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BDS2 > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What are the routes of administration for respiratory drugs?

A

via:
inhalation
Oral
IV

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2
Q

What are the types of delivery aids that can be used to deliver respiratory drugs?

A

Inhalers - Meter dose inhaler (MDI), Breath activated device (spinhaler, turbohaler)

Spacers - Medication ejected into chamber before inhalation

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3
Q

What is ventilation?

A

Movement of air between the environment and the lungs via inhalation and exhalation

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4
Q

What drugs are used in ventilation to improve airway patency?

A

Bronchodilators
Anti-inflammatory
Anti-cholinergic drugs

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5
Q

Which drugs are used to prevent mast cell degranulation?

A

Mast cell stabilisers - Chromoglycate - stops mast cells releasing inflammatory mediators such as histamine (inhaled) - YELLOW/WHITE inhaler

Leukotriene receptor agonists - montelukast - good for mast cell disorders but not as potent as steroids (oral route - tablets)

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6
Q

What drugs are used to impair ventilation?

A

Beta blockers - blocks adrenaline which normally acts as a bronchodilator, however when blocked it can manifest in asthmatic symptoms

Respiratory depressants

  • Benzodiazepenes (Diazepam) - act on GABA receptors
  • Opioids (Morphine) - pain relief
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7
Q

What bronchodilators are used as respiratory drugs and how do they work?

A

B2 agonists:

Short acting - Salbutamol/Terbutaline (BLUE) onset 2-3 mins, lasts 4-6 hours, for bronchial constriction (all routes)

Long acting - Salmeterol (GREEN) onset 1-2 hours, lasts 12-15hrs, used to prevent bronchial constriction, always used with an inhaled steroid e.g. Seretide (PURPLE) which is Fluticasone and salmeterol

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8
Q

What antiinflammatories are used as respiratory drugs and how do they work?

A

corticosteroids - reduce inflammation in bronchial walls (effective topical or systemic)

  • Beclomethasone (BROWN)
  • Budesonide (BROWN)
  • Flucitasone (ORANGE)
  • Mometasone (PINK)
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9
Q

What anticholinergics are used as respiratory drugs and how do they work?

A

Anticholinergics - inhibit muscarinic ACh receptors in autonomic nerves, basal tone only = increase bronchial dilation, decrease Mucus secretion e.g. Ipratropium (inhaled route) (GREEN/WHITE)

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10
Q

What drugs are used to improve gas exchange?

A

Respiratory stimulants such as

Theophyllines - postive chronotropic (^HR), positive inotropic (^contractility), bronchodilator, therefore better gas exchanging properties due to better air exposure in alveoli and blood flow
- Cause - Diuresis, arrythmia, CNS stimulation

Oxygen - is a drug and should be treated as such

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11
Q

What are the signs and symptoms of Obstructive Airways Disease?

A

Symptoms:

  • Cough (Dry? sputum and if so what colour? Blood?)
  • Wheeze - expiratory noise
  • Stridor - Inspiratory noise
  • Dyspnoea - distress on effort to breathe
  • Pain - generic, or upon inspiration (pleuritic pain)

Signs:

  • Resp rate - 12-15/min
  • Symmetry of air entry/chest expansion
  • Percussion note - resonant/dull
  • Vocal resonance
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12
Q

What are the investigations for obstructive airways disease?

A
  • Sputum examination
  • Chest radiograph
  • Pulmonary function - PEFR (maximum flow rate), FEV1 (forced expiratory volume - vol of exhaled air in 1 second), FEV1/FVC - FEV1/total amount of air exhaled in fev test (vital capacity)
  • Bronchoscopy
  • VQ scan
    (ventilation/perfusion mismatch)
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13
Q

What are the main differences between obstructive and restrictive lung disease?

A

Obstructive characterised by reduction in AIRFLOW, so shortness of breath –> in exhaling air, whereas restrictive is reduction in LUNG VOLUME so difficulty in taking air into the lung.

In obstructive disorders the air will remain inside the lung after full expiration, whereas restrictive disorders occur due to stiffness inside the lung tissue or chest wall cavity

Obstructive disorders - COPD, Asthma, Bronchiecstasis

Restrictive disorders - Interstitial lung disease, scoliosis, neuromuscular cause, marked obesity

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14
Q

What are three types of respiratory infections?

A

Pneumonia - Strep pneumoniae causes inflammation (pneumonitis) of the alveoli and they become fluid filled (consolidation) preventing oxygen exchange

Legionairre’s disease - Leigonella pneumophilia causes an atypical pneumonia often transmitted by stagnant water dental chair

Tuberculosis (TB) - Mycobacterium Tuberculosis - only 10% of cases symptomatic, if so cough, fever and weight loss

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15
Q

What is Asthma and what are the signs/symptoms?

A

Reversible airflow obstruction - Bronchial hyper-reactivity

Triad of:

  • Airway smooth muscle constriction
  • Inflammation of mucosa
  • Increased mucus secretion

Diurnal process -worse in the morning

  • Cough, wheeze, shortness of breath
  • Triggered by infections, environmental stimuli (dust, smoke, chemicals), cold air

Atopy - genetic predisposition to allergy

  • Mast cell degranulation (IgE released - primary allergen antibody)
  • Eosinophils, T cells, interleukins activated
  • B2 agonists, Chromoglycate, steroids prevent mast cells degranulating
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16
Q

How is asthma treated?

A

Depending on severity from 1-5

  1. Occasional beta agonist only
  2. LD inhaled steroid/chromoglycate
  3. HD inhaled steroid
  4. Long acting beta agonist, theophylines, anti-muscarinic drugs
  5. Oral steroid
17
Q

What is COPD?

A

Chronic Obstructive Pulmonary Disease

Combination of 2 diseases:
- Chronic bronchitis - inflammation of mucous membranes of bronchial tubes and hypertrophy of mucous glands

  • Chronic emphysema - destruction of alveoli and distal bronchiales, dilation of others to fill space results in chronic hypoxia due to reduced gas transfer

Marked by reduced PEFR and FEV1

18
Q

What are the marked effects of respiratory failure?

A
  • Reduced surface area for gas exchange
  • Thickening of alveolar mucosal barrier
  • Poor ventilation (from restrictive defects and reversible narrowing)
19
Q

Where does COPD arise?

A

Smoking

Environmental - fibrosis (coal, silicon), tumours (asbestos = mesothelioma)

Hereditary - Emphysema

Occupational lung disease can lead to respiratory disease - mesothelioma - tumour of lung lining

20
Q

How do you manage COPD?

A

Smoking cessation

Mucolytic agents (carbocisteine)

LA Bronchodilator - Salmeterol

IF <50% FEV - give inhaled steroids

Oxygen support

21
Q

What are the different types of respiratory failures that arise from COPD?

A

Type 1 RF - hypoxaemia, thickening of alveolar barrier

Type 2 RF - Hypercapnia, airway blockage/narrowing, ventilation failure, can be caused by neuromuscular problems (guillen-barre/MND), or from severe spinal deformity (kyphoscoliosis)

22
Q

What does a V/Q value of > 1 indicate?

A

Ventilation exceeds perfusion

23
Q

What does a V/Q value of <1 indicate?

A

Perfusion exceeds ventilation

24
Q

What is perfusion?

A

Process by which deoxygenated blood passes through the lung and becomes oxygenated

25
Q

What is the normal V/Q for the lung?

A

0.8 (4/5)

26
Q

How does V/Q tie into COPD?

A

Normal - CO2 drive controls ventilation oxygen saturation usually ok

COPD:
CO2 tolerance - hypoxia drives ventilation

If giving O2 in excess it causes V/Q mismatch and causes respiratory acidosis and death:

in COPD there is respiratory vasoconstriction due to the lung being underventilated so the vasculature ‘downsizes’ to match

Sudden oxygen increase can open up the vasculature suddenly causing a V/Q mismatch

This redistributes blood to areas of the lung where ventilation is poor causing CO2 retention and resultant acidosis and death

27
Q

What is cystic fibrosis?

A

Inherited disorder

CFTR gene mutation - chromosome 7 - recessive gene, both parents must have gene, 1/4 offspring affected - of the 3/4 not affected 2/3 are carriers, 1/4 is healthy and not affected nor is a carrier

Defect in cell chloride channels

Produces excess sticky mucous

Lung/Pancreas mainly affected

Pancreas covered in mucous so digestive enzymes blocked

Causes poor digestion of fats/proteins

Results in steatorrhea

28
Q

What are the symptoms of Cystic Fibrosis?

A

Lungs - prone to infection - s.aureus/psedumonas aeruginosa

Pancreas - steatorrhoea (excess fat in faeces) due to pancreatic enzyme blockage from mucous, diabetic symptoms due to pancreatic dysfunction

Liver - bile is thick and tenacious - struggles to get out of liver leaving hepatobiliary tree dehydrated which can result in cirrhosis

Reproductive system - reduced ferility in males

29
Q

What is the treatment for cystic fibrosis?

A

Physiotherapy - used to help remove the mucous secretions from the lungs

Medication
Lungs - bronchodilators to open airways, antibiotics to reduce chest infection frequency, steroids to reduce airway inflammation, Dnase to break down mucous
Digestive - pancreatic enzyme replacement, nutritional supplements

Exercise - necessary to keep lung function optimal, necessary to build physical bulk and strength

Transplantation - not a cure,
end stage lung disease
heart-lung transplant (2-12 yrs)

30
Q

How can lung cancer be classified?

A

Small cell carcinoma (20%)
- oat cell carcinoma - very small cells that are possibly malignant because of their inability to regulate their size and growth

Non-small cell carcinoma (80%) - squamous carcinoma, adenocarcinoma, large cell undifferentiated carcinoma

31
Q

What are the effects of lung cancer?

A
  • Cough
  • Haemoptysis
  • Pneumonia
  • Metastasis - bone, liver, brain
  • Other - dysphagia, superior vena cava obstruction compression from tumour, recurrent laryngeal nerve palsy - horseness
32
Q

What is obstructive sleep apnoea syndrome? (OSAS)

A

Airway obstruction whilst asleep - 10s or more, airway muscle tone drops

May be snorers
Caused by pharyngeal muscle relaxation (tongue occludes pharynx temporarily)
Drowsiness in daytime - falling asleep whilst driving
- Inc risk of MI due to low O2
- NON respiratory - Central sleep apnoea - brain doesnt send correct signals to muscles that control breathing

OSAS patients are of high risk of hypoventilation and CO2 retention when under sedation

BDS2 (8 decks)

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