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anticholinergic Flashcards

1
Q

What is the Clinical Indications for Use of anticholinergic?

A
  1. COPD maintenance
    - -> via Inhaled anticholinergic bronchodilator

2.COPD with airflow obstruction
–> Inhaled for combined anticholinergic and β
agonist bronchodilators

  1. Allergic and non allergic perennial rhinitis
    - -> Anticholinergic Nasal spray (itrapromium bromide)
  2. cardiac medication
    - ->Intravenous anticholinergic (atropine sulfate)
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2
Q

what is the effect of anti-cholinergic?

A
  • increase HR
  • pupil dilation
  • drying of upper airway
  • reduced tearing
  • urinary retention
  • constipation
  • reduced mucociliary action
  • Inhibit bronchoconstriction
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3
Q

What is the normal result of activation of the cholinergic pathway?

A

if M3 receptor is stimulated by ACh or drug
- Results in increased intracellular Ca++
and bronchoconstriction,
mucous & histamine release

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4
Q

What is the action of anti cholinergic?

A

inhibits the pathway of parasympathetic receptors

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5
Q

What structure or form does anti-cholinergic drug come in

A

Tertiary , Quaternary forms

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6
Q

what is the characteristics of tertiary anti-cholinergic drug ?

A

Easily absorbed in the bloodstream

Cross the blood brain barrier

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7
Q

what is the characteristics of Quaternary forms anti-cholinergic drug ?

A
  • Poorly absorbed in the bloodstream or central
    nervous system
  • Better for inhalation
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8
Q

What is an advantage of Quaternary forms anti-cholinergic drug ?

A
  • doesnt cause any systemic effect
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9
Q

example of tertiary anti-cholinergic drug ?

A

Atropine and scopolamine

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10
Q

function of scopolaminne?

A

treat motion sickness and postoperative nausea and vomiting

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11
Q

What is the Pharmacological Effects of Tertiary ammonium compound effects?

A
  • Respiratory tract
  • Central nervous system
  • Eyes
  • Cardiac
  • Gastrointestinal
  • Genitourinary
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12
Q

What is the Pharmacological Effects of Tertiary ammonium compound effects?

A

Side effects are localized to the site of drug

exposure

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13
Q

What is the relationship between parasympathetic tone and bronchdilation

A

inverse relationship

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14
Q

What is the mechanism of action of anti-cholinergic

A

it blocks ach from attaching to the muscarnicic receptor

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15
Q

What factor causes Vagally mediated reflex bronchoconstriction

A 
Irritant aerosols
cold air
high airflow rates
smoke,
fumes
histamine release
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16
Q

How does these factors cause bronchoconstriction

A

Afferent impulse to CNS –> reflex cholinergic
efferent impulse –> constriction of airway smooth
muscle –> mucus and cough

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17
Q

What structures carry out the effects of the stimulation of PNS

A

airway epithelium
submucosal glands
smooth muscle
mast cells

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18
Q

What is the effect of stimulationn of PNS in airway?

A

increase bronchomotor tone

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19
Q

What are the 3 Muscarinic Receptor Subtypes?

A

M1, 2, 3

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20
Q

the function of M1?

A

Parasympathetic post ganglia

  • Facilitate neurotransmission and bronchoconstriction
  • Cause secretion and rhinitis in the nose
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21
Q

the function of M2?

A
  • Inhibit continued use of acetylcholine

* Blockade may enhance acetylcholine release, counteracting bronchodilation (tiotropium is selective for M1 and M3

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22
Q

the funciton of m3?

A
  • Smooth airway muscle and submucosal glands
  • Cause bronchoconstriction
  • Cause secretion and rhinitis in the nose
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23
Q

What does nonspecific blockade?

A

the drug action isn’t specific to any receptor subtype?

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24
Q

what is an example of nonspecific blockade

A

ipratropium

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25
Q

what is the effect of blocking M3?

A

improve airflow because:

  • Reduces bronchoconstriction
  • Reduces pulmonary secretions
  • Reduces histamine release
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26
Q

What is the side effect of anticholinergic?

A 
– Dry mouth (most common)
– Coughing due to dryness
– Mydriasis (eyes should be protected)
– SVN (make sure drug is contained and dont come in contact with patient face): also pharyngitis, dyspnea, flulike symptoms,
bronchitis, upper respiratory infection
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27
Q

which anticholingeric is used in asthma patient?

A

Tiotropium ® Respimat
**Anti muscarinics not superior to β agonists for
asthma

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28
Q

when is Tiotropium ® Respimat used for asthma?

A
  • Nocturnal asthma
  • Psychogenic asthma
  • Asthmatics being treated for another condition
    with β blockers
  • An alternative to theophylline
  • In acute/severe episodes not responding to β
    agonist
  • use with SABA for AE asthma due to its synergistic , e.g. combivent`
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29
Q

When is Spiriva Respimat indicated?

A

Indicated as add on treatment to high dose
ICS&LABA in patients with severe persistent
symptoms and have experienced an
exacerbation in the previous year

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30
Q

how does Spiriva Respimat help with symptoms?

A

improved dyspnea
QofL scores
spirometry
lung deflation

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31
Q

how can Tiotropium be given for asthma

A

Combivent (combined with SABA)

nebuilzer

*usually given after b-agonist as it has rapid onset

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32
Q

What is an example of Quarternary drug?

A

atrovent

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33
Q

what is the drug structure of atropine sulfate

A

tertiary amine derivative of

atropine

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34
Q

how is atropine sulfate delivered?

A

nebulized and parenteral

administration

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35
Q

when is atropine sulfate indicated?

A

mostly used as IV cardiac drug

Effect => ↑ HR (vagal blockade)

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36
Q

what is the drug structure of glycopyrrolate

A

quaternary amine compound

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37
Q

when is glycopyrrolate indicated?

A
  • NM blockage reversal
  • drying agent used pre -intubation to reduce secretion
  • used in OR to wake patient up due to similar effect to atropine
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38
Q

what is the drug structure of ipratropium bromide

Atrovent

A

quarternary amine derivative of atropine

non selective anti muscarinic

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39
Q

What is ipratropium bromide

Atrovent effect?

A

local effects on large diameter, central

airways

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40
Q

the onset, peak and duration of ipratropium bromide

Atrovent

A

onset: 5- 15 min;
peak: 1 -2 hrs (slower than SABA)
duration: 4 - 6

SAAC

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41
Q

What is the indication of ipratropium bromide

Atrovent

A

bronchodilator therapy
for COPD or Asthma
in Acute Resp.distress

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42
Q

the precaution of ipratropium bromide

Atrovent

A

not as rapid a
response for acute
bronchospasm as
SABA

glaucoma, urinary
retention

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43
Q

adverse effect of atrovent

A

bad taste
dry mouth
eye problems
headache

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44
Q

what is the Route/dose/frequency of atrovent?

A
  1. inhaled via nebulizer OR nubules
    - -> 1-2 mls of 250 mcg/mL in 3 mls N/S
    - ->prn
  2. pMDI
    –>20 mcg/puff
    –> 4-8 puffs prn for acute exacerbations of
    Asthma and COPD with salbutamol
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45
Q

what is the drug structure of tiotropium
bromide
Spiriva

A

quaternary amine derivative of atropine

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46
Q

characterisitc of spiriva?

A

similar to ipratropium, but long acting

receptor selectivity M1 , M3

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47
Q

the onset, peak and duration of spirivia?

A
  • onset: 30 min;
  • peak: 3 hrs
  • duration: 24 hrs
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48
Q

indication of spirivia?

A 
- Long term maintenance of
bronchodilation due to COPD
- bronchodilation; good for
moderate to severe
COPD
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49
Q

contraindication of spirivia?

A

lactose intolerance
18yrs+
Not for acute bronchospasm

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50
Q

Route/dose/frequency of spirivia

A

inhaled

  • ->DPI Handihaler
  • 18mcg
  • once daily
  • ->SMI Respimat
  • once daily q a.m.
51
Q

What other drug can atrovent or LAMA be combined with

A

another LABA

Tiotropium- Olodaterol / Inspiolto ®

52
Q

dose/frequency of inspiolto?

A

SMI: 2.5μg OD via respimat

53
Q

what is the brand that combine ipratropium and salbutamol together?

A

Duoneb, combivent respimat

54
Q

what is the dosage of duoneb?

A

0.5 mg ipratropium and 2.5 mg salbutamol

55
Q

what is the dosage of respimat?

A

20 μg ipratropium and 100 μg salbutamol/puff

qid

56
Q

What is the indication of LAMA?

A

same as with Tiotropium

57
Q

What is the risk of LAMA

A

Risk: paradoxical bronchospasm

58
Q

What is an example of LAMA?

A

glycopyrronium - seebri
aclidinium bromide - genuair / Tudorza
umeclidinium - Ellipta

59
Q

dose/frequency of glycopyrronium?

A

Seebri® Breezhaler®

59mcg/puff

60
Q

What is the effect of Seebri® Breezhaler®

A
  • Reduced breathlessness
  • Improved dyspnea
  • delay moderate or severe exacerbation
  • Use less rescue
    medication
61
Q

dose/frequency of aclidinium bromide?

A

BID 400mcg

62
Q

What is advantage of aclidinium bromide

A

Very low and transient systemic exposure
–> reduce potential side effects

Potent antagonist for all muscarinic receptors

63
Q

What is soime LABA/LAMA combination?

A

Aclidinium/Formoterol : Duaklir® Genuair®

umeclidinium / vilantero : Anoro ®Ellipta

64
Q

dose/frequency of Aclidinium/Formoterol?

A

DPI
400 μg/12μg per inhalation
bid

65
Q

What is umeclidinium bromide

A

a LAMA
Long Acting Once Daily Dosing TX of
bronchoconstriction of airflow obstruction

66
Q

dose/frequency of umeclidinium bromide?

A

Incruse® Ellipta

DPI: 62.5 μg/inhalation, once daily

67
Q

dose/frequency of Anoro ®Ellipta?

A

62.5 μg umeclidinium & 25 μg vilanterol/puff

OD

68
Q

What is the triple therapy in canada?

A

TRELEGY ELLIPTA

  • fluticasone furoate 100mcg
  • umeclidinium 62.5mcg
  • vilanterol 25mcg

**addition of an ICS to LAMA+LABA

69
Q

indication of triple therapy

A
  • long term, once daily
  • maintenance treatment of chronic obstructive pulmonary disease
  • for frequent or severe AECOPD who symptoms cannot be controlled by LAMA+LABA
70
Q

what is a Phosphodiesterase-4 Inhibitor?

A

Roflumilast, Daxas®

71
Q

indication of Phosphodiesterase-4 Inhibitor?

A

anti-inflammatory therapy for COPD
- for frequent or severe AECOPD who symptoms cannot be controlled by triple therapy***
- reduce the number of flare-ups or worsening of COPD symptoms (exacerbation).
- patients with severe and very severe airflow limitation caused by excessive airway secretions linked to chronic
bronchitis

72
Q

dose/frequency of Roflumilast?

A

tablet, oral
500mcg
OD

73
Q

What is the MOA of PDE4?

A

PDE4 is expressed in

  • airway smooth muscle,
  • pulmonary nerves
  • proinflammatory
  • immune cells.

*contribute to asthma inflammation

74
Q

What is the action of Roflumilast

(Daxas®)?

A 
inhibits PDE 4
targeting 3 componenets of COPD:
- bronchoconstriction mucus
- hypersecretion 
- airway remodelling
75
Q

What is the precautions of Roflumilast

Daxas®

A
  • not recommended for patients with primary emphysema
  • Roflumilast is not a bronchodilator and
    should not be used for treating sudden
    shortness of breath.
76
Q

dose/frequency of Roflumilast

(Daxas?

A

500 mcg

OD, PO

77
Q

what is the side effect Roflumilast

(Daxas?

A

N&D, headaches, tremors, weight loss

78
Q

What is the contraindication of Roflumilast 500mcg

A

Cannot be used under 18,
pregnant
liver function problems

79
Q

what is Xanthines

A
  • central ventilatory drive stimulant
  • respiratory muscle strength &
    endurance
80
Q

what is the indication of Xanthines

A
  1. apnea of prematurity
    - -> caffeine citrate (safer, higher therapeutic
  2. COPD
    - ->Theophylline: alternative to β 2 agonist and anticholinergics
    - ->Not used in acute exacerbations
  3. use in asthhma
    - -> Theophylline: maintenance therapy if persistent asthma despite β 2 , ICS
    - -> a weaker bronchdilator than beta 2
    - -> use late in ER treatment of asthma
81
Q

what is exampe of Xanthines?

A

methylxanthines

  • ->Theophylline
  • ->Theobromine
  • ->Caffeine
82
Q

Wat is the effect of Xanthines

A 
• CNS stimulation
• Cardiac muscle stimulation
• Diuresis
• Bronchial, uterine, and vascular smooth muscle
relaxation
• Theophylline is generally classified as a bronchodilator
• Peripheral and coronary vasodilation
• Cerebral vasoconstriction
-->Used in headache remedies
83
Q

Wat is te MOA of xanthines

A

• Smooth muscle relaxation via inhibition of
phosphodiesterase (?)
• Antagonism of adenosine receptor (?)
• Enhancement of catecholamine release (?)

84
Q

Wat is te lung effect of xantines?

A
  • bronchodilation
  • increase resp muscle strength
  • increase resp muscle endurance
  • central ventilatory drive
85
Q

wat is te cardiac effect of xantines

A

increase cardiac output
decrease pulm vascular resistance
increase myocardial perfusion in
ischemia

86
Q

what is the route/dose of xantines

A

theophylline, Theo dur

IV
0.8 and 1.6 mg/ml in 5%
dextrose

Tabs
400 and 600 mg tabs (slow
release)

87
Q

wat is te terapeutic range of xantines

A

55 -110 m mol/L

dangerous if above:
20 mcg/L
110 mmol/L usually toxic

88
Q

What is te side effect of xantines?

A

CNS
anxiety, dizziness, headache, restless, insomnia,
irritability, seizures

GI
nausea/vomiting, diarrhea , anorexia,

Renal
excessive diuresis

CVS
palpitations, arrhythmias, tachycardia,
hypertension/hypotension

89
Q

what increase Conditions that increase theophylline levels:

A 
Viral hepatitis
Left ventricular failure
corticosteroids
alcohol
beta blockers propranolol
renal failure
90
Q

Wat decrease theophylline levels:

A

Smoking
Isoproterenol IV
barbiturates
Benzodiazpines Valium

91
Q

When is xanthines used in asthma?

A

Only after other relievers and controllers have

failed

92
Q

When is xanthines used in COPD?

A

If ipratropium bromide and β 2 agonist fail to

provide control

93
Q

what does mast cell and basophils release

A

leukotrienes (LT)

94
Q

wt is the function of leukotrienes

A

tpotent broncho constrictors and stimulate other cells to cause:

  • Airway edema
  • Mucus secretion
  • Ciliary beat inhibition
  • Recruitment of other inflammatory cells
95
Q

What is an example of Antileukotriene Agents

LTRA

A

Zafirlukast Accolate ®

Montelukast Singulair ®

96
Q

Dose/frequency/route of accolate?

A

Oral 20mg Dosage

BID

97
Q

onset,peak, duration of accolate?

A

onset: 30 min
peak: 3-4 hr ;
duration 12 hr

98
Q

What is te side effect of Antileukotriene

A
  • Headache
  • Infection
  • Nausea
  • Diarrhea
  • Pain
99
Q

Dose/frequency/route of Montelukast Singulair?

A

for children
Oral Dosage
chewable or granules 4mg (2-5yrs),
5mg (6- 14yrs)

adult 10 mg

100
Q

onset,peak, duration of Montelukast

Singulair?

A

Onset 30 min
; peak 3- 4 hr
duration 24 hours

OD

101
Q

What is the advantage of Antileukotriene in treating asthma?

A
  • safe, with few side effects

- effective for patient wit aspirin sensitivity and exercise induced asthma

102
Q

What is the disadvantagge of Antileukotriene

A
  • systemic drug exposure, not limited to lung

- unknown long term toxicitity

103
Q

What is severe asthma?

A

“Asthma which requires treatment with :

  • high dose ICS and a second controller for the previous year, or
  • systemic corticosteroids for 50% of the previous year to prevent it from becoming ‘uncontrolled’ or
  • which remains ‘uncontrolled’ despite this therapy
104
Q

How to define uncontroll asthma

A

Poor symptom control

  • ACQ consistently >1.5
  • ACT <20
  • child asthma control test cACT ) <20

Frequent severe exacerbations
Two or more systemic steroid bursts (≥3 days
in the previous year

Serious exacerbations

  • hospitalisation,
  • intensive care stay
  • mechanical ventilation

Airflow limitation
FEV 1 <80% predicted of personal best

105
Q

what is difficult to treat asthma?

A

Difficult to treat asthma can be hard to control
despite high intensity asthma medications, due to:

Poor medication adherence
Poor inhaler technique
Ongoing exposure to sensitising or irritant agents
Comorbidities (rhinosinusitis, obesity, GERD, obstructive sleep apnoea)
Incorrect diagnosis confounded with upper airway dysfunction, cardiac
failure or lack of fitness
Psychosocial issues

106
Q

What is thhe problem with severe asthma compared to normal asthma population

A

Have higher morbidity rates

Are at increased mortality risk

107
Q

Wat is a biologic

A

A pharmaceutical product that is produced by biotechnology, generated by lviing cells

108
Q

Wat are the examples of biologic

A
  • growth factors
  • antibodies
  • clotting factors
  • antibody factor
  • recmobinant proteins
109
Q

What is te characteristic of Severe eosinophilic asthma

A

Severe eosinophilic asthma is characterised by persistent eosinophilic airway inflammation, and includes disease that is driven
by either allergic or non allergic triggers 1,2

110
Q

Wat is the problem wit eosinophilic

A

Eosinophils are a source of a wide variety of

cytokines and other mediators

111
Q

Wat are 2 But inflammatory infiltrating eosinophils tat are recruited into te lung

A

Type 1:
Homeostatic regulatory eosinophils

type 2:
Inflammatory infiltrating eosinophils

112
Q

Wat does Eosinophil activation leads to production ?

A

IL 5

113
Q

wat is the function of IL 5

A

IL-5 has a direct effect on
eosinophil growth, activation and
surviva

114
Q

Wat are examples of anti IgE

A

Xolair® Omalizumab

–> a Monoclonal Antibody

115
Q

Wat is Omalizumab

A

is a subcutaneously injected monoclonal

antibody.

116
Q

indication of omalizumb?

A
  1. treatment of moderate to severe asthma
    in adults and adolescents 12 years of
    age and older who have a positive skin test
  • or reactivity to a perennial aeroallergen
    2. treating seasonal allergic rhinitis
117
Q

Whats te MOA of omalizumb

A

MOA: drug blocks the binding of IgE to mast cell
–> causing reduction of mediators that
can be released in allergic response

118
Q

dose/form of omalizumb

A

reconstituted and has a concentration of
150mg/1.2ml once mixed.

Dosing is q2 - 4 wks, depending of serum IgE level

119
Q

clincal use of omalizumb

A

a prophylactic agent used in moderate to severe persistent asthma

It may allow reduction of asthmatic rescue
agents.

It may allow reduction of high dose ICS or
prevent an increase in the dose of inhaled
corticosteroids.

120
Q

what is te contraindication of omalizumb

A
  1. not indicated for acute relief or rescue therapy
  2. not a replacement for ICS
  3. not optimal as monotherapy in persistent asthma.
121
Q

Wat is Il-5 inibitors for

A

Three drugs targeting IL 5 or its receptor
have been developed to treat severe
eosinophilic asthma.

122
Q

What are some example of iL-5 ?

A

mepolizumab NucalaTM
reslizumab CinqairTM
benralizumab Fresenra TM)

123
Q

indication of iL5

A
  • inadequately controlled severe asthma
    with high dose inhaled corticosteroids
  • (ICS) and an additional asthma
    controller(s) & (e.g. LABA) +

-have a blood eosinophil count of
**≥150 cells/mL) at initiation of treatment OR 300
cells/mL in the past 12 months

MDRS (23 decks)

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