PBL 5 Flashcards

1
Q

Define aspergilus antibodies

A

this is a laboratory test performed on your blood, it is ordered when the doctor thinks that you have an infection caused by fungus asperigillus, it is usally treated with prescription antifungal medication

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2
Q

define eczema

A

this is a condition where patches of skin become inflamed, itchy, red, cracked and rough

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3
Q

define PEF

A

this is the normal peak expiratory flow, this is when you take your PEF regularly and keep a record of it therefore when you see changes in it or feel your asthma getting worse you can see how your peak flow changes

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4
Q

define nebulisation

A

this is a piece of medical equipment that a person with asthma or other respiratory conditions can use to administer medication quickly to lungs, it turns liquid medicine to fine mist that a person can inhale through a face mask or mouthpiece

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5
Q

define asthma

A

this is a chronic inflammatory airway disorder, it is marked by airway hyperresponsiveness with recurrent episodes of wheezing, coughing, tightness of the chest and shortness of breath

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6
Q

describe the 3 characteristics of asthma

A
  • airflow limitations
  • airway hyper-responsiveness
  • inflammation of the bronchi with eosinophils, t lymphocytes and mast cells
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7
Q

what is atopic asthma

A
  • begins in childhood and is linked to triggers such as allergens that can cause release of excessive IgE
  • this causes inflammation mediates to trigger airway inflammation and bronchoconstriction
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8
Q

what do the eosinophils do in the bronchial wall

A
  • they release substances such s histamine, and leukotrienes which cause bronchoconstriction and cause the formation of a mucus plug
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9
Q

what is the difference between asthma and COPD

A
  • Asthma has variability in obstruction to airflow and responds to broncho dilators
  • COPD there is fixed airway. narrowing with reduced FEV1/FVCC and less than 15% response to bronchodilator
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10
Q

what are the potential causes and risk factors of asthma

A
  • Obesity – reasons are unclear but some people think it is due to low-grade inflammation in the body that occurs with extra weight
  • Air pollution – exposure to the main component of smog (ozone) raises the risk of asthma
  • Smoking – cigarette smoke irritates the airways, smokers have a high risk of asthma
  • Occupational exposures – exposures to certain elements in the workplace which can cause asthma symptom
  • Allergies – having an allergic condition such as atopic dermatitis or alleric rhinitis
  • Viral respiratory infections – respiratory problems during infancy and childhood can cause wheezing some children whoe xpericne viral respiratory infections go on to develop chronic asthma
  • Family history – if you have a parent with asthma you are three to 6 times more likely to develop asthma
  • Occurs more frequently in boys than in girls
  • Maternal smoking during pregnancy appears to result in lower lung function in infants compared to those whose mothers did not smoke
  • Hygeine hypothesis
  • damp houses
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11
Q

what are the three types of inhalers

A
  • These help relive symptoms when they occur – reliver inhalers
  • Stop symptoms developing – preventer inhalers
  • Some need both – combination inhalers
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12
Q

how do ICS work

A

– they suppress inflammation mainly by switching off multiple activated inflammatory genes through reversing histone acetylation via the recruitment of HDAC2

  • ICS (also known as glucorticoid steroids) reduces airway hyperresponsiveness and controls asthma symptoms
  • ICS is first line therapy for all patients with persistent astha
  • Inhaled long acting beta 2 agonist are added to ICS to further improve asthma control and are given as combination inahlers, these imrpvoe compliance and control asthma at lower does of corticosteroids, ICS provide much less clinical benefit in COPD and the inflammation is resistant due to the action of corticosteroids
  • Improves the FVC, FEV1/FVC and PEF
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13
Q

how do SABAs work

A

– these work fast to relax the muscles of the airways, they are a beta 2 agonist and prevent them from getting to tight, they relieve asthma symptoms from 3 to 6 hours, this can be salbutamol, works within 5 minutes, they do not control inflammatory processes, used for mild to intermittent asthma, once using them for more than 2 a week you should go onto a ICS or LABA to control the inflammation
- blocks parasympathetic activity

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14
Q

How does a nebuliser work

A

– necessary in severe asthma as the uptake form inflaers is low and not adqqeuate to reduce bronchoconstriction

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15
Q

how does LABA work

A

– long acting beta 2 agonist, haa a duration of action of 12 hours which is longer than the SABA, shouldn’t be used on there own should be used with an ICS

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16
Q

what is salbutamol

A

beta 2 agonist can also affect the heart

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17
Q

what is combination inhalers

A

theses are LABAs and ICS combined

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18
Q

name some lung function tests

A

• Peak flow. Your doctor may take a peak flow reading when you come in for a scheduled visit or for emergency treatment during an asthma attack. This test measures how quickly you can breathe out. You may also use a peak flow meter at home to monitor your lung function.
The results of this test are known as peak expiratory flow (PEF). A peak flow test is done by blowing into a mouthpiece as hard and as fast as you can with a single breath (expiration).
• Spirometry. During spirometry, you take deep breaths and forcefully exhale into a hose connected to a machine called a spirometer. A common spirometry measurement is forced expiratory volume, which measures how much air you can breathe out in one second.
The results of this test are known as forced expiratory volume (FEV). Spirometry can also measure how much air your lungs can hold and the rate at which you can inhale and exhale.
• Nitric oxide measurement. This exam measures the amount of nitric oxide gas you have in your breath when you exhale. High nitric oxide readings indicate inflammation of the bronchial tubes.
• Pulse oximetry. This test measures the amount of oxygen in your blood. It’s measured through your fingernail and only takes seconds.

19
Q

what are medications given in an asthma attack

A
  • Short-acting beta agonists, such as albuterol. These are the same medications as those in your quick-acting (rescue) inhaler. You may need to use a machine called a nebulizer, which turns the medication into a mist that can be inhaled deep into your lungs.
  • Oral corticosteroids. Taken in pill form, these medications help reduce lung inflammation and get your asthma symptoms under control. Corticosteroids can also be given intravenously, typically to patients who are vomiting or who are experiencing respiratory failure.
  • Ipratropium (Atrovent HFA). Ipratropium is sometimes used as a bronchodilator to treat a severe asthma attack, especially if albuterol is not fully effective.
  • Intubation, mechanical ventilation and oxygen. If your asthma attack is life-threatening, your doctor may put a breathing tube down your throat into your upper airway. Using a machine that pumps oxygen into your lungs will help you breathe while your doctor gives you medications to bring your asthma under control.
  • ICU
20
Q

what are the symptoms of an asthma attack

A
  • your symptoms are getting worse (cough, breathlessness, wheezing or tight chest)
  • your reliever inhaler (usually blue) isn’t helping
  • you’re too breathless to speak, eat or sleep
  • your breathing is getting faster and it feels like you can’t catch your breath
  • your peak flow score is lower than normal
  • children may also complain of a tummy or chest ache
  • You should see your GP or asthma nurse within 48 hours of leaving hospital, or ideally on the same day if you didn’t need hospital treatment.
21
Q

what are the risk factors of an asthma attack

A
  • Going near allergy
  • High levels of pollution
  • Smoke
  • Beta blockers
  • NSAIDS
22
Q

what is the treatment of an asthma attack

A
  • Give oxygen – venture mask or nasal cannula
  • Treat with SABA
  • For life threatening or severe asthma give nebulized salbutamol
  • If nebulizer is not avaliabe use a pressurized emtered dose inhaler with a large volume spacer
  • Neublized ipratropium bromide
  • Monitor PEF
23
Q

explain her result

A
  • The aspergillus antibodies indicate that mould is part of the allergy that she is having
  • Eosinophils indicate that she is having an allergy attack
  • This would show in her detoriation of asthma when she moved house and it was more damp and mouldy
  • Could have skin prick test to prove
  • Her arterial blood oxygen is lower than normal
  • Her arterial blood gas shows hypocapnia which is her carbon dioxide being lower than normal, this shows that she is breathless and hyperventilation but can still clear carbon dioxide from the blood - her pH would be greater than 7.45, carbon dioxide less than 4.6kPa
  • A lowered carbon dioxide level would indicate reduced ventilation – life threatening asthma
  • Patient has hypoxia but a normal pCO2 which is type I respiratory failure
  • She could develop type II if her condition continued
  • Alkalosis but pH still in normal range this is due to the hypocapnia
  • Pulse oximeter goes from 92% to 93% this is result of giving oxygen
24
Q

how do you classify asthma

A

life treating asthma

  • PEFR lower than 33% predcited
  • SAO2 lower than 92%
  • tacycardia
  • PaO2 less than 8KpA
  • PC02 normal
  • silent chest
  • cyanosis
  • feeble respiratory effort
  • acute sever asthma with any one of
  • PEFR lower than 35% predicted
  • respirator rate greater than 25 a minute
  • heart rate greater than 110
  • inability to complete sentences in one breath
25
Q

name some other bronchodilators used in severe acute asthma

A
  • intravenous salbutamol
  • intravenous aminophylline
  • intravenous magnesium
26
Q

name an other treatment for asthma

A
  • IgE treatment

- this includes monoclonal antibodies against IgE

27
Q

what is type I respiratory failure

A

– Hypoxaemia only – type I respiratory failure is only type I
– PaO2 < 8 kPa
( hypocapnoea?)

28
Q

what is type II respiratory failure

A

– Hypoxaemia and normo/hypercapnia
– PaO2 < 8 kPa
– PaCO2 >6.5 kPa

29
Q

What are the three histoloigcal features of asthma

A

Bronchial smooth muscle hypertrophy = bronchospasm

Mucus hypersecretion

Airway inflammation

30
Q

Explain the allergic reaction to aspergillus fumigatus

A

Allergen eg aspergillus is inhaled

Meets dendritic cell which engulfs allergen
and presents to CD4+ T cells via MHC class 2

CD4+ T cells differentiate from Th0 to Th2
CD4+ cells

TH2 cells release IL-4 and IL-13, which
activate B-cells to differentiate to plasma
cells and produce IgE

Th2 cells release IL-5 which attracts eosinophils

IgE binds to mast cell/basophil surface= sensitisation

Re-exposure to allergen leads
to cross-linking with surface IgE🡪

mast cell degranulation🡪

histamine and leukotriene release = asthma

31
Q

What are the symptoms of astama

A

Intermittent episodes of:

  • Dyspnoea
  • Wheeze
  • Cough
  • Chest tightness
32
Q

How do you diagnose asthma

A

History- symptoms and atopy

Peak flow- diurnal variation of ≥20% over >3 days/ week
for 2 weeks

Spirometry: FEV1/FVC <70%

Reversible: FEV1 increases by >15% or 200ml
post-bronchodilator

33
Q

what is the FEV1 differnece between normal and obstructive airway condition

A

FEV1 higher - FEV1/FVC greater than 70%

FEV1 reduced in obstructive conditions this causes the FEV1/FVC ratio to be lower than 70%

34
Q

What is the treatment of asthma

A

Step 1: Short-acting B2-agonist (SABA) eg salbutamol when required

If using salbutamol 3 or more times a week, or nighttime
symptoms 1 or more nights a week🡪

Step 2: Inhaled corticosteroid (200-800mcg per day, usually
400mcg)

Step 3: Add long-acting B2-agonist (LABA) eg salmeterol
- Good response, continue
- Benefit from LABA but still inadequate control- increase
corticosteroid to 800mcg per day
- No response- stop LABA, increase corticosteroid to 800mcg.
Still inadequate control add leukotrienne receptor antagonist (eg monteleukast) or theophylline

Step 4: increase corticosteroid dose to 2000mcg/day
- Add a fourth drug eg LABA, leukotrienne receptor antagonist, theophylline or B2 agonist tablets

Step 5: continue inhaled corticosteroid at 2000mcg/day. Add oral
corticosteroid

Anti-IgE monoclonal antibodies eg omalizumab

35
Q

what are the symptoms of a severe asthma attack

A

Unable to complete sentences in one breath

Respiratory rate >25/min

Pulse rate >110bpm

Peak expiratory flow rate (PEFR) 33-50% of predicted/ best

36
Q

what are the symptoms of a life threatening asthma attack

A

PEFR <33% of predicted/ best

Silent chest, cyanosis, feeble respiratory effort

Bradycardia or hypotension

Exhaustion, confusion or come

PaO2

37
Q

what is near fatal asthma

A

Raised PaCO2 >6kPa or patient requiring ventilation

- exhaustion leads to poor ventilatory effort and less carbon dioxide is blwon up

38
Q

what is the treatment of an asthma attack

A

Inhaled high-dose salbutamol

Oral steroids eg prednisolone 40-50mg

Oxygen if SpO2<94%

39
Q

what is the difference between dyspnoea and hypopnoea

A

Dyspnoea- difficulty in breathing/ shortness of breath

Hyponoea- reduced respiratory rate (apnoea- absence of breathing)

40
Q

what are the main inflammatory cells in astham

A

Eosinophils, mast cells, basophils, Th2 CD4+ T cells

41
Q

what is the diagnostic diurnal varation in asthama

A

Diurnal variation of ≥20% over >3 days/ week for 2 weeks

42
Q

what is the diagnositc FEV1/FVC ratio in ashtam

A

less than 70%

43
Q

what is the diagnostic reversibility in astama

A

Increase in FEV1 by >15% or 200ml post-bronchodilator

44
Q

what is a bad feature in an asthama attack

A

Raised PCO2