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Sven's Flashcards > 210 - Asthma > Flashcards

210 - Asthma Flashcards

1
Q

what is the definition of asthma?

A

chronic inflammatory disorder of the airways characterised by airways hyper-respoinsiveness with airflow obstruction that is reversible spontaneously or with treatment

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2
Q

what are the clinical characteristics of asthma

A
  • recurrent wheeze
  • SOB
  • diurnal variation - peak flow lowest in morning
  • chest tightness
  • cough
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3
Q

What is extrinsic (atopic) asthma?

A

IgE mediated asthma - most common & runs in families
a type I hypersensitivity reaction - has a extrinsic cause - aeroallegen (dust mite, fur, mould, fungi, pollen). Usally develops in children below 10 and affects males more

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4
Q

what is occupational asthma?

A

IgE hypersensitivity reaction that develops later in life to workplace allergens

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5
Q

what is intrinsic asthma?

A

non atopic (non immune) - less common and develops later in life & less responsive to treatment. Causes include infection, cold, exercise, stress, irritants (ozone)

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6
Q

what are environmental risk factors for asthma

A

smoking exposure, pollutants, viral infections, childhood abx use, caesarean birth, not breast fed

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7
Q

What is the early response in asthma?

A

only in IgE mediated asthma, devops in mins & reversible with beta2 agonists.
Caused by a type I hypersensitivity reaction - antigen cross links with IgE on mast cell & causes degranulation of histamines (bronchoconstricts, ↑mucous production & ↑ microvascular leakage), prostaglandins & leukotrienes (both bronchoconstrict). IL-5 encourages eosinophil recruitment & late response

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8
Q

what is the late response in asthma?

A

develops 3-12 hrs after trigger & less response to B2 agonist (requires steroids)
Involves airway inflammation & oedema and also bronchoconstriction, ↑mucous, hyperresponsiveness
Caused by *eosinophils - attracted by IL-5 (mast cells) & damage by major basic protein (epi damage & ↑ perm, ciliostasis & water secretion), eosinophil cation protein (epi sheding) & leukotrienes. *TH-2 cells - attracted by IL-4 (mast cells) to activate b cells *b cells activated by IL-13 (b cells) to produce further IgE

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9
Q

what long term damage occurs in asthma?

A

airway remodelling due to repeated inflammation & over production of growth/repair factors.
effects: bronchial wall thickening & fibrosis, smooth muscle hypertrophy, goblet cell hypertrophy, loss of surface epithelium

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10
Q

what investigations can be carried out for suspected asthma?

A
  • PEFR monitoring
  • spirometry - onstructive pattern FEV1:FVC 12% FEV1 improvement
  • methacholine test - spirometry before and after taking histamine
  • skin prick test for allergies
  • CXR
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11
Q

what are the signs and symptoms of an acute asthma attack?

A

SOB, pink colour, ↑RR & HR, accessory muscle use, ↑exp phase

*red flags - cyanosis, silent chest (with bradycardia), lack of distress (confusion)

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12
Q

what are the gradings for asthma attacks?

A
  • mild - PEFR >75%, pulse 96%
  • moderate - PEFR 50-75%, pulse 100-110, RR 20-25, SATS >92%
  • severe - PEFR 33-50%, pulse >110, RR>25, SATS >92%, unable to talk in full sentences
  • life threatening - PEFR <33%, confused, bradycardia, hypotension, poor resp effort, ABG acidotic, normal to hig pCO2, hypoxia (low pO2)
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13
Q

what short acting beta2 agonists (SABA) are used to treat asthma, how do they work and what are the side effects?

A
  • salbutamol, terbutaline
  • act on b2 adrenoreceptors on bronciole walls, ↑production of cAMP, which activates protein kinase A & leads via myosin light chain kinase to relax bronchial smooth muscle. Also reduces inflam mediator release & ↑ cilia activity. Works in mins but lasts 4-6hrs
  • side effects - tremor, tachycardia, hypokalaemia
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14
Q

what corticosteroids are used to treat asthma, how do they work and what are the side effects?

A
  • beclometasone (brown), fluticasone (red), budesonide (brown)
  • ↓mast cell/eosinophil/t-cell/dendritic number in mucosa reducing the immune response and hyper-responsiveness. reduces goblet cell hyperplasia & vascular permeability. Takes up to 2 weeks to act
  • side effects - hoarse throat, sore throat, candidal infect, at high dose - bruising, immunosupression, osteoporosis, growth retardation, weight gain, moods, hyperglycaemia
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15
Q

what long acting B2 agonists (LABA) are used to treat asthma, how do they work and what are the side effects?

A
  • salmeterol, formoterol
  • as SABA but lipophilic side chain anchors molecule next to receptor. Slower to take effect but last 12hrs. Must be used with steroids as do not ↓inflammation
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16
Q

what do the combined LABA/corticosteroids Symbicort, seretide and fostair contain?

A
  • symbicort - formeterol & budesonide
  • seretide - salmeterol & fluticasone
  • fostair - formeterol & beclometasone
17
Q

what leukotrine receptor antagonists are used to treat asthma, how do they work and what are the side effects?

A
  • montelukast, zafirlukast - for exercise, nocturnal, NSAID, obesity asthma
  • block leukotriene C4, D4 & E4 binding to receptor reducing bronchocontriction & wheeze, mucous, vascular permeability & eosinophil recruitment. work within hrs
  • Side effects - headache, GI symptoms
18
Q

what xanthines are used to treat asthma, how do they work and what are the side effects?

A
  • Theophylline, aminophylline
  • bronchodilate by inhibiting phosphodiesterse (enzyme for break down of cAMP)
  • Has a narrow therapeutic range & variability in metabolism in px - longer 1/2 life with erythromycin, fluconazole, liver & heart disease. shorter 1/2 life with rifampicin, carbamazepine, drinking & smoking
  • side effects due to toxicity - N&V, tachycardia, tremor, agitation, seizures - must monitor plasma conc.
19
Q

what are the steps of asthma control?

A
  • 1 - SABA
  • 2 - SABA + low dose inhaled corticosteroid
  • 3 - SABA + LABA + low to med does corticosteroid
  • 4 - SABA + LABA + high dose corticosteroid + if needed theophylline, leukotriene receptor antagonist
20
Q

what is omalizumab?

A

anti IgE antibody binds to IgE

21
Q

what is mepduzimab?

A

anti IL-5 antibody - stops eosinophil recruitment

22
Q

what treatment should be given in an acute asthma attack?

A
  • 100% O2
  • B2 agonist
  • antimuscarinic - ipratropium inhibit parasympathic bronchoconstriction
  • steroids - prednisolone or hydrocortisone oral or iv
23
Q

what treatment should be given in a life threatening asthma attack?

A

ITU admission, intubation & ventilation, IV MgSO4 (inhibits bronchoconstriction & ↓ histamine release), iv aminophylline

24
Q

what is contraindicated in asthma?

A
  • NSAIDS (blocks COX-2 inhibitor which catalyses arachidonic acid to thromboxane instead of bronchoconstrictive prostanoids & leukotriene)
  • beta blockers

Sven's Flashcards (32 decks)

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