted is normal
  • *Low = airway restriction**
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4
Q

How are the results of spirometry expressed?

A

FEV1 / FVC

in %, best of three readings

Normal is >0.7

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5
Q

What does it mean to have an obstructive spirometry pattern?

A

FEV1/FVC below 0.7 = obstruction

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6
Q

What does it mean to have a restrictive spirometry pattern?

A

Normal FEV1/FVC > 0.7
but FVC is low = restriction

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7
Q

Name a few obstructive diseases?

A

COPD, asthma, emphysema, bronchiectasis, bronchiolitis,
cystic fibrosis

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8
Q

Name a few restrictive diseases?

A

Pulmonary
Pulm fibrosis, Pulm oedema, TB !

Non pulm
kyphoscoliosis, neuromuscular disease, connective tissue disease, obesity, pregnancy

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9
Q

What is reversibility?

A

Bronchodilator responsiveness - see if lung function gets better with meds

If
reversible - + asthma likely diagnosis
not reversible - fixed obstructive patho
partially reversible - coexist

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10
Q

How might you assess reversibility?

A

Spirometry → Administer bronchodilator → repeat

Test with 400 microgram salbutamol

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11
Q

Compare and contrast asthma & COPD?

A

Asthma
variable airflow obstruction
reversible

COPD
fixed airflow obstruction
may be mixture

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12
Q

What is COPD?

A

Chronic Obstructive Pulmonary disease

persistent airflow limitation, not fully reversible

progressive, assoc chronic bronchitis & empysema

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13
Q

What is chronic bronchitis?

A

Cough with sputum for 3 months
2 or more years

  • *Hypertrophy & hyperplasia of bronchi** = bronchoconstriction, - airflow,
  • *narrowing of airways**
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14
Q

What is emphysema?

A

Histological!

Enlarged airspaces distal to terminal bronchioles, with destruction of alveolar walls

loss of elastic recoil = - expiratory airflow
loss of alveoli = loss of SA for exchange
= airway collapse during expiration

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15
Q

Risk factors for COPD?

A

Cigarette smoke
Occupational exposure to pollutants, dust, chemicals, smoke

alpha-1 antitrypsin deficiency

recurrent lung infections

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16
Q

How might cigarette smoke cause COPD?

A

Mucus gland hypertrophy in large airways
= increase in WBC (N, M & L) & release of inflam mediators →

structural changes in lung = emphysema

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17
Q

Presentation of COPD (4)?

A

Productive cough
with white or clear sputum

Breathlessness - even at rest
prolonged expiration, poor chest expansion
lungs hyperinflated = barrel chest
Pursed lips on expire = prevent alveolar & airway collapse

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18
Q

Extra-pulmonary manifestations of COPD?

A

Pulmonary hypertension
= fluid retention, peripheral oedema
= (severe) RV hypertrophy, cyanosed

Weight loss, reduced muscle mass, general weakness, osteoporosis, depression

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19
Q

Function of alpha-1 antitrypsin in normal person?

A

secreted by liver, acts in parenchyma

Inhibits elastase
= protease that breaks down elastin

Elastin = important for
structural integrity of alveoli

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20
Q

How might alpha-1 antitrypsin deficiency caused COPD present?

A

Early onset, family history!
auto recess
smoking still +++ risk tho

a-1 a = hepatic secreted elastase inhibitor, deficiency = breakdown of alveoli = emphysema

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21
Q

Investigations for COPD (4)?

A

Lung function test
FEV < 80
FEV1/FVC < 0.7 = obstruct

CXR / CT
normal / hyper inflated lungs = low flattened diaphragm, long narrow heart shadow
reduced peripheral lung markings
bullae = airspace >1cm, complete destruct of lungs

FBC = chronic hypoxia

alpha-1 antitrypsin levels / genotypes
esp in premature disease & lifelong non smokers

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22
Q

What is peak flow?

A

= test of peak flow rate during forced expiration following max inspiration

Varies with:
diurnal (high afternoon low early)
age, gender, height

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23
Q

How might you differentiate between asthma & COPD (in investigations)?

A

Repeat peak flow to exclude asthma

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24
Q

Classification of stages of COPD?

A

Stage 1 - FEV1 <80%
Stage 2 - FEV1 50-79
Stage 3 - FEV1 30-49
Stage 4 - FEV1 <30%

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25
Q

Lifestyle tx before pharm tx (5)?

A

stop smoking!!! duh

pneumococcal and influenza vaccinations

pulmonary rehab if indicated

make a self management plan with patient

treat comorbidities

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26
Q

Pharma tx principles for COPD?

A

1st line = SABA / SAMA

2nd- Steroid responsive / asthma features?
yes - LABA + ICS
no - LABA + LAMA

3rd
(LABA + LAMA) + ICS 3 months
= if 2nd & still affect QoL
(LABA + LAMA) + ICS
= if 1 severe or 2 modern exa / year
(LABA + ICS) + LAMA
QoL or 1s2m/y

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27
Q

What are SAMA / LAMAs? Examples?

A

Antimuscarinics = competitive inhibitor of Acetylcholine → reduce smooth muscle tone
= bronchodilation

-ium ending!

Short = ipratropium

Long = titropium, glycopyroonium, aclidinium

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28
Q

What are SABA/LABAs? Examples?

A

Beta 2 agonists = smooth muscle relaxation, (K+ to cells)

Short = salbutamol. terbutaline

Long = salmeterol, formoterol

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29
Q

What are ICS? Examples?

A

Inhaled corticosteroids = alternates transcription so reduces IL & chemokines, increases antiinflam proteins → reduce mucosal inflammation, widen airways & reduce mucus secretion

Examples = beclometasone, budesonide, fluticasone

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30
Q

Pathophysio of asthma!

A

Airflow limitation

Airway hyper responsiveness

Bronchial inflammation → plasma exudate oedema, smooth muscle hypertrophy, mucus plugging and epithelial damage

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31
Q

Cells involved in airway inflammation in asthma?

A

Main mediator = IgE

Mast cells → histamine = bronchoconstrict, prostaglandin, cytokine, IL345

Eosinophils → by IL3 & 5

Dendritic cells & lymphocytes: present allergens to lymphocytes & release cytokine

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32
Q

Two main types of asthma?

A

Allergic / eosinophilic asthma (70%)
allergens & atopy

Non-allergic / non eosinophilic (30%)
Exercise, cold air & stress
smoking, obesity

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33
Q

Non-acute attack symptoms of asthma?

A

Nocturnal worse: cough / dyspnoea
frequent in children

intermittent dyspnoea, wheeze, sputum

May be linked to ‘provoking †’ = allergens, infections, men-cycle, exercise, cold air

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34
Q

Features of an asthma attack?

A

reduced chest expansion / prolonged expiratory time / bilateral expiratory polyphonic wheezes / tachypnoea

severe = silent chest / cyanosis (PaO2 < 8kPa) / bradycardia / PEFR < 33%

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35
Q

Immediate management if life threatening attack?

A

Oxygen to maintain O2

Nebulised 5mg salbutamol + ipratropium - repeat / IV

Prednisolone ( ± hydrocortisone IV)

ABG, repeat in 2hrs
PEFR regularly
Oximetry → SaO2 > 92%
CXR if no response

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36
Q

How might you diagnose asthma?

A

RCP3 questions - nocturnal / usual in a day? / interfere with daily living?

1- Lung function test

  1. Nitric oxide FeNO test
  2. Peak flow readings

blood & sputum test → eosinophilia in sputum = specific!

Skin prick allergen test

Asthma control test
25 good, 20-24 on target, 20 = off

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37
Q

What will an asthmatic lung function test look like?

A

Peak expiratory flow rate PEFR - measure on waking, prior to b.d. & before bed, after bronchodilator

→ diagnostic if > 15% improvement on FEV1 or PEFR follow b.d.

Spirometry = assess reversibility
Exhaled nitric oxide = assess efficacy of corticosteroids
Carbon monoxide test = normal

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38
Q

How might you distinguish asthma from COPD?

A

COPD = later disease, smokers
Progressive short of breath with wheeze as a part of symptom complex

= less day to day variation
winter symptoms and sputum production in COPD

* but can overlap!

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39
Q

Treatment algorithm for asthma in >17? (NICE)

A

Short term, 1st: SABA
Maintenance 1st: ICS + SABA

+ LTRA
then onwards, LTRA optional
+ LABA
+ LABA in MART

Sebastian’s steroids went ultra fast in a lazy supermarket

MART = maintenance and reliever therapy

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40
Q

Treatment algorithm for asthma in 5-16?

A

Short = SABA

Maintenance
ICS + SABA
ICS + LTRA
ICS + LABA

Then
Maint: ICS + LABA in MART
Short: ICS + LABA in MART

Then
Main: up ICS + LABA in MART or fixed
Short: ICS + LABA in MART
or change to SABA

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41
Q

Beta agonists for asthma
Effective time, examples and type of agonist?

A

Short acting BA - 4 hours
Salbutamol = partial agonist
Terbutaline

Long acting BA - 12 hours
Salmeterol
Formoterol = full agonist

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42
Q

How does LABA last longer and what should you be careful of with badly controlled asthmatics?

A

LABA = longer since more lipophilic = remain in tissue longer

In badly controlled asthmatics - high concentration may lead to tolerance due to B2-receptor desensitisation

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43
Q

Types of ICS for asthma?

A

= semi-synthetic glucocorticoids

Budesonide, beclomatasone, prednisolone

(mineralo involves aldosterone so Na+)

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44
Q

What is an LTRA?

A

Leukotriene receptor antagonist
e.g. montelukast

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45
Q

What is bronchiectasis?

A

Chronic infection of the bronchi & bronchioles → airway distortion & dilatation with inflam process in wall of the airway

Results from pulmonary inflammation & scarring due to infection, bronchial obstruction or fibrosis

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46
Q

Risk factors for bronchiectasis?

A

women > men, increase w/age

pathological endpoint for many diseases

HIV, UC, RA!

  • *post INFECTIONS**
    e. g. pneumonia, TB, measles, pertussis
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47
Q

Causes of bronchiectasis?

A

Infections!!
again, pneumonia, TB, measles, pertussis, whooping cough

Congenital
CF, Kartagener’s

Mechanical obstruction
foreign body, lymph node, tumour

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48
Q

Briefly describe pathophysiology of bronchiectasis (again)?

A

Failure of mucociliary clearance + impaired immune = insult to bronchial wall → uncontrolled inflammation → bronchitis → bronchiectasis → fibrosis

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49
Q

Present - bronchiectasis?

A

Productive cough with large amounts of foul smelling, discoloured (khaki / green) sputum
occasional haemoptysis

Infection = + sputum volume, + purulence

  • *Finger clubbing**! esp CF
  • *Chest pain**!

Dilated, thick bronchi on CT

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50
Q

Investigations for bronchiectasis?

A

Usually lower lobes affected!

CXR
cystic shadows: cysts w/ fluid
dilated bronchi & thickened walls = tramlines & ring shadows

High Res CT
Thickened, dilated bronchpi + cysts
always > assoc. blood vessels

Spirometry = obstructive
Bronchoscopy to sputum culture!

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51
Q

Common causal organisms for bronchiectasis?

A

H. influenza

S. pneumoniae

S. aureus

P. aeruginosa

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52
Q

Treatment for bronchiectasis?

A

Improve mucus clearance
chest physio, mucolytics, postural drain

  • *Antibiotics**
  • *H. influenza** = amoxi / co-amoxiclav / doxycyline but if resistant = IV cephalosporin
  • *S. aureus** = flucloxacillin
  • *P. aeroginosa** = high dose oral ciprofloxacin

Anti-inflammatory agents = long term azithromycin can reduce exacerb freq

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53
Q

What is cystic fibrosis?

A

Disease of exocrine gland function affecting mainly caucasians

auto recess!
multi system usually w/ pancreatic insuff

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54
Q

Pathophysio of cystic fibrosis?

A

Mutation on chromosome 7
= defective CF transmembrane regulator (CFTR) protein

defective Cl- secretion & increased Na+ absorption in airways = increased H2o absorp → thickened secretion in number of organs

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55
Q

How might CF manifest in the lungs?

A

= dehydrated airway surface liquid,
= mucus stasis, airway inflam & recurrent infection

predisposed to chronic pulmonary infections + progressive obstruct

final = bronchiectasis

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56
Q

How might CF present extra-pulmonarily?

A

Salty sweat!!

Reduced pancreatic enzymes → pancreatic insufficiency (DM & steatorrhoea)

Distal intestinal obstruction syndrome
= reduced GI motility, maldigest & malabsorp

Male urogenital abormality, female amenorrhea

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57
Q

How might you test for cystic fibrosis?

A

fam hist + clinical hist

Sweat test
= high [Na+] & [Cl-], >60mmol/L

Genetic screening for CF mutations

Faecal elastase test
tests for protease - produced by pancreas
in CF - low to none

cough swab, sputum culture

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58
Q

Treatment for cystic fibrosis?

A

Stop smoking
FEV1 & BMI every appt

Prophylactic
antibiotics
pseudomonal & flu vaccine

Pharm
BA & ICS = symptomatic relief
Mucolytics = clear airway mucus
Replace pancreatic enzyme

Bilateral lung transplant

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59
Q

Antibiotics for -

s. aureus
h. influenza
MRSA
p. aeruginosa

A
  • *s. aureus** = flucloxacillin
  • *h. influenza** = amoxicillin
  • *MRSA** = rifampicin & fucidin
  • *p. aeruginosa** = ciprofloxacillin & nebulised colomycin
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60
Q

Complications for cystic fibrosis?

A

gallstones, liver cirrhosis

end stage = bronchiectasis

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61
Q

What is sarcoidosis?

A

Multisystem inflammatory disease affecting the lungs & intrathoracic lymph nodes

= interstitial lung disease

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62
Q

Pathophysio of sarcoidosis?

A

T cell mediated granulomatous disease

non-caseating sarcoid granulomas consisting mainly of T cells

mainly mediastinal lymph nodes & lung

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63
Q

risk factors for sarcoidosis?

A

20-40 years, women

afro-caribbeans more frequent
& severe - particularly extra-thoracic disease

fam hx (first degree)

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64
Q

Presentation - sarcoidosis

A

Incidental find on CXR common
= infiltrate & extracellular matrix deposition in lung distal to terminal tubule

lymphadenopathy = swole lymph nodes in neck!
painless, no swallow difficulty

can affect any organ but predilection to lung & lymph node

cancer symptoms / systematic

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65
Q

Acute sarcoidosis - symptoms?

A

Erythema nodusum - on shins, thigh & forearm ± polyarthralgia
both may spontaneous resolve / come and go

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66
Q

Investigations for sarcoidosis?

A

DIAG = tissue biopsy
→ non-caseating granuloma

**CXR for staging**
Bronchoalveolar lavage (BAL) - increased lymphocytes in active disease

Lung function test
Blood = raised ESR, ACE!!!
LFT, Ca2+, lymphopenia

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67
Q

Staging for sarcoidosis?

A
  • *0** - normal
  • *1** - bilateral hila lymphadenopathy (BHL)
  • *2** - pulm infiltrate with BHL
  • *3** - pulm infiltrate without BHL
  • *4** - prog pulm fibrosis, bulla formation = honeycombing & bronchiectasis
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68
Q

Treatment for sarcoidosis?

A

No treatment for
those with bilateral hilar lymphadenopathy = no tx = spont resolve
symptomatic at stage 1, asymptomatic at stage 2

treat acute, transplant for severe

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69
Q

How might you treat acute sarcoidosis?

A

Bed rest

NSAIDs

Corticosteroids
= prednisolone oral then wean
severe = IV methylpred
steroid resistant = methotrexate but needs close monitoring

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70
Q

What is idiopathic pulmonary fibrosis?

A

Chronic condition characterised by progressive fibrosis of unknown aetiology

= interstitial lung disease

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71
Q

Risk for IPF?

A

commonly related to other interstitial diseases - sarcoidosis, chronic hypersensitivity pneumonitis, autoimmune stuff

50+ age!
fam hx - familial PF

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72
Q

What is interstitial lung disease?

A

group of diseases affecting the lung insterstitium (tissue & space around air sacs of lungs)

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73
Q

Features of IPF?

A
  • *Chronic exertional dyspnoea**
  • *bilateral inspiratory crackles**
  • *clubbing**
  • *acrocyanosis** (peripheral discoloration indicative of cyanosis)
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74
Q

Investigations for IPF?

A

High Res CT = key
in basal lung / periphery
subpleural reticulation / reticular opacity
traction bronchiectasis
emphysema / loss of lung volume
honeycombing

Lung function tests
Bloods
Biopsies - bronchoalveolar lavage / transbronchial biopsy etc

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75
Q

Management in IPF?

A

Supportive
O2, exercise, opiates

Treat cough

Pharma w/ specific criteria
Pirfenidone (anti-inflam), nintedanib (slow fibrosis)

Lung transplant where appropriate

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76
Q

Pulmonary hypertension - criteria?

A

using
mean pulmonary artery pressure (mPAP)

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77
Q

Conditions associated with pulmonary hypertension?

A

1e = Connective tissue disease - SLE

Left heart failure - MI / systemic
(test using brain natriuretic peptide, ECG etc)

COPD, pulmonary embolism

Sarcoidosis, glycogen storage disease & haem disorders

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78
Q

How might you treat pulmonary hypertension?

A

Warfarin - intrapulmonary thrombosis

Diuretics for oedema

Prostanoids = IV epoprostenol

Oral endothelin receptor antagonist = bosenten

Phosphodiesterase-5 inhibitors = sildenafil

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79
Q

What is hypersensitivity pneumonitis?

A

ILD

Inhalation of allergens provoking a hypersensitiivity (type 3 / 4 reaction)

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80
Q

Nature of hypersensitivity pneumonitis?

A

adult onset, occupation related!

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81
Q

Compare and contrast asthma x hypersensitivity pneumonitis?

A
  • *Asthma**
  • type I IgE
  • inflam around airway (bronchial)
  • eosinophilic inflam
  • eventual - irreversible airway changes
  • *Hypersensitivity pneumonitis**
  • type III or type IV IgG
  • inflam around alveoli and lung interstitium
  • neutrophilic inflam
  • eventual = fibrosis
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82
Q

Pathophysio of hypersensitivity pneumonitis?

A

allergic reaction to inhaled antigen → granulomatous inflammation of lung parenchyma

= sensitised by repeat inhalation of the antigen

  • *acute / subacute** = recurrent
  • *chronic** = fibrosis, emphysema & perm lung damage
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83
Q

Occupations at risk and subtypes of hypersensitivity pneumonitis?

A

Farmer’s lung = most common
exp to fungus in mouldy hay

Bird/pigeon fanciers lung = also common
exp to avian proteins & droppings

Cheese-workers lung = exp to mouldy cheese

Malt-workers lung = exp to mould malt

Humidifier fever! = contaminated humidifying systems in AC / humid in factories, esp printing works

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84
Q

Present - farmer’s lung?

A

acute dyspnoea & cough
hours after inhalation

may resolve upon withdrawal of antigen

earliest = bronchiolitis
then = non-caveating granulomas
comp = pulmonary fibrosis
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85
Q

Acute & chronic presentation for hypersensitivity pneumonitis?

A

fever, rigors, myalgia
dry cough, dyspnoea, crackles no wheeze, tight chest
→ related to lvl of exposure

chronic

  • usually no hist of preceding acute symptoms
  • partial improvement when remove trigger
  • cyanosis / clubbing / weight loss
  • T1 resp failure
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86
Q

How might you diagnose hypersensitivity pneumonitis?

A
  • *CXR**
  • fibrotic shadow in upperzone of lung (mottling / consol)
  • diffuse small nodules / + reticular shadowing
  • *Lung function test**
  • reversible restrictive defect
  • reduced gas transfer during acute attacks

Bronchoalveolar lavage
→ analyse lymphocyte count & CD4/8 ratio

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87
Q

How might you treat hypersensitivity pneumonitis?

A

acute
remove allergen, O2
oral prednisolone followed by reducing dose

chronic
avoid exposure
long term steroids

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88
Q

Name some defensive mechanisms that protects the respiratory tract from infections?

A

Skin!

  • *Intestines**
  • acidic stomach, enzymes, commensal bacteria, thick mucosa barrier

Urinary system
sterile & flows outwards

Vagina
acidic pH / mucus barrier / commensal bacteria

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89
Q

Defensive mechanism of the lungs to protect against pathogens in respi tract?

A

Mucus barrier & cough

Humoral & cellular immunity
WBC & soluble factors

Commensal flora

Swallowing
push into intestines = strong acid

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90
Q

Upper respiratory tract infections?

A
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91
Q

What is pharyngitis / tonsilitis?

A

Infections in throat that causes inflammation

tonsils = primarily affected = tonsilitis
throat = pharyngitis
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92
Q

Causes of pharyngitis?

A

Viral = 80%
rhinovirus / adnovirus
Epstein Barr virus, acute HIV

Bacterial
Group A beta haemolytic strep pyogenes (GABHS)

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93
Q

Presentation for pharyngitis?

A

sore throat / fever

  • *oropharynx & soft palate = red**
  • *tonsils inflamed and swollen**

1-2 days → tonsil lymph nodes enlarge

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94
Q

Treatment for GABHS caused pharyngitis?

A

Amoxicillin

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95
Q

How might you decide if a sore throat is caused by a bacterial infection or not?

A

→ Centor criteria

3-4 positive = 40-60% likely bac

tonsillar exudate
tender anterior cervical adenopathy
fever over 38 degrees by hx
absence of cough

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96
Q

What is sinusitis?

A

Infection of paranasal sinuses

mostly bacterial sometimes fungal

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97
Q

Causes for sinusitis?

A

Strep pnuemoniae (40%)

Haemophilus influenza (30-35%)

assoc. Upper RI infect / asthma

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98
Q

Present / diagnosis of sinusitis (2 key)?

A

Frontal headache ± fever

Purulent rhinorhea = nasal cavity filled with mucus fluid
= purulent nasal discharge

Unilateral facial pain, potentially with tenderness

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99
Q

Treatment for sinusitis?

A

Nasal decongestant e.g. xylometazoline

  • *Broad spectrum antibiotics**
    e. g. co-amoxiclav (h.i. can be resistant to amoxicillin)

complications
brain abscess, sinus vein thrombosis, orbital cellulitis

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100
Q

Acute epiglottitis - what is it?

A

Inflammation of epiglottis
= flap of cartilage behind roof of tongue → depressed during swallow to cover windpipe

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101
Q

Risk / epidemiology of acute epiglottitis?

A

Formerly in children < 5y/o
severely ill, life threat
now = rare → HiB vaccine

adults
severe = h. influenza
can be from pharyngitis / other bac infect of airway
immunocompromised - AIDS

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102
Q

Clinical presentation for acute epiglottitis?

A

Sore throat
pain on swallowing = odynophagia

Inspiratory stridor = high pitched wheeze when breathing in

if long hx, fatigue, weight loss, diarrhoea

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103
Q

Investigate / results for acute epiglottitis?

A

Sagittal view
upper respiratory tract XR

= thumb sign

104
Q

Treatment for HiB caused acute epiglottitis?

A

Doxycycline or co-amoxiclav

20% amoxicillin resistant
not susceptible to macrolides (erythromycin / clarithromycin)

105
Q

What is whooping cough? What causes it?

A

disease of childhood, 90% <5 yo

caused by Bordatella pertussis = gram neg coccobacillus (rod)

106
Q

Clinical presentation for whooping cough?

A

Chronic cough in spasms (<14d)
inspiratory whoop = in younger
usually end in diarrhoea

rhinorhoea, conjunctivitis
may px as subconjunc haemorrhage

107
Q

Investigations & results for whooping cough?

A

Lungs clear to auscultation

Respiratory culture - 90% positive for B. pertussis [gram neg]

PCR/ ELISA for IgG against pertussis toxin

108
Q

Treatment for whooping cough?

A

Antimicrobials = clarithromycin
reduce symptoms earlier (1-6 weeks), less effective later

Should eliminate carriage in household = chemoprophylaxis

Vaccination
acellular pertussis as a part of dTaP

109
Q

Diagnose:

3y, M
prominent barking cough, febrile, has inspiratory stridor

febrile, cyanosed with intercoastal recessions

A

Croup / acute laryngotracheobronchitis

110
Q

Cause & pathophysio for Croup / acute laryngotracheobronchitis?

A

Parainfluenza viruses

inflammatory oedema extend to vocal cords & epiglottis = narrow of airway

progressive airway obstruction = cyanosis

111
Q

Treatment for croup?

A

Nebulised adrenaline for short term relief

Oral / intramuscular corticosteroids (dexamethasone) w/ oxygen & fluids

112
Q

Pneumonia - what is it?

A

Acute lower respiratory tract infection

= inflammation of the lung parenchyma

113
Q

People at risk of pneumoniae?

A

Immunocompromised
infants & the elderly
nursing home residents

Comorbidities
COPD, chronic lung diseases
people w/ impaired swallow conditions *neuro etc)
Diabetes, congestive heart

114
Q

Pathology of pneumonia?

A

Bacteria translocate to normally sterile distal airway → overwhelm resident host defence → inflammatory response → bac cleared

115
Q

Pneumonia symptoms?

(think of big 3 areas - not signs!)

A

Infection
fever, sweats, sputum
no sputum in atypical org

Chest
short of breath, pleuritic chest pain (worse on deep breath)

Illness
weakness, malaise
sometimes extra pulm features

116
Q

rusty sputum & pleuritic chest pain, raised WBC, multi-lobar consolidation
- causing organism?

A

S pneumoniae

117
Q

Differentiate S pneumonia from S aureus?

A

S pneumonia = multi lobar

S aureus = multi lobar + multiple abscess

118
Q

flu like symptoms, ± sputum, neuro / GI features
upper lobe cavity

  • causing organism?
A

Legionella spp.

(but exclude TB first as TB also upper lobe)

119
Q

± sputum, pneumonia features with a rash - causing organism?

A

rash = mycoplasma spp. !

120
Q

Signs of pneumonia?

A

Infection
+ HR, RR, low BP
fever, dehydration

Chest
= signs of lung consolidation on percussion & auscultation
dull to percussion
decreased air entry
crackles ± wheeze
increased vocal resonance

121
Q

Investigations for pneumonia?

A

CXR

FBC + Biochemistry
WBC (= marker of sev)
C-reactive protein = inflammation marker, diag + assess

Pulse oximetry

Microbiological tests

122
Q

CXR signs for pneumonia?

A

airspace opacification
filling of the alveoli with infectious material and pus
patchy → confluent as infection develops

air bronchograms
air-filled bronchi running through pus-filled alveoli
(black branches in white)

123
Q

Microbiological tests for pneumonia?

A

Sputum culture & sensitivities

Urinary antigen
Legionella & S pneumonia

PCR
viruses & mycoplasma

Consider acid fast bacilli stain & culture (TB) if features suggestive

124
Q

Community acquired pneumonia - causative organisms (6)?

A

Strep pneumoniae = most common

H influenza

Klebsiella pneumoniae

Atypical
Mycoplasma pneumoniae
Chlamydophila pneunominae
Legionella sp.

125
Q

How might you assess severity of CAP?

A

using the CURB-65 score

126
Q

CURB 65 criteria?

(pls know)

A

Confusion

Urea (> 7mmol/L)
might not be present in community so ignore

Respiratory rate (> 30 / min)

BP < 90/60

Age > 65

127
Q

Response according to CURB 65?

A

0-1 mild, admit if special circ

2 - moderate - admit!

3-5 - admit & monitor closely

4-5 admit to critical care

(no urea in comm so 0, 1-2 mod, 3-4 severe)

128
Q

CAP treatment based on CURB score? Tx duration?

A

mild 0-1
amoxicillin
alt: clarithromycin or doxycycline

moderate 2
amoxicillin plus clarithromycin

severe 3-5
IV co-amoxiclav + clarithromycin
alt: cefuroxime & clarithromycin

  • *5 days** mild to mod, + if severe
  • *14-21 days** S aureus, gram neg & legionella
129
Q

Other indicators of severity for pneumonia?

A
  • *Delerium** = confusion
  • *Renal impairment** = + urea

Increased oxygen demand, hypoxaemia
+ RR, lactic acid production
BP drop

→ signs of sepsis!

130
Q

Treatment for pneumonia

S. pneumonia
nature of bac
tx?

A

gram positive
alpha haemolytic optochin sensitive

beta lactam = amoxicillin, cefuroxime, cefotaxime

  • *alt**
  • *macrolides** = clarithromycin, fluoroquinolones, ciprofloxacin
131
Q

Treatment for pneumonia

H. influenza
nature of bac
tx?

A

gram neg cocobacilli

  • *beta lactam** = amoxicillin, co-amoxiclav
  • *tetracyclines** = doxycycline

NOT macrolides!!

132
Q

Treatment for pneumonia

S. aureus
nature of bac
tx?

A

gram pos

beta lactams = flucloxacillin, cefuroxime

if MRSA = vancomycin, linezolid

133
Q

Treatment for pneumonia

Klebsiella pneumonia
nature of bac
tx?

A

gram neg, entero

beta lactam = co-amoxiclav, cephalosporins

134
Q

General ‘atypical’ pathogen tx principle?

A

special antibiotics

=
macrolides
Erythro / claritho

fluoroquinolones
ciprofloxacin

tetracyclines
doxycycline

135
Q

Legionella features?

A

warm water
tanks, AC, travel

severe illness, resp failure
extra pulmonary = diarrhoea, GI & consudion

136
Q

Mycoplasma features?

A

younger adult, milder illness

extrapulm features = rash (erythema multiforme), haemolytic anaemia, Raynauds, bullous myringitis, enceph

137
Q

Prevention of pneumonia?

A

Vaccine!

Polysaccharide pneumococcal vaccine for > 65
Pneumococcal conjugate for children

138
Q

Complications of pneumonia?

A

Respiratory failure

Hypotension
due to comb of dehydration + vasodilation from sepsis

Parapneumonic effusion

Empyema

139
Q

What is parapneumonic effusion? Investigate?

A

any pleural effusion secondary to pneumonia (bacterial or viral) or lung abscess

→ thoracocentesis to remove fluid from pleural space, aka pleural tap
→ CXR = signs of pleuritic effusion

140
Q

What is of empyema?

A

pleural effusion, but fluid is infected by bacteria!
= pus / purulent fluid in pleural space

fluid = yellow / turbid, pH < 7.2, low glucose

141
Q

Signs of empyema?

A
  • *ongoing fever**
  • *failure of WBC / CRP to settle on antibiotics**

Pleuritic pain (on deep insp)

Signs of pleural collection
= stormy dull percussion, reduced air entry

142
Q

Treatment for empyema / complicated parapneumonic effusions?

A

Drainage - chest tube / cardiothoracici surgery

Antimicrobials
co-amoxiclav
meropenam for anaerobic coverage

143
Q

Lung abscess - people at risk?

A

in aspiration pneumonia, inapp tx CAP

  • *alcoholics, those with poor dentition**
  • *metastatic infection** from right heart & venous system - IVDU, Lemierre’s

TB, septic emboli

144
Q

Causative organisms & nature - lung abscess?

A

Strep milleri
= alpha haemolytic optochin resistant

Klebsiella pneumonia
& other gram neg bac

Anaerobes!!!
ensure microbio coverage

145
Q

Treatment for lung abscess?

A

= prolonged antibiotics for 6 weeks +, surgical drainage if required

146
Q

Hospital acquired pneumonia - criteria? signs?

A

Acquired at least 48 hours after hospital admission

new fever, purulent secretions,
new radiological infiltrates / CRP increase, + O2 requirements

147
Q

Hospital acquired pneumonia - causative organisms?

A

S. aureus (& MRSA)
strongly ventilator associated

Pseudomonas aeruginosa

  • *Acinetobacter baumanii**
  • *Klebsiella pneumoniae**
  • *E. coli**
148
Q

Treatment for early onset hospital acquired pneumonia (CAP organisms)

A

Metronidazole

Beta lactams with inhibitor of beta lactamase = co-amoxiclav, piperacillin-tazobactam

149
Q

General, go to antibiotic if hospital acquired?

A

Start broad then focus

  • *→ doxycycline**
  • *→ piperacillin-tazobactam or cefurioxime**
150
Q

Treatment for s. aureus HAP?

A

beta-lactam = flucloxacillin, cefuroxime

if MRSA - vancomycin

151
Q

Treatment - pseudomonas aeruginosa?

A

Anti-pseudomonal penicillin

= piperacillin-tazobactam

152
Q

What is bronchitis - acute vs chornic?

A

acute = self limited inflammation of the epithelia of the bronchi due to upper airway infection

chronic = condition in COPD, cough > 3m in 2 conseq years

153
Q

Signs & causes of bronchitis?

A

cough, often wheeze > 5 days
± phlegm

no fever / signs of infection!

majority viral, rarely bacterial in healthy adults

154
Q

Investigate & treatment, bronchitis?

A
  • *CXR** - normal
  • *Viral & bacterial throat swabs** = PCR for resp viruses & mycoplasma, culture for others

Usually none if viral!

155
Q

What is tuberculosis?

A

= infectious disease caused by mycobacterium spp. with significant morbidity & mortality world wide

→ HIV linked!

156
Q

Causative organisms (4) & spread?

A

Mycobacterium

  • tuberculosis* = most common
  • bovis* = unpasteurised milk
  • africanum*
  • microti*

→ aerosolised droplet spread!
but not all infected will develop active disease!

157
Q

Nature of mycobacterium? Stain used?

A

aerobes, slow growing (15-20h)

Acid fast bacilli
= resistant to staining by acid

use Ziehl-Neelsen stain
= goes red / pink

158
Q

People at risk of tuberculosis?

A

Origin
immigration (sub-saharan africa), hotspots

immunosuppressed
age
HIV
therapy (chemo etc)

  • *IVDU, alcohol, smoking**
  • *malnutrition, homeslessness**
159
Q

Subtypes (manifestations) of TB?

A

Primary TB
= first infection with mycobacterium spp.

Latent TB
= immune system contains the nfection & cell mediated immunity memory developed to bac

Reactivation TB / Post-primary TB
= majority! dormant → active
= depression of host immune system (older, severe infection)

160
Q

Pathophysiology of primary tuberculosis?

A

bac + macrophages → granuloma
= primary Ghon focus

as it grows → cavity in apex of lung
bac expelled when patient coughs

Primary focus in mediastinum lymph node = Ghon complex

161
Q

Nature of the granuloma formed in TB?

A

Caseating granuloma

on CXR: small calcified nodule,
often on lower of upper lobe / upper of lower lobe

Can also be found in GI!
ileocaecal region

162
Q

TB presentation?

A

night sweats & weight loss!
anorexia, low grade fever, malaise

cough 3/52
chest pain
breathlessness
haemoptysis

163
Q

Investigations for TB?

A

CXR
patchy / nodular shadow in upper zone w/ loss of volume, fibrosis
normal in miliary TB

Sputum
auramine-phenol fluorescent test
= highlights bac as yellow-orange on a green background
Ziehl-Neelsen stain = red if TB

Culture
solid = Lowenstein-Jensen slopes / Middlebrook agar

Nucleic acid amplication = differentiate m. tb from others

Lumber puncture & CSF exam
= miliary TB

164
Q

Testing for latent TB?

A

Skin test = Mantoux test
= cell mediated response to underskin TB antigen
→ type 4 hypersensitivity reaction
false neg if miliary / immunosuppressed

Interferon gamma release assays (IGRAs)
= more specific as can use specific antigen (diff bet vac and TB)
e.g. ESAT-6 & CFP10

165
Q

Treatment for TB?

A

NOTIFIABLE to PUBLIC HEALTH ENGLAND + contact tracing

RIPE!!

Rifampicin 6m

Isoniazid 6m

Pyrazinamide 2m

Ethambutol 2m

166
Q

Mechanism & SE Rifampicin?

A

bac cidal, anti protein synthesis
SE red urine, hepatitis

167
Q

Mechanism & SE Isoniazid?

A

bac cidal, anti cell wall synthesis
SE hepatitis & neuropathy

168
Q

Mechanism & SE Pyrazinamide?

A

bac cidal
SE hepatitis, arthralgia / gout + rash

169
Q

Mechanism & SE Ethambutol?

A

bac static, anti cell wall synthesis
SE optic neuritis

170
Q

Prevention for TB?

A

active case finding to reduce

Vaccination
Bacillus Calmette–Guérin (BCG)
= live attenuated, from M bovis
= in UK = mostly in areas with incidence bc ? cost effective

(CXR for contact tracing)

171
Q

What is respiratory failure?

A

Occurs when inadequate gas exchange in the lungs

→ ABG to sample

172
Q

Types of respiratory failure & criteria?

A

Type 1
= hypoxaemia (PaO2 < 8kPa)
normal / low Co2

Type 2
= hypoxaemia (PaO2 < 8kPa)
hypercapnia (PaCO2 > 6.5 kPa)

173
Q

Causes of respiratory failure?

A 
Hypoxaemia = V/Q mismatch
Hypercapnia = alveolar hypoventilation

reduced ventilation
increased dead space
diffusion limitation

174
Q

What is the V/Q ratio?

A

V = ventilation
flow of air in and out of alveoli

Q = perfusion
flow of blood to alveolar capillaries

175
Q

What does it mean to have / causes of a high V/Q ratio?

A

alveolae has poor perfusion
(compared to ventilation)
= vascular problem!

causes = e.g. pulm embolism

176
Q

What does it mean to have / causes of a low V/Q ratio?

A

alveolar has poor ventilation
(compared to perfusion)
ventilation problem!

= hypoxaemia (low al O2 lvls)

causes = airway disease, interstitial lung disease → reduced ventilation

177
Q

Causes of T1RF?

A

= hypoxaemia

pneumonia, pulm oedema
COPD, asthma
pneumothorax, pulm embolism = MC!!

178
Q

Treatment for T1RF?

A

Usually responds well to oxygen therapy

179
Q

Causes for T2RF?

A

→ hyperventilation

Exacerbation of obstructive lung disease
= COPD (most common)
asthma, cystic fibrosis, bronchiectasis

Respiratory depressants = opiate overdose

180
Q

What should you not do for acute deterioration in COPD?

A

treat with high flow oxygen

→ can lead to oxygen induced hypercapnia
(from + V/Q mismatch & physiological dead space)

→ that’s why COPD / asthma O2 saturation target = 88-92%

181
Q

What is a pneumothorax?

A

Collection of air within the pleural space = space between parietal & visceral pleura

182
Q

Types of pneumothorax?

A

Spontaneous = sans trauma
older with underlying lung disease
younger with apical blebs

Traumatic
can be open (communicate with outside air and pleural space) or closed

183
Q

What is a pleural bleb?

A

a small collection of air in the pleural space <1-2cm

184
Q

Present - pneumothorax?

A

Sudden onset dyspnoea
Pleuritic chest pain!

Tachycardia
Reduced chest expansion
Diminished breath sounds

Hyper resonant to percussion

185
Q

Investigations for pneumothorax?

A

CXR

186
Q

Signs of tension pneumothorax?

A

tachycardia, tachypnoea
low O2 low BP
distended neck veins

CXR
Trachea deviated away from the affected side

187
Q

Treatment for tension pneumothorax (& spontaneous pneumothorax)

A

Needle aspiration first

then chest drain
(for spont pneumothorax too)

(at midclavicular line 2nd intercoastal space)

188
Q

What is pleural effusion?

A

Abnormal collection of serous fluid within the pleural space

can also be: simple fluid, blood, pus (empyema)

189
Q

Function of the pleural fluids?

A

Lubricate pleural surfaces

Generates surface tension

190
Q

Pathophysiology - pleural effusion/

A

Imbalance of fluid entry & exit within the pleural space

+ entry: inflammation, pulmonary hypertension, nephrotic syndrome, cirrhosis

- exit: inflam mediators, damage (chemo), physical compression, decreased intrapleural pressure

191
Q

Causes of pleural effusion?

A

Transudate = minimal protein & cellular content
→ alteration in hydrostatic / oncotic pressure

Exudate = high protein & cellular content
→ infection or malignancy

192
Q

Symptoms of pleural effusion?

A

Signs develop when >300ml
Signs localised to side of effusion

reduced chest expansion & breath sounds

stony dull percussion

reduced vocal resonance
reduced tactile vocal fremitus (vibration of chest wall when speaking)

193
Q

CXR signs of pleural effusion & criteria?

A

Need minimum 200-250 ml of fluid to detect
→ on PA chest xray!

= dense white consolidations!
aka opacification

meniscus at the costophrenic angle :)

194
Q

Investigations for assessment of pleural effusion?

A

CXR to confirm

→ Pleural tap (thoracentesis) & analysis
needle inserted under anaesthesia
guide under ultrasound

→ sample for - pH, cytology, microbiology

purulent in empyema
turbid = infected
milky = lymph fluid

transudate / exudate based on protein content
(usually 🔪 30g/L)

195
Q

Treatment for pleural effusions?

A

Exudate → drain

Transudate → TUC

Pleurodesis = injection that causes adhesions of visceral & parietal pleura → prevent reaccumulation of effusion = e.g. tetracycline

196
Q

What is Goodpasture’s syndrome?

A

Acute glomerulonephritis + pulmonary alveolar haemorrhage

presence of circulating antibodies against antigen in basement membrane of kidney & lung

197
Q

Pathophysio & antibodies in Goodpasture’s syndrome?

A

Autoimmune
= type II antigen-antibody reaction → diffuse pulm haemorrhage, glomerulonephritis ± AKI/CKD

antibody = anti-GBM antibodies

198
Q

Risk & epidemiology of Goodpasture’s syndrome?

A

adults (>16)
rare in children

common in men

199
Q

Presentation - Goodpasture’s syndrome?

A

Upper RI infect symptoms
sneezing, nasal discharge, congest, runny nose + fever

  • *Haemoptysis**
  • *Acute glomerulonephritis**

Cough, tiredness
Anaemia
(from persistent intrapulmonary bleeding)

200
Q

just for fun

if similar presentation to goodpasture’s but no antibodies & kidney less involved, in children?

A

Idiopathic pulmonary haemosiderosis

201
Q

Investigations & diagnosis for Goodpasture’s?

A

Presence of anti-GBM antibodies in blood

CXR
transient patchy shadows / pulm infiltrates due to pulm haemorrhage
often in lower zone

Kidney biopsy
crescentic glomerulonephritis

202
Q

Treatment for Goodpasture’s?

A

→ in some may spontaneously improve

Vigorous immunosuppresive treatment
= corticosteroids = prednisolone

Plasmaphoresis = remove antibodies from blood and back

203
Q

Complications - Goodpasture’s

A

Renal failure

shock!

204
Q

Some non-specific occupational lung disorders / complications?

A

Acute bronchitis / oedema!

Pulm fibrosis

Occupational asthma

Hypersensitivity pneumonitis

Bronchial carcinoma

205
Q

What is coal worker’s pneumoconiosis?

A

Pneumoconiosis = accumulation of dust in lungs & reaction of tissues to its presence

→ inhalation of coal dust particles in 15-20 years

206
Q

Presentation & Management - coal worker’s pneumoconiosis?

A

Asymptomatic mostly!

but High Res CT → round opacities in upper zone

avoid exposure to coal dust, claim compensation

207
Q

What is silicosis? At risk populations?

A

Inhalation of silica particles (silica dioxide) = toxic to alveolar macrophages & fibrogenic

at risk: stonemasons / sand-blasters / pottery & ceramic workers / foundry workers

208
Q

Presentation & management - silicosis?

A

Progressive dyspnoea & increased incidence of TB

avoid exp, claim compensation

209
Q

Investigations & results - silicosis?

A

Potential PMH / current TB

CXR
diffuse nodular pattern in upper & midzone
thin streaks of calcification (egg-shell calcification) of the hilar zone

Spirometry
restrictive ventilatory defect

210
Q

What is asbestosis? Who are at risk?

A

Inhalation of asbestos = banned now
widely used in roofing, insulation, fireproofing as resistant in heat & pH

mostly crocidolite (blue) = readily trapped in lung

211
Q

Presentation - asbestosis?

A

Progressive dyspnoea, finger clubbing, bilateral basal end inspiratory crackles

+ risk pleural plaques and + risk mesothelioma & bronchial adenocarcinoma

212
Q

Management for asbestosis?

A

only symptomatic manage
= corticosteroids

213
Q

What is a (malignant) mesothelioma?

A

= tumour of the mesothelial cells of pleura

STRONGLY associated w/ ASBESTOS exposure

214
Q

Aetiology & locations of mesotheliomas?

A

men, 40-70’s

Exposure to asbestos = cause
but only 20% have pulmonary asbestosis

Other locations = peritoneum, pericardium, testes

215
Q

Presentation - mesothelioma

A

Severe chest pain

  • *Weight loss, finger clubbing**
  • *recurrent pleural effusions** → malignancy!

Signs of mets = lymphadenopathy, hepatomegaly, bone pain / tenderness, abdominal pain / obstruction

(invasion of chest wall possible → intercoastal nerves)

216
Q

Diagnosis - mesothelioma

A

CXR & CT
= unilateral pleural effusion
= pleural thickening

Pleural biopsy
Bloody / straw coloured pleural fluid

217
Q

Treatment - mesotheliomas

A

Surgery for extremely localised mesothelioma

Generally resistant to all surgery, chemo, radio

Poor prognosis :<

218
Q

Wegener’s granulomatosis / Granulomatosis with polyangitis

  • what is it?
A

Multisystem disorder characterised by granulomatous disease and vasculitis of small and medium cells

ANCA positive

219
Q

Pathophysio of granulomatosis with polyangitis?

A

Neutrophils activated inappropriately by autoantibodies (Anti-neutrophil cytoplasmic antibodies ANCA) before tissue migration

→ neutrophil recruitment when there is no infection → granulomas & vasculitis

220
Q

Presentation of granulomatosis with polyangitis?

A

Lesions in upper respi tract, lungs & kidneys

Severe rhinorrhea (congested) & subsequent mucosal ulceration → characteristic saddle nose deform

cough, pleuritic pain, haemoptysis
skin purpura or nodules

PN, arthritis
renal disease → rapid progressive glomerulonephritis

221
Q

Differential for granulomatosis with polyangitis -

Churg-Strauss syndrome - what is it? Features?

A

affects small arteries, male

rhinitis / asthma, eosinophilia, systemic vasculitis

high eosinophil count

ANCA positive

222
Q

Investigations & diagnosis for granulomatosis with polyangitis?

A

Bloods
c-ANCA positive
+ PR3 antibodies
raised CRP, ESR

CXR
nodular masses or pneumonic infiltrates with cavitation = clear migratory pattern

CT
diffuse alveolar haemorrage

Urinalysis → proteinuria & haematuria → if pos: renal biopsy

223
Q

Treatment for GPA?

A

Depends on extent of disease

Severe disease → steroids

Azathioprine / methotrexate for maintenance

224
Q

Bronchial carcinoma - types?

A

Two main types

Small cell lung carcinoma

Non SCLC - in which
squamous carcinoma
adenocarcinoma
large cell and differentiated carcinoma
carcinoid tumours

225
Q

Small cell carcinoma - risk factors & source & nature?

A

STRONGLY assoc cigarette smoking

arises from endocrine cells
central bronchus
secretes polypeptide hormones

226
Q

Presentation, tx & prognosis, small cell lung carcinoma?

A

often arises in a central bronchus

early development of widespread metastases

chemo = primary tx
poor prognosis

227
Q

Small cell lung tumours - supportive treatment?

A 
**Primary = chemotherapy** 
brachytherapy = radioactive source placed close to exams

Pleuritic drain - symptomatic relief

Stents for obstructions - SVC, tracheal

228
Q

Small cell lung cancer - endocrine complications

A

= ectopic ADH, ACTH secretion

SIADH

Cushing’s syndrome

(also Lambert Eaton)

229
Q

Non - small cell carcinoma - tx?

A

Often treated best to surgical oblation with lymph node sampling

chemo /radio for follow up

More susceptible to new therapy e.g. tyrosine kinase

230
Q

Lung cancer most strongly associated with cigarette smoking?

A

Squamous cell carcinoma

231
Q

Squamous cell carcinoma - nature & locations?

A

arise from epithelial cells
associated with production of keratin

central tumours, frequent central necrosis, loca spread

→ obstructive lesions of bronchus
→ late mets

232
Q

What is a pancoast tumour?

A

Squamous cell carcinoma that start in the top part of the lung (the apex).

Associated with Horner’s syndrome

233
Q

Symptoms of a pancoast tumour?

A

severe pain in the shoulder or the shoulder blade (scapula)

pain in the arm and weakness of the hand on the affected side

Horner’s syndrome
= flushing on one side of the face and that side doesn’t sweat. The eye on the same side has a smaller (constricted) pupil with a drooping or weak eyelid.

234
Q

Most common lung cancer overall, also in non-smokers?

A

Adenocarcinoma

235
Q

Nature of adenocarcinoma?

A

commonly associated w/ asbestos

arise from mucus-secreting glandular cells

central or peripheral

236
Q

Features of adenocarcinoma?

A

Usually single lesions but may be multifocal / bilateral pattern

Peripheral lesions on CXR / CT

mets are common

237
Q

Treatment for non-small cell lung cancer (80%)?

A

main = Surgical excision for peripheral tumours with no spread

Chemo ± radio = more advanced disease e.g. monoclonal antibodies

comp’s = radiation pneumonitis, fibrosis

238
Q

Main lung lymphoma - name, type of cells, tx?

A

Baltoma
= Bronchus Associated Tissue Lymphoma

B cell lymphoma
responds to standard chemo regimes

239
Q

Name for benign tumours in the lung & nature?

A

Hamartomas

Irregular proliferation of benign tissue not normally found in lung tissue

240
Q

Common destinations for lung mets? (LBAB)

A

Liver

Bone

Adrenal glands

Brain

241
Q

Common origins of lung mets

(causes of secondary lung cancer?)

A

Breast cancer

Bowel Cancer

Kidney cancer = most common!!
= renal cell carcinoma

Bladder cancer

242
Q

Consequences of arterial thrombosis?

A

Coronary circulation = MI

Cerebral circulation = TIA / stroke

Peripheral circulation = peripheral vascular disease = claudication, rest pain, gangrene

243
Q

STEMI ECG features?

A

ST elevation, tall T waves, LBBB, T wave inversion with pathological Q waves

244
Q

Thrombolytic therapy for MI’s?

A

Streptokinase & tissue plasminogen activator

245
Q

Consequences of venous thrombosis?

A

Deep vein thrombosis = usually in legs

Pulmonary embolism = lungs

If atrial septal defect = travel to arterial system = stroke, MI, TIA

246
Q

Risk of DVTs?

A

Recent surgery

Genetics = predisposition (thrombophilias)
deficiencies: factor V Leiden, protein C or S, antithrombin

Acquired
Antiphospholipid syndrome
Lupus anticoagulant

Lifestyle
Long haul flights, pregnancy, obesity, cancer, immobility, synthetic oestrogen

247
Q

Main features of antiphospholipid syndrome?

A

CLOT

Clots = usually venous

Livedo reticularis = lace like rash on lower limbs

Obstetric loss

Thrombocytopenia

248
Q

How might you provide venous thromboembolism prophylaxis

A

Low molecular weight heparin
CI existing warfarin / DOAC

anti-embolic compression stockings
CI peripheral arterial disease

249
Q

DVT features?

A

Calf swelling and tenderness

Dilated superficial veins

Colour changes

Oedema

250
Q

Investigations for DVT?

A

Well’s score predicts risk of patient having DVT / PE

D-Dimer will exclude DVT, as is also raised in pneumonia, heart failure, pregnancy etc

Doppler ultrasound of the leg = DIAGNOSTIC
repeat 6-8 days after if suggestive Wells & D-Dimer positive

251
Q

Pulmonary embolism diagnostic test?

A

CT Pulmonary angiogram CTPA
= preferred
CI contrast allergy / kidney impairment

Ventilation perfusion (VQ) scan = alt

252
Q

DVT initial management

A

Anticoagulation

= apixaban or rivaroxaban

if symptoms < 14 days & symptomatic iliofemoral DVT
consider catheter directed thrombolysis

253
Q

Long term anticoagulation - classes, indications & examples?

A

Direct acting oral anticoagulants DOACs
= apixaban, rivaroxaban, edoxaban & dabigatran

Warfarin = vitamin K antagonist
1st for antiphospholipid syndrome (+LMWH)

Low Molecular Weight Heparin LMWH
= Enoxaparin, dalteparin
1st in pregnancy

3m if reversible cause, >3m if unclear, irreversible, recurrent. 3-6m active cancer

254
Q

How might you reverse anticoagulation in strokes?

A

Dabigatran (direct thrombin inhibitor)
= idarucizumab

rivaroxaban / apixaban (direct factor Xa inhibitor)
= Andexanet alfa

Warfarin = vitamin K, human prothrombin complex (alt fresh frozen plasma)

255
Q

Long term tx for VT if anticoag is unsuitable?

A

Inferior vena cava filters

= for recurrent PEs & those unsuitable for anticoag
= act as a sieve allow blood to flow through while catching clot

256
Q

How might you investigate unprovoked DVT or PE

A

check for antiphospholipid antibodies (antiphospholipid syndrome)

check for hereditary thrombophilia if 1st degree relative also affected by DVT / OE

257
Q

What is Budd-Chiari syndrome?

A

Blood clot develops in hepatic vein, blocking blood flow (assoc. hypercoagulable states)

→ causes acute hepatitis

→ present
abdominal pain
hepatomegaly
ascites

Phase 2A (12 decks)

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