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drugs y3 > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Example of B2 agonist

A

salbutamol (SABA)

salmeterol (LABA)

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2
Q

how do beta agonists work

A
  • stimulates the B2 receptor located on smooth muscle of the bronchial tree, causing it to relax, causing vasodilation
  • also causes K+ to move from extracellular to intracellular, decreasing K+ concentration in the blood
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3
Q

when are beta2 agonists used

A
  • asthma
  • COPD
  • hyperkalaemia
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4
Q

contradictions for b2 agonists

A

cardiac conditions, arrhythmias

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5
Q

side effects of b2 agonists

A

tremor, muscle cramps, anxiety, palpitations, arrhythmias, tachycardia

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6
Q

possible interactions of B2 agonists

A
  • beta blockers reduce effectiveness
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7
Q

how to give salbutamol as nebs in asthma

A

with oxygen

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8
Q

how to give salbutamol as nebs in COPD

A

with air to prevent CO2 retention

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9
Q

examples of anti-cholinergics / anti-muscarinics

A

SAMA - ipratropium

LAMA - tiotropium

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10
Q

how do anti-muscarinics work

A

competitive inhibitor for AcetylCholine on muscarinic receptors, decreasing smooth muscle tone, increasing HR and conductivity and decreasing glandular and tract secretion

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11
Q

when are anti-muscarinics used

A

COPD - SAMA used to relieve, LAMA used to prevent

Asthma - SAMA added to SABA to relieve or LAMA added to LABA and inhaled corticosteroid to prevent

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12
Q

contraindications for anti-muscarinics

A

those at risk of glaucoma (due to risk of increased intra-ocular pressure), arrhythmias, urinary retention

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13
Q

side effects of anti-muscarinics

A

arrhythmias, GI disturbance, resp tract irritation, sinusitis, constipation, cough, dry mouth

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14
Q

possible interactions for anti-muscarinics

A

drugs with other anti-muscarinic effect e.g., tricyclic anti-depressants

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15
Q

example of inhaled corticosteroids

A

beclomethasone

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16
Q

how do inhaled corticosteroids work

A

enter cells and modify gene transcription, down-regulating pro-inflammatory interleukins, cytokines and chemokine and up-regulating anti-inflammatory proteins
- they decrease mucosal inflammation, widen airways and decrease mucus secretion

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17
Q

when are inhaled corticosteroids used

A

asthma and COPD - used as preventers and to decrease exacerbations

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18
Q

contraindications for inhaled corticosteroids

A

history of pneumonia and in children be cautious - can cause growth suppression

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19
Q

side effects for inhaled corticosteroids

A

oral candidiasis, pneumonia risk

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20
Q

example of systemic corticosteroids

A

prednisolone

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21
Q

how does prednisolone work

A
  • binds to glucocorticoid receptors and up regulates anti-inflammatory genes and down-regulates pro-inflammatory genes
  • mineralocorticoid effects by stimulating Na and water retention and K+ secretion in the renal tubule
22
Q

when is prednisolone used

A
  • allergic and inflammatory disorders
  • autoimmune suppression
  • cancer to decrease tumour swelling
  • HRT in adrenal insufficiency and hypopituitarism
23
Q

contraindications for prednisolone

A

infection and children (can cause growth suppression)

24
Q

side effects of prednisolone

A

immunosuppression, mood changes (insomnia, psychosis, suicidal thoughts, confusion), muscle weakness, easy bruising, DM, osteoporosis, adrenal atrophy

25
Q

interactions of prednisolone

A

NSAIDs increase risk of GI bleed, cytochrome P450 inhibitors decrease efficacy

26
Q

examples of mucolytics

A

carbocisteine

27
Q

how do mucolytics work

A

decrease sputum viscosity, facilitating expectoration

28
Q

when are mucolytics used

A

COPD (decrease eaccerbations), Bronchiectasis (via steam inhalation)

29
Q

contraindications for mucolytics

A

peptic ulcers (can disrupt the gastric barrier)

30
Q

side effects of mucolytics

A

peptic ulcers, rarely gastric bleed

31
Q

examples of xanthines

A

theophylline

32
Q

how do xanthines work

A
  • competitive non-selective phosphodiesterase inhibitors, which increase intracellular cAMP, inhibiting leukotriene synthesis, thus decreasing inflammation and innate immunity
  • non-selective adenosine receptor antagnoist (preventing the blocking of irregular heart signals)
33
Q

when are xanthines (theophylline) used

A

asthma and stable COPD as a bronchodilator

34
Q

when are xanthines contraindicated

A

cardiac disease (arrhythmias), peptic ulcer disease, hyperthyroidism, hypertension, epilepsy, hypokalaemia risk

35
Q

side effects of xanthines (theophylline)

A

arrhythmias, N&V, diarrhoea, gastric irritation, palpitations, tachycardia, headache, insomnia, convulsions

36
Q

interactions of xanthines (theophylline)

A

may have additive effects if used with b2 agonists such as increasing chance of hypokalaemia

37
Q

how does oxygen therapy work

A

increase pO2, increasing diffusion of oxygen to issues

38
Q

when do you use oxygen therapy

A
  • pneumothorax
  • CO poisoning
  • acute hypoxaemia
  • chronic hypoxaemia
39
Q

how does oxygen therapy work in pneumothorax

A

O2 causes decrease in N2, increasing diffusion of nitrogen out of the body

40
Q

how does oxygen therapy work in CO poisoning

A

decreases carboxyhemoglobin half life

41
Q

contraindications for oxygen therapy

A

chronic type 2 resp failure (severe COPD) - can result in hypercapnia

42
Q

side effects of oxygen therapy

A

discomfort

43
Q

types of oxygen therapy

A
  • reservoir mask (non-rebreathe)
  • venturi mask
  • nasal cannula
  • simple facemask
  • non-invasive ventilation (BiPAP / CPAP)
44
Q

target O2 levels

A

94-98%

45
Q

target O2 levels in someone with chronic type 2 RF

A

88-92%

46
Q

when to use a reservoir / non-rebreathe mask

A

acute settings

  • if SpO1 <85%
  • continuous supply
47
Q

when to use a Venturi mask

A
  • oxygen and air blended

- if target is less (in CT2RF)

48
Q

when to use a nasal cannula

A
  • if possible

- variable O2 conc

49
Q

when to use a simple facemask

A
  • variable O2 conc

- if nasal cannula cannot be used

50
Q

when to use NIV

A
  • if CO2 retention and hypoxic

- last resort as difficult to wean off

drugs y3 (10 decks)

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