Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CPTP > COPD and Asthma > Flashcards

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
Q

Action of cortisol

A

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
Q

Indications for steriods

A 
AI and vasculitic conditions
Cerebral oedema
MSCC
Addison's disease
Acute severe asthma/COPD
Analphylaxis
Rheumatoid
27
Q

SE of steriods

A 
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
Q

Stopping steriods

A

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
Q

Interactions with steriods

A

Antihypertensives = increased risk of hypotension
NSAID’s = increased risk of PUD and GI bleed
High risk of hypokalemia with theophylline, B2 agonists

30
Q

Omalizumab

A

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
Q

Asthma PC

A

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
Q

Drug that exacerbate asthama

A

i) B-blockers = increased risk of bronchospasm
ii) NSAIDs = Block prostaglandin synthesis so reflex increase in leukotriene production which increased bronchoconstriction

33
Q

Acute asthma Mx

A

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
Q

BTS Asthma algorithm

A

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
Q

COPD PC

A

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
Q

Algorithm for COPD

A

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
Q

O2 therapy in COPD

A

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
Q

Paediatric asthma Mx

A

Step 1 = SABA
Step 2 = ICS/montelukast
Step 3 = Consider adding montelukast refer to specialist

39
Q

Complete control of Asthma

A

No nocturnal symptoms, no attacks or need for rescue medication, no exercise limitation, normal lung function PEF >80% predicted

40
Q

Bad sign in acute asthma

A

paC02 climbing or in normal range = alarm bells, pt tiring and going into T2RF

41
Q

When to call ICU in acute asthma

A

Poor resp effort, falling PEF, persistent hypoxia, hypercapnia, low GCS,

42
Q

Moderate asthma attack

A

PEF 50-75% predicted, Increased symptoms

43
Q

Acute severe asthma attack

A

HR >110bpm, RR > 25, Inability to complete sentences in one breath, PEF 33-50%

44
Q

Life threatening asthma attack

A

PEF <33%, Unable to speak, O2 sats <92%, normal/high CO2, poor respiratory effort, reduced GCS, hypotension

45
Q

On discharge after asthma attack

A

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

CPTP (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions