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Medicine (Year 5) > Respiratory (Misc) > Flashcards

Respiratory (Misc) Flashcards

1
Q

types of smoking cessation therapy

A

nicotine replacement therapy (NRT), varenicline, or bupropion

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2
Q

how should pharmacological therapy be used to aid smoking cessation

A
  • Should be given to patient on or before a particular target stop date
  • prescription should only last util 2 weeks after the target stop date (2 weeks NRT or 3/4 weeks of varenicline/bupropion)
  • ## if treatment is unsuccessful do not offer a repeat within 6 months unless special circumstances have contributed to failure
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3
Q

nicotine replacement therapy modes

A

gum, patches, lozenges and nasal sprays

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4
Q

nicotine replacement therapy contraindications

A

Cautions
* Cardiovascular disease and peripheral arterial disease
* Diabetes mellitus
* Hyperthyroidism
* Renal/hepatic impairment
* Peptic ulcers

Contraindications

  • Severe cardiovascular disease (e.g. arrhythmia, post-myocardial infarction, recent stroke or TIA)
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5
Q

adverse effect of NRT

A
  • Dizziness
  • Nausea
  • Myalgia and flu-like symptoms
  • Palpitations
  • Dyspepsia
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6
Q

MOA OF VARENICLINE

A

Varenicline is an alpha-4 beta-2 nicotinic acetylcholine receptor partial agonist. It blocks and stimulates the receptor leading to reduced craving. It also inhibits the pleasure derived from smoking.

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7
Q

varenicline contraindication

A

Cautions

  • History of psychiatric illness – can increase risk of suicidal thoughts/behaviour
  • Breastfeeding
  • Severe renal impairment
  • Withdrawal symptoms on stopping – gradual withdrawal may need to be considered

Contraindications

  • Pregnancy
  • <18 years
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8
Q

varenicline adverse effects

A

Nausea
Headaches
Insomnia
Abnormal dreams

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9
Q

bupropion

A

Bupropion is an atypical antidepressant that has been demonstrated in trials to be effective in smoking cessation.

It is a noradrenaline and dopamine reuptake inhibitor and nicotinic antagonist.

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10
Q

contraindications of bupropion

A

Cautions

  • There is a risk of seizures (1 in 1000)
  • Hepatic cirrhosis
  • Renal impairment
  • Blood pressure

Contraindications

  • Patients with a history of seizures
  • Pregnancy
  • Bipolar disorder
  • <18 years
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11
Q

bupropion adverse effects

A

Adverse effects

Seizures (1 in 1000)
Insomnia
Dry mouth

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12
Q

Smoking and Pregnancy

A
  • Pregnant people should be offered carbon monoxide testing at all antenatal appointments to assess exposure to tobacco smoke – this is because it can be difficult to disclose smoking during pregnancy due to the stigma surrounding it

Management
* Refer to stop-smoking support (e.g. NHS Stop Smoking)
* Consider nicotine replacement therapy
* Varenicline and bupropion are contraindicated

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13
Q

MOA of CO poisoning

A

Carbon monoxide binds to haemoglobin more strongly, forming carboxyhaemoglobin, leading to tissue hypoxia. Carboxyhaemoglobin can take several hours to dissociate, meaning blood cannot carry as much oxygen in this timeframe.

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14
Q

Sources of Carbon Monoxide

A
  • Poorly-maintained housing (e.g. blocked chimneys, lack of ventilation, gas ovens)
  • Smoke in burning buildings
  • Aerosols
  • Running petrol/diesel engines in confined spaces, even if the windows are open
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15
Q

presentation of CO poisoning

A

Questions to ask can be remembered using the mnemonic COMA:

  • Cohabitees – is anyone else in the property affected? – including pets
  • Outdoors – do the symptoms improve outside the building?
  • Maintenance – are any fuel-burning appliances and vents properly maintained?
  • Alarm – does the house have a carbon monoxide alarm?

Features seen in carbon monoxide poisoning are non-specific, making it difficult to diagnose:

  • Headaches – most common:
  • Often described as tension-type headaches
  • Nausea and vomiting
  • Vertigo
  • Altered consciousness
  • Confusion
  • Fatigue
  • Non-specific pain – usually the chest or stomach
  • Weakness
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16
Q

Features of severe CO toxicity may be:

A
  • Pink skin and mucosae
  • Personality changes
  • Arrhythmia
  • Parkinsonism
  • Coma
  • Death
  • Classic ‘cherry red’ skin is rarely seen in life and is usually seen post-mortem
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17
Q

CO investigations

A

REMEMBER: Pulse oximetry may be falsely normal – it cannot differentiate oxyhaemoglobin and carboxyhaemoglobin

Venous or arterial blood gas – gold standard:

  • Shows increased carboxyhaemoglobin levels:
  • <3% is normal for non-smokers
  • <10% is normal for smokers
  • > 30% indicates severe exposure

Serum lactate:

May be elevated in severe poisoning

ECG:

  • May show cardiac ischaemia or arrhythmia

Serum troponin:

  • May show cardiac ischaemia

Serum glucose:

Always test in any patient with reduced consciousness

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18
Q

management of carbon monoxide poisoning

A
  • 1st-line: 100% high-flow O2 via non-rebreather mask
  • Evidence suggests that this reduces the half-life of carboxyhaemoglobin
  • Evidence surrounding hyperbaric oxygen is controversial
  • Any patient who has suffered smoke inhalation should be assumed to have carbon monoxide poisoning and should also be treated as such

complications include: myocardial infarction

19
Q

causes of pulmonary embolism

A

thrombus
fat
gas
aminionic fluid

20
Q

RF pulmonary embolism

A
  • Up to 30-50% have no identifiable cause (unprovoked)
  • Deep vein thrombosis (DVT)
  • Previous VTE
  • Active cancer
  • Recent surgery (within the last 2 months), especially major orthopaedic surgery
  • Significant immobility (e.g. hospitalisation or bed rest >5 days)
  • Lower limb paralysis, trauma, or fracture
  • Pregnancy and the postpartum period
  • > 60 years of age
  • Combined oral contraceptive use
  • Obesity
  • Long-distance sedentary travel (e.g. long-haul flights)
  • Varicose veins
  • Superficial venous thrombosis
  • Any cause of hypercoagulable state (e.g. factor V Leiden, antiphospholipid syndrome)
  • Behçet’s disease
  • Nephrotic syndrome (due to loss of antithrombin III and plasminogen in urine)
21
Q

presentation of PE

A

There is a classic triad of dyspnoea, haemoptysis, and pleuritic chest pain, however in reality this only presents in around 10% of patients.

  • Dyspnoea – most common presenting complaint (usually acute)
  • Pleuritic chest pain (usually acute)
  • Tachycardia
  • Tachypnoea
  • Signs of a DVT:
  • Usually pain and swelling in one leg (or both), and there may be redness, warmth, and distended veins
  • Presence of risk factors in the history
  • Cough
  • Fever
  • Haemoptysis – present in around 8% of patients
22
Q

if a patient with a PE is haemodynamically unstable…

A

suggests a massive pulmonary embolism and usually requires critical care.

  • Tachycardia
  • Hypotension
  • Acute right ventricular dysfunction (e.g. elevated jugular venous pressure)
  • Syncope or pre-syncope
23
Q

Pulmonary em bolism rule-out criteria (PERC)

A

The PERC rule can be used to rule out a PE when the suspicion of diagnosis is relatively low, but reassurance is desired. The PERC is negative when none of the criteria are present, making the probability of a PE is <2%. A score >0 (i.e. if any feature is present) is a positive PERC.

If the suspicion of a PE is higher, the PERC should be skipped and a 2-level PE Wells score should be calculated.

24
Q

Two-level PE Wells score

A

If a PE is suspected, then a Two-level PE Wells score should be calculated. A PE is likely if there are >4 points and unlikely if there ≤4 points.

25
Q

investigations for PE

A

Chest x-ray:
Should be offered to all patients, usually normal

ECG:

  • Sinus tachycardia is most commonly seen
  • ‘S1Q3T3’ sign may be seen - S wave deepest in lead 1, Q wave in 3 and T wave inversion in 3
  • RBBB
  • AF
  • Right axis deviation

PE likely (>4 points on two-level PE Wells score)

Immediate CT pulmonary angiogram (CTPA):

  • If there is a delay in performing a CTPA, give interim anticoagulation
  • If CTPA positive: continue anticoagulation
  • If CTPA is negative: consider proximal leg vein ultrasound if DVT suspected
  • If the patient has renal impairment: use V/Q scan instead of CTPA (this is because a CTPA uses contrast)

PE unlikely (≤4 points on two-level PE Wells score)

  • Immediate D-dimer test:
  • If D-dimer positive: arrange CTPA (or V/Q scan if renal impairment present)
  • If there is a delay in performing CTPA, give interim anticoagulation
  • If D-dimer negative: stop anticoagulation and consider an alternate diagnosis
26
Q

management of PE: Non-pregnant patients without renal dysfunction

A

*When you first suspect a PE give LWMH immediately *

  • First line Direct oral anticoagulant (DOAC) such as apixaban or rivaroxaban
  • Second line (if DOAC unsuitable) Low molecular weight heparin (LMWH) followed by dabigatran or edoxaban
  • LMWH followed by warfarin

* If the patient has cancer: use DOAC and follow above steps

*If the patient has antiphospholipid syndrome:LMWH followed by lifelong warfarin

27
Q

PE management: Severe renal dysfunction (eGFR <15 /min)

A

LMWH, unfractionated heparin, or LMWH followed by warfarin

28
Q

PE management: Pregnant patients

A
  • 1st-line: subcutaneous LMWH or IV heparin
  • Warfarin is contraindicated in pregnancy
  • DOACs are not used in pregnancy as there is no information surrounding their use
29
Q

PE management with haemodynamic instability

A

These are patients with massive PE and haemodynamic instability (i.e. hypotension)

1st-line: thrombolysis e.g. alteplase (takes 90 mins)

30
Q

Length of anticoagulation in all patients

A
  • If the DVT was provoked (there was an obvious event causing it e.g. prolonged immobilisation): continue anticoagulation for 3 months
  • If the DVT was unprovoked: continue for 6 months
  • If the patient has active cancer: continue for 6 months
31
Q

warfarin INR targets

A

the INR target is 2.5, keeping in the range of 2.0 – 3.0

32
Q

Pulmonary hypertension (PH)

A

is characterised by increased blood pressure in the arteries of the lungs and the presence of increased pulmonary vascular resistance. This can cause strain on the right side of the heart, leading to right ventricular hypertrophy and failure.

Pulmonary hypertension is diagnosed if the mean pulmonary arterial pressure is >25 mmHg at rest or >30 mmHg with exercise.

33
Q

WHO Classification system for pulmonary hypertension

A

The World Health Organisation has produced a system for classifying PH based on cause and associations:

  • Group I – idiopathic or associated with connective tissue disorders (e.g. systemic lupus erythematosus)
  • Group 2 – secondary to left heart disease/valvular disease/restrictive cardiomyopathy
  • Group 3 – secondary to chronic lung disease/environmental hypoxaemia
  • Group 4 – due to chronic thrombotic/embolic disease
  • Group 5 – metabolic disorders/systemic disorders/haematological disease/other causes
34
Q

Pulmonary hypertension presentation

A
  • Insidious dyspnoea
  • Fatigue
  • Peripheral oedema
  • Chest pain
  • Syncope
  • Elevated jugular venous pressure (JVP)
  • Tricuspid regurgitation
  • Right ventricular parasternal heave
  • Ascites
35
Q

pulmonary hypertension investigations

A

Chest X-ray:
Rules out other lung diseases
May show enlarged pulmonary artery or hilar vessels

ECG:
May show right ventricular hypertrophy (RVH) or right axis deviation

Echocardiography:
Assess right ventricular function and estimate pulmonary arterial pressure

Right heart catheterisation:
Directly measures pulmonary pressure and confirms the diagnosi

36
Q

1.

management of pulmonary hypertension

A

manage underlying cause
- consider sildenagil - phosphodiesterase-5 inhibitor
- lung transplant

37
Q

pulmonary hypertension complications

A
  • Right ventricular hypertrophy and right ventricular failure
  • Peripheral oedema
  • Hepatic congestion
  • Exertional syncope
  • Cardiac arrest
38
Q

Obstructive Sleep Apnoea

A

a sleep-related breathing disorder characterised by recurring episodes of partial/complete obstruction of the upper airway during sleep leading to apnoea (complete airflow obstruction and temporary absence of breathing). This leads to irregular breathing at night and excessive drowsiness during the day.

39
Q

RF OSA

A

Risk Factors

  • Obesity – strongest risk factor
  • Increasing age
  • Male sex
  • Family history
  • Smoking
  • Alcohol
  • Macroglossia (enlarged tongue) and adenoid tonsil hypertrophy
  • Down’s syndrome
  • Type 2 diabetes
  • Jaw morphology
40
Q

OSA presentation

A

Presentation

Patients often have unexplained daytime sleepiness. If possible, anyone that sleeps alongside the partner should be present when taking a history. Features are:

  • Excessive daytime sleepiness and feeling unrefreshed after sleep
  • Snoring
  • Their partner may notice periods of apnoea
  • Choking during sleep
  • Headaches on waking
  • Insomnia
  • Problems with memory or cognition
  • Hypertension can occur as a result
41
Q

investigations for OSA

A

Epworth Sleepiness Scale:
* Assesses the severity of daytime sleepiness

Polysomnography (sleep studies) – diagnostic test:
* This may involve measuring pulse oximetry at night or measuring multiple factors, such as an EEG, ECG, EMG, airflow assessments etc.

42
Q

management of OSA

A

First line weight loss

Second line continuous positive airway pressure (CPAP) if moderate-severe OSA

Other options are:
* intra-oral mandibular advancement devices
* upper airways surgery (e.g. tonsillectomy or uvulopalatopharyngoplasty)

43
Q

patient advice for OSA

A
  • Patients must notify the DVLA if their OSA causes excessive sleepiness
  • Patients should try to lose weight (if necessary) and be offered help with this
  • Patients should try to avoid sleeping supine where possible

Medicine (Year 5) (34 decks)

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