COPD and Asthma Flashcards

1
Q

B2 adrenergic receptor agonist

A

Short acting - Salbutamol, terbutaline
Long acting - Salmetrolol and lomoterol

Long acting B2 receptor agonists are analogues of SABA with long lipophilic chains allowing the active drug to remain @ the site for longer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

MOA B2 agonists

A

Acts on B2 adrenorecptors in SM of upper airways. They stimulate adenylate cyclase enzymes to increase production of CAMP the ensuing cascade leads to K+ channels hyperpolarising the sarcolemma and reduced Ca2+ intracellularly therefore SM relaxation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Indications

A

Acute severe asthma. COPD, hyperkalemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

SE of B2 agonists

A

Fine tremor, palpitations, headaches and anxiety
Lactic acidosis, hypokalemia if used in high doses

Side effect risk increase if given systemically

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Administration of B2 agonists

A

Nebuliser 5mg for acute severe asthma

Inhaled via spacer for asthma - education of inhaler technique is crucial to ensure correct dose. If >3x weekly use further treatment required

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Use in obstetrics

A

Salbutamol/terbutaline can be used to delay uncomplicated pre-mature labour by 48hrs. Inhibiton of uterine contractions can give time to administer steroids and aid lung maturation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Muscarinic antagonists

A

SAMA - ipatropium , LAMA - tiatropium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

MOA muscarinic antagonists

A

Competitive antagonists at the M3 receptor on bronchial SM and mucus glands. They bind to the receptor site changing its shape preventing ach binding. This leads to SM relaxation and reduced mucus secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

CI B2 agonists

A

IHD, HTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Indications muscarinic antagonists

A

COPD - tiatropium

Asthma - ipatropium (only if B2 CI due to IHD or HTN)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

SE of muscarinic antagonists

A

Normal anticholingeric SE - blurry vision, urinary retention, constipation, dry eyes

Close angle glaucoma, AF and palpitations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Methylxanthine

A

Theophylline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

MOA theophylline

A

Inhibit phosphodiesterase isoenzymes resulting in increased cAMP levels and SM relaxation = bronchodilation. Prevent leukotriene synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

SE methylxanthines

A

Acts as a nonselective adenosine antagonist hence can give tachycardia, arrhythmias and palpitations

Headaches, insomnia, hypokalemia and seziures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Indications methylxanthines

A

IV amiophylline - acute severe asthma.

Chronic asthma esp children, COPD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Cautions theophylline

A

Porphyria and when coadministered with epinephrine

Metabolised by CYP450 enzymes therapeutic levels can be altered by inducers and inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Theophylline toxicity

A

PC = vomiting, agitation, cardiac arrhythmia and seizures

When given IV ensure continuous cardiac monitoring and regular K+ levels. Hypokalemia potentiated by B2 agonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

CYP450 inducers

A

Chronic alcohol, carbamazepine, rifampicin, lamotrigine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

CYP450 inhibitors

A

Macrolides, quinolones, PPI, CCB and antifungals

20
Q

Leukotriene receptor antagonist

A

Montelukast

21
Q

MOA Montelukast

A

Act to block the leukotriene receptor. Leukotrienes are pro-inflammatory eicosanoids released from mast cells.

Inhibiting leukotrienes prevents mucus secretion and bronconstriction. Not effective in acute scenarios.

22
Q

SE montelukast

A

abdo pain, GI upset, headache
depression, suicidal thoughts
?EGPA link

23
Q

Corticosteriods

A

Prednisone, methylprednisolne, hydrocortisone and dexamethasone

24
Q

MOA corticosteriods

A

Acts as agonists to mimic action of endogenous cortisol. Once bound to the glucocorticoid cytosolic receptor, exposes the DNA binding domain. This leads to the steroid-receptor complex binding to promoter regions of target genes

25
Action of cortisol
Inhibit bone and collagen formation Stimulate gluconeogensis Activates antiinflammatory molecules, inhibits IL-12, TNFa Counteracts insulin = increase glucose in blood Retains h20 and Na+
26
Indications for steriods
``` AI and vasculitic conditions Cerebral oedema MSCC Addison's disease Acute severe asthma/COPD Analphylaxis Rheumatoid ```
27
SE of steriods
``` Striae, hirsutism, acne, thin skin and easy bruising Central obesity, proximal myopathy HTN, DM Cataracts Cushings syndrome Osteoporosis (short stature in children) Psychosis and insomnia Immunosuppression - infections, candida ```
28
Stopping steriods
Never stop steroids abruptly, due to exogenous supply of cortisol the adrenal glands can atrophy leading to deficiency of cortisol and an adrenal crisis
29
Interactions with steriods
Antihypertensives = increased risk of hypotension NSAID's = increased risk of PUD and GI bleed High risk of hypokalemia with theophylline, B2 agonists
30
Omalizumab
IgE monoclonal Ab used for people with severely resistant asthma >4 courses of oral steroids a year. Binds to free IgE and IgE on the surface of B lymphocytes
31
Asthma PC
Episodic symptoms of SOB, wheeze and chest tightness. Diurnal variation worse @ morning and night, FHx of atopy, Inv - spirometry shows >15% post bronchodilator reversibility. Skin prick tests and high IgE levels
32
Drug that exacerbate asthama
i) B-blockers = increased risk of bronchospasm ii) NSAIDs = Block prostaglandin synthesis so reflex increase in leukotriene production which increased bronchoconstriction
33
Acute asthma Mx
High flow 02 stat. IV 100mg hydrocortisone Nebulised 5mg salbutamol (Can give back to back) If deterioration call ITU, IV Mg2SO4 Repeat PEF 15-30mins post treatment to gauge improvement
34
BTS Asthma algorithm
Step 0 = No formal diagnosis SABA i.e. salbutamol PRN 3x weekly Step 1 = SABA and ICS Step 2 = + LABA (Given as combination inhaler) Step 3 = i) No response to LABA stop and increase ICS ii) Continue LABA +/- increase ICS Consider trial of LAMA, leukotriene or theophylline Step 4 = Increase ICS to high dose, add 4th drug Step 5 = Oral steroids at lowest dose possible SABA should be given for all steps. If using more than 3x weekly symptoms aren't controlled
35
COPD PC
Chronic progressive dysponea, sputum prodcution, recused exercise tolerance. 40+y/o linked to smoking or pollution Goals of treatment = smoking cessation, symptom relief, improved QoL and exercise tolerance. reduced mortality, exacerbation and progression
36
Algorithm for COPD
SAMA/SABA for all - FEV1 >50% LABA or LAMA - FEV1 <50% LAMA or LABA + ICS LAMA, LABA and ICS proven to reduce exacerbation, hospital admissions and improve exercise tolerance. Pul rehab and smoking cessation crucial
37
O2 therapy in COPD
In COPD loss of hypercapnic drive. This in normal physiology causes pt to breathe. In COPD pt breathe relying on hypoxic drive, hence if high flow o2 is administered they may hyperventilate leading to T2RF Therefore target sats 88-92%. Monitor regularly with ABG, give O2 via targeted venturi mask. If pH < 7.35 or CO2>6 consider NIV and notify ITU
38
Paediatric asthma Mx
Step 1 = SABA Step 2 = ICS/montelukast Step 3 = Consider adding montelukast refer to specialist
39
Complete control of Asthma
No nocturnal symptoms, no attacks or need for rescue medication, no exercise limitation, normal lung function PEF >80% predicted
40
Bad sign in acute asthma
paC02 climbing or in normal range = alarm bells, pt tiring and going into T2RF
41
When to call ICU in acute asthma
Poor resp effort, falling PEF, persistent hypoxia, hypercapnia, low GCS,
42
Moderate asthma attack
PEF 50-75% predicted, Increased symptoms
43
Acute severe asthma attack
HR >110bpm, RR > 25, Inability to complete sentences in one breath, PEF 33-50%
44
Life threatening asthma attack
PEF <33%, Unable to speak, O2 sats <92%, normal/high CO2, poor respiratory effort, reduced GCS, hypotension
45
On discharge after asthma attack
Treatment with oral/inhaled steroids and bronchodilators GP follow up with 2 days, clinic within 4 weeks PEFR >75% best and when they can manage at night without nebulisers