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taz- year 3 med > Resp > Flashcards

Resp Flashcards

1
Q

what are some common resp presenting complaints?

A
  • Dyspnoea
  • Chest Pain
  • Wheeze
  • Cough
  • Sputum
  • Haemoptysis
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2
Q

what are important things to ask about when a patient presents with:

  • Dyspnoea
  • Chest Pain
  • Wheeze
  • Cough
  • Sputum
  • Haemoptysis
A
  • Dyspnoea – MRC score, Exercise Tolerance,
    triggers, relieving factors, diurnal variation, orthopnoea, PND
  • Chest Pain – site, severity, radiation, triggers,
    relieving factors, associated symptoms
  • Wheeze – triggers, relieving factors, diurnal
    variation, associated cough
  • Cough – dry or productive, triggers, relieving
    factors, diurnal variation, association with eating
    or dyspepsia, positional, nasal secretions,
    associated fever
  • Sputum – how much over 24 hours, colour,
    consistency
  • Haemoptysis – quantity and frequency, fever /
    night sweats, appetite, weight loss
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3
Q

what is the MRC dyspnoea score? what are the 5 grades?

A

Grade of breathlessness related to activities:

  • 1 Not troubled by breathlessness except on strenuous exercise
  • 2 Short of breath when hurrying or walking up a slight hill
  • 3 Walks slower than contemporaries on level ground because of breathlessness, or has to stop for breath when walking at own pace
  • 4 Stops for breath after walking about 100m or after a few minutes on level ground
  • 5 Too breathless to leave the house, or breathless when dressing or undressing
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4
Q

what is the WHO performance status and what are the 5 grades?

A
  • 0 Normal - Fully active without restriction
  • 1 Restricted in physically strenuous activity but ambulatory and able to carry out light work e.g., light house work, office work
  • 2 Ambulatory and capable of all self-care but unable to carry out any work activities. Up and about more than 50% of waking hours
  • 3 Capable of only limited self-care, confined to bed or chair more than 50% of waking hours
  • 4 Completely disabled. Cannot self-care. Totally confined to bed or chair
  • 5 Dead
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5
Q

what are 4 causes of a low Pa02 (hypoxia)

A
  • Hypoventilation
  • Diffusion impairment
  • Shunt
  • V/Q mismatch
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6
Q

What is the A-a gradient useful for calculating?

How do you calculate it? What is normal and what suggests a pathology?

A

A=Alveolar a=arterial Can be useful to work out it there is a respiratory problem

PAO2 = PIO2 – PaCO2/0.8
- PAO2 = Alveolar partial pressure of oxygen
- PIO2 = Room air (approx. 20 kPa)
- PACO2 is virtually the same as arterial partial pressure of carbon dioxide (PaCO2)
A-a gradient in young healthy people should be less than 2 kPa, and less than 4 kPa in older people >4 kPa implies lung pathology

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7
Q

What are the acid base disturbances for:

  • metabolic acidosis
  • metabolic alkalosis
  • respiratory acidosis
  • respiratory alkalosis
A
  • metabolic acidosis- decreased pH, PaCO2, [HCO3-]
  • metabolic alkalosis- increased pH, PaCO2, [HCO3-]
  • respiratory acidosis decreased pH, increased PaCO2, [HCO3-]
  • respiratory alkalosis increased pH, decreased PaCO2, [HCO3-]
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8
Q

a 26 year old female nurse thought to be hyperventilating
- On air pH7.56, pCO2 2.7, PO2 11.5, B.E. -2, HCO3 23

Calculate her A-a gradient and therefore if there is an underlying lung pathology?

A

PAO2 = PIO2 – PaCO2/0.8
= 20 – 2.7/0.8 = 20-3.4 = 16.6 kPa
PA-aO2 = 16.6-11.5 = 5.1 kPa
- THEREFORE PROBLEM WITH THE LUNGS

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9
Q

the Hepatology consultant from the liver unit refers a 31 year old man with liver failure and new hypoxia. On examination – jaundice, ascites.
On air pH 7.35, PO2 7.2, PCO2 8.6, HCO3 35, Sats 87%

Calculate her A-a gradient and therefore if there is an underlying lung pathology?

A

PAO2 – PaO2 = 2.1kPa, i.e. NORMAL lungs.

- There is under ventilation secondary to drugs, encephalopathy, or just ascites.

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10
Q

What are some common causes of resp emergencies

A 
Anaphylaxis and Angioedema
Asthma
COPD Exacerbations
Pneumonia
Massive Haemoptysis
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11
Q

What are the clinical features of anaphylaxis

A

Occurs in minutes -
Pruritus
urticaria & angioedema
hoarseness progressing to stridor & bronchial obstruction
wheeze & chest tightness from bronchospasm

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12
Q

How would you treat anaphylaxis

A

DO NOT DELAY! GET HELP
Remove trigger, maintain airway, 100% O2
Intramuscular adrenaline 0.5 mg (Repeat every 5 mins as needed to support CVS)
IV hydrocortisone 200mg
IV chlorpheniramine 10 mg
If hypotensive: lie flat and fluid resuscitate
Treat bronchospasm: NEB salbutamol
Laryngeal oedema: NEB adrenaline

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13
Q

How would you classify the severity of asthma and what are the features of each

A 
Mild:  
- No features of severe asthma 
- PEFR >75%
Moderate: 
- No features of severe asthma 
- PEFR 50-75%
Severe (if any one of the following): 
- PEFR 33 – 50% of best or predicted 
- Cannot complete sentences in 1 breath 
- Respiratory Rate > 25/min 
- Heart Rate >110/min
Life threatening (if any one of the following): 
- PEFR < 33% of best or predicted 
- Sats <92% or ABG pO2 < 8kPa 
- Cyanosis, poor respiratory effort, near or fully silent chest 
- Exhaustion, confusion, hypotension or arrhythmias 
- Normal pCO2
Near Fatal:
- Raised pCO2
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14
Q

What is the acute management of an asthma attack

A
  • ABCDE
  • Aim for SpO2 94-98% with oxygen as needed, ABG if sats <92%
  • 5mg nebulised Salbutamol (can repeat after 15 mins)
  • 40mg oral Prednisolone STAT (IV Hydrocortisone if PO not possible)
    If severe:
  • Nebulised Ipratropium Bromide 500 micrograms
  • Consider back to back Salbutamol
    If life threatening or near fatal:
  • Urgent ITU or anaesthetist assessment
  • Urgent portable CXR
  • IV Aminophylline
  • Consider IV Salbutamol if nebulised route ineffective
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15
Q

What is the management of an acute COPD exacerbation

A
  • ABCDE approach
  • Oxygen: via a fixed performance face mask due to risk of CO2 retention - aim for SaO2 88-92% being guided by ABGs
  • NEBs – Salbutamol and Ipratropium
  • Steroids – Prednisolone 30mg STAT and OD for 7 days
  • Antibiotics if raised CRP / WCC or purulent sputum
  • CXR
  • Consider IV aminophylline
  • Consider NIV if Type 2 respiratory failure and pH 7.25-7.35
  • If pH <7.25 consider ITU referral
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16
Q

When should you consider pneumonia in a patient?

A

Consolidation on CXR with fever +/- purulent sputum +/ raised WCC and / or CRP

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17
Q

How should you manage pneumonia

A
  • ABCDE
  • If any features of sepsis – immediately treat using sepsis pathway – NO DELAY in initiating IV antibiotics and fluids
  • Otherwise treat with antibiotics as per CURB-65 score, local pneumonia guidelines and awareness of any patient drug allergies
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18
Q

What scoring system should you use for pneumonia and what are the features

A

CURB-65 Score

C Confusion, MMT 2 or more points worse
U Urea > 7.0
R > 30 / min
B < 90 mm Hg systolic or < 60 mm Hg diastolic
65 Age above 65 years

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19
Q

What is the definition of a massive haemoptysis

A

> 240mls in 24 hours OR >100mls / day over consecutive days

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20
Q

How would you manage a massive haemoptysis

A
  • ABCDE
  • Lie patient on side of suspected lesion (if known)
  • Oral Tranexamic Acid for 5 days or IV
  • Stop NSAID’s / aspirin / anticoagulants
  • Antibiotics if any evidence of respiratory tract infection
  • Consider Vitamin K
  • CT aortogram – interventional radiologist may be able to undertake bronchial artery embolisation
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21
Q

What are some examples of Sympathomimetics? What are their main indication? What is the mechanism of actions?

A
  • Short acting: Salbutamol, Terbutaline (effects ~4-6hrs)
  • Long acting: Formeterol, Salmeterol (effects ~12 hrs) – often given in combination with steroid inhaler
  • Main Indications- Bronchospasm
  • MOA- ß2-selective adrenergic agonists Increase cAMP in SMC’s resulting in relaxation and thus bronchodilation
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22
Q

What are some common side effects of B2 agonists

A

Tremor, headaches, GI upset, palpitations, tachycardia, hypokalaemia

Make sure inhaler technique is correct

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23
Q

What are some examples of antimuscharinics? What is the main indication? What it the Mechanism of action?What are some common side effects? Which patients should you take caution giving them to

A
  • Short acting eg ipratropium
  • long acting- tiotropium
  • main indication- COPD- bronchospasm
  • MOA- Muscarinic antagonist Decreases cGMP which affects intracellular calcium resulting in decreased SMC contractility
  • side effects- Dry mouth, constipation, cough, headache
  • Use with caution in those with angle- closure glaucoma & Benign Prostatic Hypertrophy
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24
Q

What are some examples of Xanthines? What is the main indication? What it the Mechanism of action?What are some common side effects?

A
  • eg Aminophylline, Theophylline
  • main indications- Asthma & COPD
  • MOA- Block phosphodiesterases resulting in decreased cAMP breakdown causing bronchodilation
  • other effects- Positive chronotropic and inotropic effects, diuretic action
  • side effects-Headache, GI upset, reflux, palpitations, dizziness
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25
Q

What is the therapeutic window for xanthines

A
  • Plasma level 10-20 mg/L.

- Toxic effects are serious arrhythmias, seizures, N&V, hypotension

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26
Q

What are some examples of inhaled steroids (glucocorticoids)? What is the main indication? What it the Mechanism of action?What are some common side effects?

A
  • eg Beclomethasone, Budesonide, Fluticasone
  • main indication- Asthma & COPD
  • MOA- Increase airway calibre by decreasing bronchial inflammation +/- modifying allergic reactions
  • side effects- Cough, oral thrush, unpleasant taste, hoarseness
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27
Q

What are some examples of corticosteroids (glucocorticoid)? What is the main indication? What are some common side effects?

A
  • eg Prednisolone (PO), Hydrocortisone (IV/IM), Dexamethasone (PO/IV), Triamcinolone (IM)
  • main indications- Supress inflammation, allergy & immune responses
  • side effects- Adrenal suppression (especially courses > 3 weeks), hyperglycaemia, psychosis, insomnia, indigestion, mood swings
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28
Q

What may you also need to give along side steroids

A

May need PPI (reduce GORD), Bisphosphonates (bone protection) and steroid card. Used both in short- term and long-term. Long-term steroid courses should NOT be withdrawn abruptly.

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29
Q

what is the definition of asthma

A

Airflow limitation + Bronchial Hyper-Responsiveness + Bronchial Inflammation → Reversible airway obstruction

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30
Q

what are the clinical features of mild asthma

A

Symptoms
- Episodic SOB + wheezing attacks
- Symptoms worse at night
- Nocturnal cough may bepresenting Sx in children
- Peak flow lowest in morning → precipitates attacks on waking
- Attacks precipitated by range of triggers
- Attacks of variable frequency, duration, severity
Signs
- Tachypnoea
- Audible wheeze
- Hyper-inflated + hyper-resonant chest
- ↓Air entry; polyphonic wheeze

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31
Q

how would you diagnose asthma

A

Minimum Diagnostic Testing = Spirometry + Bronchodilator reversibility (≥5yrs) + FeNO (≥17yrs).

Asthma may be diagnosed if any of the following criteria are met (in adults)

  • Obstruction: An FEV1/FVC ratio <70% (it is an obstructive lung disease)
  • Reversibility: PEF rate variability of ≥ 20%
  • Reversibility: A post-bronchodilator improvement in lung volume of ≥200 ml or of FEV1 of ≥12%
  • Inflammation: FeNO ≥40ppb
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32
Q

what is the conservative management of asthma

A
  • Quit smoking
  • Avoid triggers: Pets, mould, foodstuffs, dustmites, active/passing smoking, occupational agents, β blockers, NSAIDs
  • Teach inhaler technique, peak flow (monitor BD), relaxed breathing methods (e.g. Papworth)
  • Suspected occupational asthma: serial PEF at home/work + referral to respiratory specialist
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33
Q

what is the medical management of chronic asthma

A

1- SABA
2- +IGC (low-dose)
3- +LABA/MART
4- +LTRA

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34
Q

what should be done on discharge of asthma patient

A
  • Asthma plan
  • notify/see GP w/in 24-48hrs
    ± specialist review in 2w if severe (adult)/life- threatening (paediatric)
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35
Q

what is the definition of COPD

A

Chronic Obstructive Pulmonary Disorder

  • Progressive airflow limitation that is not fully reversible.
  • A type of obstructive respiratory disorder (
    FEV1/FVC < 0.7)
  • Includes chronic bronchitis (cough/sputum most days, ≥3 months, 2 years) and emphysema (histologically enlarged air spaces)
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36
Q

what are the causes of COPD

A

Smoking accounts for 90% of cases. Rarely α1 antitrypsin deficiency

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37
Q

what are the histological features of COPD

A
  • mucous gland hypertrophy
  • goblet cell hyperplasia
  • squamous metaplasia
  • mucus secretion
  • inflammatory cell infiltrate → bronchial inflammation, epithelium ulceration → 1. Scarring and thickening of walls and/or 2. Structural breakdown
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38
Q

what is V/Q mismatch

A

Ventilation perfusion mismatch or “V/Q defects” are defects in total lung ventilation perfusion ratio. It is a condition in which one or more areas of the lung receive oxygen but no blood flow, or they receive blood flow but no oxygen due to some diseases and disorders.

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39
Q

why may you get V/Q mismatch in COPD

A

V/Q mismatch due to:
1. Damage + mucus plugging of small airways 2º to chronic inflammation
COPD Pneumonia 2. Premature closure of small airways during expiration 2º to loss of elasticity

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40
Q

what is the most common causative organism for a COPD pneumonia

A

Haemophilus influenzae

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41
Q

what are the symptoms of COPD

A
  • Productive cough w/ white/clear sputum (green = infected)
  • Progressive dyspnoea/SOB
  • Frequent infective exacerbations → purulent sputum
  • Systemic Sx:
    o Weight loss, muscle mass loss and weakness
    o Depression, Osteoporosis
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42
Q

what are some signs of COPD

A
  • Expiratory wheezes throughout
  • Respiratory: tachypnoea, accessory muscle use (+ pursed lips), prolonged expiratory phase, ↓
    chest expansion, hyperinflation
  • Hypercapnic: CO2 retention flap, bounding pulse, peripheral vasodilation, morning headache →
    confusion → drowsiness
  • Circulatory: pulmonary hypertension → cor pulmonale, peripheral oedema, ↑JVP, ascites,
    abdominal discomfort
  • Complications: exacerbations, infection; polycythaemia, cor pulmonale,
    pneumothorax; cancer
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43
Q

what is the gold standard investigation for staging COPD

A

Spirometry

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44
Q

what are the target sats for a copd patient

A
  • Target Sats 88- 92% until ABG

- If ABG CO2 normal→ target 94-98%

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45
Q

what are some other investigations you could do for COPD

A
  • Spirometry (GOLD staging): FEV1 + Post-dilator FEV1:FVC <0.7 (i.e. non-reversible obstructive)
  • FBC: Haemoglobin and PCV (2º polycythaemia), WCC
  • CXR: flattened diaphragm, >6 anterior ribs, bullae
  • Blood gases: hypoxia (< 8kPa), hypercapnia (>7kPa)
  • Sputum culture
  • CT: useful when CXR normal
  • ECG: often normal, P pulmonale, RBBB, RVH
  • ECHO; α1 anti-trypsin levels
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46
Q

what is the general management of COPD

A
  • Smoking cessation (↑survival)
  • weight loss, exercise
  • Pulmonary rehab: as soon as SOB on regular activity
  • Vaccination: flu (annual) + pneumococcal (one-off)
  • Mucolytics (e.g. carbocysteine) if chronic productive cough
  • PRN SAMA (ipatropium) or SABA (salbutamol)
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47
Q

what antibiotic should be used for a infective COPD exacerbation

A

1st line amoxicillin 500mg TDS (clari, doxy)

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48
Q

what is pneumonia

A

infection and inflammation of lung parenchyma; a LRTI. 20% in-hospital mortality

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49
Q

what is CAP

A

Community Acquired Pneumonia: infection of lung parenchyma occurring outside of a healthcare setting; wide range of ages (but most common at extremes)

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50
Q

what are some abscess forming causative organisms of pneumonia

A
  • staph aureus
  • klebsiella
  • pseudomonas
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51
Q

what are some common causative organisms of CAP and how to treat

A
  • strep pneumonia (80%) treat with beta lactams/cephalosporins
  • H influenza- commenest in COPD

many others

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52
Q

what is HAP? what are some common causative organisms of HAP

A

Hospital Acquired Pneumonia: occurring within healthcare setting

  • Commonest: Staph. aureus
  • Pseudomonas (common bronchiectasis/commonest CF)
  • Klebsiella
  • Bacteroides
  • Clostridia
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53
Q

what is aspiration pneumonia? what are some common causative organisms of aspiration pneumonia? how do you treat?

A

Aspiration Pneumonia: secondary to aberrantly inhaled extra-pulmonary agents

  • Risk factors: low GCS, neuromuscular diseases, drugs (opiates, barbiturates, etc)
  • inhaled agents can be oral or gastric agents → chemical or infective pneumonitis
  • Common bacterial are: Strep. pneumoniae, staph. aureus, H. influenzae, Pseudomonas

treat with Cephalosporin IV + metronidazole IV

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54
Q

what is the conservative management of pneumonia

A

Pneumococcal vaccination

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55
Q

what is the medical management of pnemonia

A
  • Oxygen: aim for 92-94% if no COPD (COPD aim 88-92%); aim PaO2 >8.0kPa
  • IV fluids: if hypotensive/dehydrated
  • Thromboprophylaxis: if admitted > 12hrs; LMWH e.g. tinzaparin; TED stockings
  • Analgesia: for pleurisy; NSAIDs or paracetamol
56
Q

what abx should be given for mild CAP

A
  • Amoxicillin 500mg TDS
  • or Clarithromycin 500mg BD
  • or Doxycycline 200mg
57
Q

what abx should be given for moderate CAP

A
  • Amoxicillin 500mg and Clarithromycin 500mg

- or Doxycycline 200mg

58
Q

what abx should be given for severe CAP

A
  • Co-amoxiclav 1.2g TDS/IV and
  • cephalosporin 1.5g and
  • Clarithromycin 500mg IV
59
Q

what is the definition of tuberculosis

A

A mycobacterial infection with high global infection rates, but low active disease rates. Presents with primary, latent and reactivation phases. Commonly pulmonary or lymphatic in active disease, but can affect other areas such as CNS, skin, bone and GI.

60
Q

why can you not gram stain for TB and what should you do instead

A

Weakly Gram-stain due to lipid rich cell wall; acid-fast (Ziehl Nielsen Stain).

61
Q

how Is tb spread

A

Airborne infection spread via respiratory droplets

62
Q

what is the pathogenesis of tb

A
  • Once inhaled in ‘Primary TB’, alveolar macrophages ingest the bacteria
  • Bacteria proliferate intracellularly causing the release of chemo-attractants and cytokines. Hilar
    lymph nodes drain
  • A delayed hypersensitivity reaction occurs resulting in a rim of activated macrophages isolating a central necrotic mass of tissue and forming a caseating granuloma
  • The initial focus of disease is called the ‘Ghon focus’ (below) (+ hilar LN = Ghon complex)
  • Granulomatous regions heal completely and may become calcified (Ranke Complex)
  • Cell-mediated immune memory develops + regionally isolated, dormant bacteria → ‘Latent TB’
63
Q

what is the Mantoux test

A

The Mantoux test is a widely used test for latent TB. It involves injecting a small amount of a substance called PPD tuberculin into the skin of your forearm. It’s also called the tuberculin skin test (TST).

64
Q

How would you investigate an active TB infection

A

• Sputum MC&S: (≥3) Auramine-Rhodamine (or Ziehl Nielsen) + Lowenstein-Jensen Medium
• PCR: rapid identification of MTb (esp. in lumbar fluid) + rifampicin (± multidrug) resistance
• HIV test: should be offered to all patients
• CXR
◦ Upper lobe consolidation ± cavitation, effusion
◦ Widened mediastinum (hilar/paratracheal LN)
• CT: apical fibrosis†
• Histology: hallmark = caseating granulomata

65
Q

What investigations are done for TB detection

A

Mantoux test

Interferon-gamma release assay

66
Q

What is the management of latent TB

A

• Otherwise healthy pt do not necessarily need treatment for latent TB. Pt at risk of reactivation of latent tb can be treated with the below:
◦ 3mo of isoniazid (with pyridoxine- vit b) and rifampicin
◦ or 6mo of isoniazid (with pyridoxine)
• If concerns about hepatotoxicity then 3mo of isoniazid and rifampicin may be preferred.

67
Q

How would you treat active Tb

A

• All forms of active TB must be made statutorily notifiable in the UK. TTreatment is under the care of a specialist TB clinician/ service according to the table above. Exceptions include:
◦ Active CNS disease (including spinal cord involvement ; continuation phase of treatment is extended from 4-10mo
◦ CNS and pericardial disease: use adjunctive high dose steroids (with weaning and withdrawal during the intensive treatment period)
◦ Drug resistant TB
• Adherence is important for treatment to be effective and to prevent drug resistance,
• RIPE:
◦ Rifampicin for 6mo
◦ Isoniazid for 6mo
◦ Pyranzinamide for 2mo
◦ Ethambutol for 2mo

68
Q

What do you do for drug resistant Tb

A

• NAAT for drug resistance should be requested for all pt with risk factors for drug resistance disease: previous Tb treatment, contact with drug resistant disease, birth or residence in a country where 5% or more cases are drug resistant.
• Drug resistance may be:
◦ To any single agent in the table above
◦ Multidrug resistant TB (MDR-TB)- resistant to rifampicin and isoniazid
◦ Extensively drug resistant TB (XDR-TB)- resistant to rifampicin, isonizad, one injectable agent (eg capreomycin, kanamycin or amikacin) an done fluoroquinolone.
• If rifampicin resistance is detected treat with at least 6 agents to which the mycobacterium is likely to be sensitive. Test for resistance to 2nd line drugs.

69
Q

Who should be screened for Tb

A

Interferon gamma tests are used in asymptomatic patients with risk factors for latent TB:
◦ Immigrants from high prevalence countries
◦ Healthcare workers
◦ HIV positive patients
◦ Patient starting on immunosuppression

70
Q

What are the side effects of the RIPE (TB medication)

A

• Rifampicin
◦ Causes urine/tears to turn orange (reverses when rifampicin stops)
◦ Drug induced hepatitis
• Isoniazid
◦ Peripheral neuropathy (reduced by pyridoxine- vit b6 which is given prophylactically)
◦ Colour blindness
◦ Drug induced hepatitis
• Pyrazinamide
◦ Drug induced hepatitis
◦ Hyperuricaemua (high uric acid levels resulting in gout)
• Ethambutol
◦ Optic neuropathy/reduced visual acuity

71
Q

What is the definition of bronchiectasis

A

Chronic infection → abnormal and permanently dilated airways

72
Q

What are some common causative organisms of bronchiectasis

A

H. influenzae (commonest),

Pseudomonas, S. pneumoniae, Klebsiella,

73
Q

What are the symptoms of bronchiectasis

A
  • cough- with daily and copious malodorous sputum (and halitosis)
  • SOB
  • rhinosinusitis
  • intermittent haemoptysis
  • recurrent infection
74
Q

What are some signs of bronchiectasis

A

Clubbing
Coarse crackles
Hyperinflation

75
Q

How would you investigate bronchiectasis

A
  • CXR: cystic shadows, thickened bronchial walls (tramline and ring shadows)
  • CT: “signet ring” appearance – airways larger than adjacent vessels
  • Sputum; Sinus X-rays; Skin prick test (e.g. allergic aspergillosis)
  • Immunoglobulins
  • Sweat electrolyte test for Cystic fibrosis (Na+ > 60mmol/L = Dx)
  • Bronchoscopy
76
Q

What is the management of bronchiectasis

A
  • Inspiratory muscle training + Postural drainage (twice daily)
  • Acute ± chronic antibiotics – according to pathogens. Pseudomonas = ciprofloxacin
  • Bronchodilators if airflow limitation
  • Steroids – for ABPA
  • Surgery: if localised disease
  • Heart/lung transplant
77
Q

What is cystic fibrosis

A

A genetic condition affecting serous excretion in the lungs and gastrointestinal tract

Autosomal recessive disorder of the cystic fibrosis transmembrane conductance regulator (CFTR) gene which induces low salt and chloride excretion into the airways leading to increased viscosity of airways secretions. Also affects other serous secretions of the body.

78
Q

What is the commonest causative organism of a cystic fibrosis infection in children

A

Staph. aureus (commonest paeds)

79
Q

What is the commonest causative organism of a cystic fibrosis infection in adults

A

Pseudomonas (commonest adults)

80
Q

What are the respiratory clinical features of cystic fibrosis

A
  • Same as those for bronchiectasis including recurrent infections, haemoptysis
  • Clubbing
  • Nasal polyps and sinusitis
  • Spontaneous pneumothorax, respiratory failure, right ventricular failure
81
Q

What are the GI clinical features of cystic fibrosis

A
  • Pancreatic insufficiency: Steatorrhoea, Diabetes Mellitus
  • Meconium ileus (children) or Distal intestinal obstruction syndrome (adults)
  • Gallstones
  • Cirrhosis
82
Q

How would you investigate Cystic fibrosis

A
  • Sweat electrolyte test (Na+ > 60mmol/L = Dx)
  • DNA analysis for genotype
  • Fecal elastase
83
Q

What is the management of cystic fibrosis

A

Resp

  • Postural drainage; antibiotics; bronchodilators; mucolytics (DNase), CFTR gene therapy
  • Amiloride or adenosine to improve hydration of secretions

GI

  • ↑Calorie, ↑fat diet + pancreatic enzymes, vit. supplements (ADEK), Ursodeoxycholic acid
  • Rx of osteoporosis, arthritis, sinusitis, etc.
84
Q

What is the definition of a plural effusion

A
  • Fluid in the pleural space.

- Can be divided by their protein concentrations into transudates (<25g/L) and exudates (>35g/L).

85
Q

What is it called when there is blood, pus, chyle, blood and air, in the plural space?

A
  • Blood = haemothorax.
  • Pus = empyema.
  • Chyle (lymph + fat) = chylothorax.
  • Blood + air = haemopneumothorax.
86
Q

What are some causes of a transplanted plural effusion

A

Transudate (<25g/L)

  • ↑Venous pressure (CCF, constrictive pericarditis)
  • ↓Protein (cirrhosis, nephrotic syndrome, malabsorption)
  • Hypothyroidism
  • Meig’s Syndrome: benign ovarian mass + ascites + effusion
87
Q

What are some causes of exudate plural effusion

A

Exudate (>35g/L)

  • ↑Leakiness of pleural capillaries secondary to:
  • Infection: Pneumonia (commonest), TB, abscess
  • Inflammation: RA, SLE, pancreatitis, PE, Dressler’s, yellow nail syndrome
  • Malignancy: carcinoma, metastases, mesothelioma, etc.
88
Q

What criteria should be used if the protein is 25-35g/L to distinguish transudate and exudate

A

Lights criteria

89
Q

What are the features of lights criteria

A

distinguishes when protein 25-35g/L; exudate likely if:
• pleural protein divided by serum protein >0.5
• pleural fluid LDH divided by serum LDH >0.6
• pleural fluid LDH > 2/3rds upper limits of normal serum LDH

90
Q

What are the symptoms of plural effusion

A
  • can be asymptomatic
  • could have dyspnoea
  • pleuritic chest pain
91
Q

What are the signs of plural effusion

A
  • ↓Expansion
  • Stony dull percussion
  • ↓Breath sounds
  • ↓Tactile vocal fremitus + vocal resonance
  • Bronchial breathing (above effusion, where lung is compressed)
92
Q

How would you investigate a plural effusion

A
  • CXR (all patients): blunting of costophrenic angles; opacities with meniscus
  • Ultrasound (recommended): guides diagnostic/therapeutic intervention
  • Diagnostic Aspiration (with US)
    o Percuss upper border of effusion; choose site 1-2 intercostal spaces below
    o Infiltrate pleura with 5-10mL of 1% lidocaine o Inject 21G needle-syringe above upper border of rib
    o Draw off 10-50mL → chemistry (LDH, pH, protein), cytology, microbiology
  • Pleural biopsy: if pleural fluid analysis is inconclusive; thoracoscopic/CT-guided best
  • Contrast CT: increasingly performed to find underlying cause, esp. exudative effusions
93
Q

How would you manage a plural effusion

A
  • Drainage: Seldinger Technique chest drain if:
    o Sepsis/unstable patient
    o Purulent/turbid/cloudy fluid (e.g. empyema) o Clear fluid but pH <7.2
  • Pleurodesis: with tetracycline, bleomycin or talc
  • opioids releive dyspnoea
  • surgery for persistent collections
94
Q

What is a pneumothorax

A

Air in the pleural space

95
Q

What is the difference between a primary and secondary pneumothorax

A
  • Occurs when a pleural bleb (primary: healthy individuals; tall, thin males)
  • pulmonary bulla ( secondary: smoker >50yrs, COPD, asthma, CF, cancer, TB) pop, allowing air to be driven into the pleural space. - Alternatively, the aetiology may be traumatic.
96
Q

What are the clinical features of a pneumothorax

A 
If small, possibly no symptoms
• Pleuritic pain
• Tracheal deviation (tension)
• Hyper-resonance
• Onset sudden
• Reduced breath sounds (and dyspnoea)
• Absent fremitus
• X-ray - collapse
97
Q

What are the clinical features of a tension pneumothorax

A
  • commonly 2º to +ve pressure ventilation, trauma
    • Imaging: mediastinal shift, flattening of hemi-diaphragm, massive lung collapse
    • Circulatory collapse: tachycardia, hypotension,
    • If tension pneumothorax is suspected TREAT EMPIRICALLY (NO CXR NEEDED)
98
Q

How would you investigate a pneumothorax

A
  • ABG – assess for hypoxemia, hypercapnia
  • CXR – lung for absence of lung markings at peripheral edges
  • CT – identify lung lesions
99
Q

How would you manage a pneumothorax

A

Conservative
• If minimal pneumothorax – no Rx, avoid strenuous exercise, observe at 2w intervals
• STOP SMOKING - ↑risk 100X Medical
• If > 2cm radiographic volume, intervene
• Primary → aspiration → (recurrence) chest drain
o 16G 3-way tap to 2nd intercostal mid-clavicular (4-6th mid-axillary) (1% lidocaine) o 50mL syringe; aspirate up to 2.5L air (50mL x 50); stop if resistance felt, or if
excessive coughing; CXR to confirm.
• Secondary (SOB or + >2cm) → chest drain (if not those criteria, aspiration)
• Tension! Large bore 14g IV cannula (2nd intercostal mid-clavicular) until chest tube can be
placed (safe triangle: 5th/6th intercostal mid-axillary)
• Chest drain swinging: rises in inspiration, falls on expiration; confirms pleural location

100
Q

What are the features to discharge a pneumothorax

A
  • If primary <2cm → discharge (if 2º <1cm → O2 + admit 24hrs)
  • Follow up at 24hrs and 7-10 days
  • Avoid flying for 1 week if post-check CXR normal (BTS); NB: CAA recommend 2 weeks
101
Q

What is a pulmonary embolism

A

Embolic occlusion of pulmonary vessels causing hemodynamic compromise.

102
Q

What are the risk factors for a pulmonary embolism

Use THROMBOSIS pneumonic

A 
THROMBOSIS
• Travel
• Hypercoagulable (e.g. thrombophilia)
• Recreational drugs
• Old (>60yrs)
• Malignancy 
• Birth control pills (pregnancy, post-partum, HRT) 
• Obesity/orthopaedics/obstetrics 
• Surgery/smoking 
• Immobilisation (fracture, surgery) 
• Sickness (PE, MI, etc)
103
Q

What are the clinical features of a pulmonary embolism

A

Signs (sudden onset)

  1. Dyspnoea
  2. Haemoptysis
  3. Pleuritic pain- Only 10% patients present with this typical triad
  4. Dizziness/syncope

Symptoms

  • Tachypnoea
  • Tachycardia
  • hypotension
  • ↑JVP
  • cyanosis
  • fever
  • Pleural rub
  • pleural effusion
  • crackles
  • peripheral oedema
  • Signs of cause e.g. DVT
104
Q

What is the score used to tell the likelihood of a DVT/PE

What score make a PE likely

A 
Well’s Score: 
suspect DVT (3)
alternative Dx unlikely (3)
tachycardia (1.5)
immobilization 3d/surgery 4w (1.5)
Hx DVT/PE (1.5)
haemoptysis (1)
malignancy (1).

Score >4 = PE likely!

105
Q

What is the gold standard diagnostic investigation for a PE

A

CTPA: DIAGNOSTIC sensitive and specific;

if unavailable V/Q scan

106
Q

What investigation should be done for a PE if you are allergic to dye for a CTPA/pregnant

A

V/Q scan

107
Q

What are some other investigations you can do for a PE

A
  • Bloods: D-dimers, FBC, U&E, baseline clotting, BNP + troponin (assess heart strain)
  • ABG: hypoxia (<8kPa), hypocapnia (<4kPa), alkalosis (2º hyperventilation); hypercapnia +
    acidosis if severe
  • CXR: near normal
  • ECG: normal, tachycardia, RBBB, right-sided strain (T inversion V1-V4), classic SI QIII TIII (rare)
108
Q

What is the management of a PE

A

↓Risk Embolism → Anticoagulation
• LMWH or Fondaparinux
• + Vitamin K antagonist (Warfarin) within 24hrs of Dx
• Continue both LMWH/Fondaparinux + Warfarin for 5 days or until INR > 2.0
• Then continue Warfarin 3 months; longer if unprovoked; 6 months if 2º to active cancer

Peri-Arrest PE (↓BP) → Thrombolysis
• Alteplase = 1st line (50mg bolus or… 100mg over 2hrs ← better evidence)
• Then SC LWMH e.g. tinzaparin 175mg/kg or… IV unfractionated heparin 10,000U bolus
• Then start warfarin regime

Peri-Arrest PE (↓BP) → Embolectomy
• Embolectomy is an alternative to fibrinolysis

Prophylaxis (All immobile patients)
• Heparin e.g. dalteparin 2500u SC OD
• Compression stockings

109
Q

What are the risk factors for lung cancer?

A 
Smoking
Airflow obstruction
Increasing age
Family history
Carcinogens eg asbestos
110
Q

What staging is used for lung cancer?

A

TNM

111
Q

What is the use of PET scanning in lung cancer?

A

Helps detect small mets not seen on staging CT

Used if patient is surgical candidate and initial CT suggests low stage

112
Q

What are the 2 main histological types of lung cancer?

A

Small cell lung cancer

Non-small cell lung cancer

113
Q

What are the different types of non-small cell lung cancer?

A

Squamous cell
Adenocarcinoma
Large cell carcinoma
Bronchoalveolar cancer

114
Q

In what stages of lung cancer is surgery considered?

A

I and II (providing patient is fit for surgery)

115
Q

What is emphysema?

A

Alveolar wall destruction causing irreversible enlargement of air spaces, distal to the terminal bronchioles

116
Q

What are the aims of long term oxygen therapy in COPD?

A

Preventing renal and cardiac damage caused by long periods of hypoxia

117
Q

At what oxygen level is LTOT offered for COPD?

A

pO2 consistently below 7.3

Or below 8kPa with for pulmonale

118
Q

What are the conditions for patients having LTOT?

A

Must be non-smokers

Must not retain high levels of CO2

119
Q

what conditions are involved in interstitial lung disease

A

Umbrella term describing a number of conditions that affect the lung parenchyma in a diffuse manner including:
• Usual Interstitial Pneumonia (UIP)
• Non-specific Interstitial Pneumonia (NSIP)
• Extrinsic Allergic Alveolitis
• Sarcoidosis
• Several other conditions

120
Q

what are the classical findings of UIP

A
  • clubbing, reduced chest expansion
  • Auscultation – fine inspiratory crepitations (like pulling Velcro slowly) – usually best heard basal / axillary areas
  • Cardiovascular – may be features of pulmonary hypertension
121
Q

what is sarcoidosis

A

A granulomatous multi-organ disease affecting principally the lymph nodes and lung, but also skin, eyes and other organs. Most prevalent in young adults (20-40), women, Afro-Carribeans (↑severity)

122
Q

how would you investigate sarcoidosis

A 
Investigations:
• PFTs: (obstructive until) fibrosis
• CXR: 4 stages
• Bloods: renal function, ACE, Calcium
• Urinary Calcium
• Cardiac involvement: ECG, 24 tape, ECHO, cardiac MRI • CT/MRI head: headaches – Neuro sarcoid
123
Q

how would you manage an acute attack of sarcoidos

A

Acute sarcoidosis = NSAIDs and bed rest

124
Q

when would you use corticosteroids in sarcoidosis

A 
Indications for Corticosteroids:
• Symptomatic stage 2+ lung disease
• Hypercalcaemia
• Uveitis
• Neurological or cardiac involvement
125
Q

what is Extrinsic Allergic Alveolitis (EAA)

A 
Type III (acute)/IV (chronic) hypersensitivity of the alveoli to previously sensitized allergens (fungal
spores or avian proteins e.g. avian IgA)
126
Q

what is the acute and chronic clinical features of Extrinsic Allergic Alveolitis (EAA)

A

4-6 Hours Post-Exposure

  • Dry cough
  • Dyspnoea
  • Crackles and wheeze
  • Fevers, rigors, myalgia

Chronic Exposure

  • Increasing and exertional dyspnoea
  • ↓weight
  • T1RF (hypoxia)
  • cor pulmonale
127
Q

how would you investigate acute and chronic Extrinsic Allergic Alveolitis (EAA)

A

Acute

  • Bloods: neutrophilia, ↑ESR, ABGs, +ve serum precipitins (indicates exposure)
  • Lung function tests: reversible restrictive, ↓gas transfer (during attacks)
  • CXR: upper zone mottling/consolidation, hilar lymphadenopathy (rare)

Chronic

  • Bloods: +ve serum precipitins but NO EOSINOPHILIA
  • Lung function: persistent changes
  • CXR: upper zone fibrosis; honeycomb lung
  • Bronchoalveolar lavage: ↑lymphocytes and mast cells
128
Q

how would you manage acute and chronic Extrinsic Allergic Alveolitis (EAA)

A

Acute: remove allergen, give O2 (35-60%), oral prednisolone 40mg/24hrs (titrate dose)

Chronic: avoid allergen, facemask/helmet, long-term steroids, compensation

129
Q

what are the features of the WHO scale of performance status

A

Gives an indication of patient’s level of fitness
• 0 Normal - Fully active without restriction
• 1 Restricted in physically strenuous activity but
ambulatory and able to carry out light work e.g.,
light house work, office work
• 2 Ambulatory and capable of all self-care but
unable to carry out any work activities. Up and
about more than 50% of waking hours
• 3 Capable of only limited self-care, confined to
bed or chair more than 50% of waking hours
• 4 Completely disabled. Cannot self-care. Totally
confined to bed or chair
• 5 Dead

130
Q

what is obstructive sleep apnoea

A

A disorder characterised by intermittent closure/collapse of the pharyngeal airway causing apnoeic episodes during sleep. These are terminated by partial arousal. These episodes are associated with oxyhaemoglobin desaturations and arousals from sleep. While these interrupt appropriate REM sleep, they are not often not recalled by the patient.

131
Q

what are some symptoms of obstructive sleep apnoea

A 
Symptoms
• Loud snoring (95%) 
• Daytime sleepiness (90%)
• Unrefreshed/restless sleep (40%) 
• Morning headache (30%) 
• Nocturnal choking (30%) 
• Reduced libido (20%) 
• Morning drunkenness (5%) 
• Ankle swelling (5%)
132
Q

how would you investigate obstructive sleep apnoea

A
  • Epsworth Sleepiness Scale questionnaire
  • Polysomnography = diagnostic; monitors SaO2, airflow, ECG, EMG during sleep
    o E.g. Multiple Sleep Latency Test (MSLT) - measures time to fall asleep in a dark
    room (using EEG criteria)
133
Q

what is the management of obstructive sleep apnoea

A

Conservative
• Weight reduction
• Avoidance of tobacco and alcohol
• DVLA should be informed if causing excessive daytime sleepiness

Medical
• Mild disease (no daytime sleepiness) → intra-oral devices (e.g. mandibular advancement)
• Moderate-severe disease → CPAP via nasal mask is recommended by NICE

Surgical
• To relieve obstruction: tonsillectomy, uvulopalatopharyngoplasty, tracheostomy

134
Q

what are the 2 classical syndromes for sarcoidosis

A

Lofgren’s- erythema nodosum, polyarthralgia, fever and BHL

Heerfort’s Syndrome- fever, parotid swelling, uveitis, +/- facial nerve palsy

135
Q

Differentials for erythema nodosum

Use pneumonic spotted

A 
Sarcoidosis 
Pregnancy 
Oral contraceptive 
Tuberculosis 
Throat infection- strep 
Everything else- IBD, NHL
Drugs- sulphonamides

taz- year 3 med (10 decks)

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