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Pharma S1Y2 > asthma > Flashcards

asthma Flashcards

1
Q

whats asthma?

A

chronic inflammatory disease of the airway

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2
Q

what are the 2 phases of asthma?

A

immediate phase –> hypersensitivity due to irritant

Delayed phase –> chemotaxis are been released by the inflammatory cells to attract more immune cells

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3
Q

what happens to the bronchial wall in asthma due to irritations and inflammation?

A

1- Smooth muscle hyperproliferation

2- increased gland secretions

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4
Q

why asthma is not considered COPD?

A

Because asthma can be reversed by drugs

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5
Q

what are the two types of asthma??

A

chronic asthma —–> stable

acute asthma —> Severe and unstable

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6
Q

how do you administer drugs in chronic asthma?

A

orally

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7
Q

how do you administer drugs in acute asthma?

A

Inhaled

IV

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8
Q

whats extrinsic asthma?

A

the irritant comes from outside the body

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9
Q

whats intrinsic asthma?

A

the irritant comes from inside the body

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10
Q

whats the triad of asthma?

A

wheezing

cough

shortness of breath

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11
Q

what drugs are contraindicated in asthma?

A

1- beta blockers
2- morphine
3- PGI
4- cholinomimetics
5- drugs that causes histamine release

cold weather
exercise
cough during crying

all of these cause bronchoconstriction so worsens the situation

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12
Q

whats are the 2 potent bronchoconstrictors ?

A

leukotrien b4

adenosine receptor

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13
Q

whats the pathophsiology of asthma?

A

the irritation will cause inflammation then immune cells come and start producing cytokines and worsen the problems

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14
Q

what are some examples of cytokines that can be released in asthma by immune cells?

A

1- histamine
2- serotonin
3- PGD
4-leukotriens ( B4)
5- platelet activating factors
6- interlukeins
7-adenosine

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15
Q

what are the 2 primary treatments used in asthma?

A

1- Bronchodilators ( beta2 agonists )

2- Antiinflammatory

3- adjuvent treatments ( used as proph)

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16
Q

can you use NSAIDS?

A

no because it will block cox pathway and then all the archnoid acid will be converted to leukotriens and ths will worsen the situations

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17
Q

what are some examples of bronchodilators?

A

1- beta agonists
2- muscarinic blockers ( muscrinic causes constriction so blockers do opposite )

3- methlyxanthine الشاي و القهوه

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18
Q

what are some examples of selective beta agonists?

A

TEROLS —> end with terol

salbutamol –> albuterol
terbutaline
salmeterol
formoterol

metaproterenol
pirbuterol

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19
Q

which ones are SABA?

A

short acting beta agonists work only for 3-4 hours

Salbutamol ( albuterol )
terbutaline
metaproterenol
pirbuterol

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20
Q

which ones are LABA?

A

long acting beta agonists –> work for 12 hours

salmeterol
formoterol

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21
Q

whats the mechanism of beta agonists?

A

they go and activate beta 2 receptors in the bronchi and increase CAMP and this will lead relaxations of muscles

CAMP always lead to smooth muscle relaxations EVERYWHERE
except in the heart and the brain

why? CAMP when increased it will activate protein kinase A ( PKA ) which will inhibit myosin light chain kinase which is responsible for contraction

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22
Q

whats none selective beta agonists?

A

adrenaline
isoprenaline

not used anymore

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23
Q

how are beta agonists administered ?

A

inhalation or IV in acute severe asthma

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24
Q

how are short acting beta agonists excreted?

A

excreted unchanged

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25
Q

when are short acting beta agonists used?

A

first line drug for the immediate phase and acute attack

NOT EFFECTIVE IN DELAYED PHASE because delayed phase is mainly due to cytokines

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26
Q

what are the adverse effects of beta agonists?

A

T—> tachycardia because direct effect and vasodilation –> reflex tachy

T —>Tremors because increased sensitivity of muscles

T—> tolerance they get downregulated يزعل منك

H—> hypokalemia –> beta 2 will take potassium from the blood and send it to muscle

revise the effects beta receptors

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27
Q

how are the LABA excreted?

A

metabolized in liver by p450 and lost in faeces

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28
Q

when are laba used?

A

used as prophylaxis before exercises and in night before sleep

it is not used for acute attacks but used in regulation with corticosteroids

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29
Q

what are ultra long acting beta agonists?

A

indacaterol
olodaterol
vilanterol
bambuterol

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30
Q

when are ultra long beta agonists used?

A

in asthma but in combination with corticosteroids NEVER ALONE

alone in COPD only

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31
Q

what are the 2 types of methylxanthine drugs?

A

natural

semi synthetic

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32
Q

whats an example natural methylxanthine drugs?

A

caffeine
theophylline
theobromine

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33
Q

whats an example of semi synthetic methylxanthine drugs?

A

aminophylline its js modified theophylline

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34
Q

whats the function of Adenosine receptor? ( A1)

A

bronchi —> bronchoconstriction

bronchi —> increase gland secretions

CNS –> depression of CNS

Heart –> inhibit conduction ( negative dromotropic effect)

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35
Q

whats the function of PDE enzyme?

A

breaks down CAMP and GAMP
CAMP, GAMP –> 123
CAMP –> 4 7 8
GAMP –> 5 6 9

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36
Q

which versions of PDE are mainly inhibited by pde inhibitors?

A

3
4

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37
Q

whats the function of methylxanthine drugs?

A

1- they block Adenosine receptor 1 which lead too :
- bronchodilation
-decreased gland secretion
-increases CNS activity
-increase heart conduction ( positive dromotropic effect)

2- Inhibit PDE enzyme which lead increased CAMP

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38
Q

what happens when theres an increase in CAMP?

A

CAMP ALWAYS LEAD TO RELAXATION IN SMOOTH MUSCLES

EXCEPT FOR THE HEART IT LEADS TO INCREASED CONTRACTILITY and THE BRAIN

different effect in heart because its the MLCK enzyme is different in the heart compared to smooth muscles

for example in kidneys anything that increase CAMP will lead to dilation and uresis

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39
Q

what are the uses of methyl xanthine ?

A

bronchial asthma (IV , OR ORAL) ( 2ND LINNEEE, right after SABA)

IV as aminophylline and orally as theophylline

Increase cns activity ( why we drink coffee and caffiene )

Migraines ( cuz of vasoconstriction

Delayed physical fatigue and increased performance

neonatal apnea syndrome ( baby doesnt cry after birth which is due to cns depression

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40
Q

how can we administer methylxanthine?

A

IV and oral BUT NO INHALERS

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41
Q

what are the adverse effects of methylxanthine?

A

1- excessive CNS stimulation ——-seizures

2- CVS tachycardia + Arrhythmia ( tachycarida due to increased conduction and vasodilation –> reflex tachy )

3-Increase HCL ( GIT disturbance )

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42
Q

when is methlyxanthine contraindicated?

A

peptic ulcer

hepatic failure

renal failure

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43
Q

what you dont add to methylxanthine?

A

anything that inhibit metabolism you have to decrease the dose (CYP 450)

44
Q

what do you do in smokers?

A

smoking and drinkers increases metabolism so you have to increase the dose

45
Q

whats the clinical uses of methylxanthine?

A

second line drug for chronic asthma

aminophylline is used as IV for severe acute asthma

46
Q

which methylxanthine can be given orally?

A

theophylline
theobromine
caffeine

47
Q

which methylxanthine can be given IV?

A

aminophylline and its used in acute asthma

48
Q

whats roflumilast?

A

ORAL, selective PDE 4 inhibitor that decreases the risk exacerbations in patients with COPD

49
Q

why we dont have methylxanthines in inhalation format?

A

because there is not a significant bronchodilation effect and risk of adverse effect is severe

50
Q

whats the relation between methylxanthines and beta agonists?

A

they should not be given together because the methylxanthine will not enhance the effect of beta agonist and it will js cause side effects

But beta agonists and muscranic blockers good combo

51
Q

what should be monitored when give methylxanthine?

A

plasma level of the drug because its easily affected by any drug that affects the metabolism

52
Q

whats the pathway of arachidonic acid after its formed?

A

2 pathways

COX 2 PATHWAY : FORMATION OF PGE2 AND PGI 2 –> INFLAMMATION AND PAIN : vasodilation, vascular permeability, cytokine release, leukocyte migration , pain

LOX pathway : formation of leukotriens LTC4, LTD4, etc —-> inflammation and bronchoconstriction : b.c , mucus secretion , edema, eosinophil migration

53
Q

which group of drugs inhibit the cox 2 pathway ?

A

NSAIDS

54
Q

which group of drugs inhibit the lox pathway?

A

leukotriene pathway inhibitors

55
Q

whats an example of lox enzyme inhibitor?

A

zileuton

56
Q

whats the function of zileuton?

A

inhibit lox enzyme and lead to anti inflammatory effect and bronchodilation

57
Q

whats the other type leukotriene inhibitors ?

A

Leukotriene receptor blocker/antagonist (LTRA)

zafirlukast
montelukast

58
Q

whats the clinical use of leukotrienes inhibitors ?

A

third line drug for asthma

Aspirin induced asthma ( aspirin will inhibit the cox 2 pathway so it will be directed to lox pathway luekotrienes inhibitors can block the lox pathway)

can be used instead of corticosteroids when they are contraindicated

easy for children to take

59
Q

in children do you use leukotrienes inhibitors or coritcosteroids?

A

corticosteroid aare bad for children because soo many severe adverse effects

so you give leukotrienes inhibitors

60
Q

whats the relationship between leukotriene inhibitors and methylxanthine?

A

leukotriene inhibitors inhibit metabolism and CYP450 so it increases the concentration of methylxanthine

must decrease the dose of methylxanthine

61
Q

examples of antimuscarinc agents?

A

atropine —> not used anymore because not selective and many side effects

ipratropium

tiotropium bromide

glycopyrronoium bromide

umeclidinium bromide

62
Q

whats the function muscarnic blockers?

A

they block m3 which is responsible for constriction once its blocked it wont cause constriction and it will give beta 2 receptors the upper hand تفضي المعلب

63
Q

which muscarinic blockers are short acting ?

A

ipratropium bromide last for 3-5 hours

64
Q

which muscarinic blockers are long acting?

A

tiotropium bromide

glycopyrronium bromide

umeclidinium bromide

last for 12-24 hours

65
Q

when are the long acting muscarinic blockers used?

A

choice for COPD

asthma in addition to LABA AND inhaled corticosteroids

66
Q

what are the adverse effects of muscarinic blockers?

A

urinary retention

dry mouth

constipation

pharyngitis

67
Q

whats the best combination in inhalers that is used now a days?

A

Short acting beta agonists ( albuterol for example )
short acting muscarinic blockers ( ipratropium )

or LAMA + LABA

68
Q

why did we develope additive combinations?

A

because using 2 different types drugs has proved to show better results than just increasing the dose

69
Q

whats another reason why did we develope the laba/lama combinations ?

A

they show better results when used combined that using them individually

a lama may block the tightening of smooth muscles around your neck to help keep the airways open

70
Q

whats the main anti inflammatory drug used in asthma?

A

corticosteroids

71
Q

whats the function of corticosteroid?

A

1- inhibit the PLA2 enzyme stops production of archnoid acid القصه من اولها

2- inhibit immune cells ( B lymphocytes, T lymphocytes, Macrophages, mast cells

3- upregulate B receptors

72
Q

how do corticosteroids inhibit the immune system?

A

they bind to GRS ( glucocorticoid receptor) and then it will result in repression of transcription factors for example : Nuclear factor kappa D (NF-KB)

73
Q

what are some examples of inhaled corticosteroids ?

A

all have son

triamcinolone
budesonide
ciclesonide
flunisolide
mometasone
fluticasone

74
Q

on which phase do corticosteroids work mainly?

A

they work on the delayed inflammatory phase only

no effect on the immediate phase

75
Q

what do you combine the inhaled corticosteroids with?

A

LABA/LAMA or both

76
Q

which corticosteroid is given iv?

A

hydrocortisone its given in acute severe asthma

77
Q

when are corticosteroids used?

A

added to bronchiodilators incase they dont work alone and in emergencies as iV as in status asthamticus

78
Q

what are the adverse effects of corticosteroids ?

A

hoarse voice –> oral candidiasis ( thrush ) due to severe immune system inhibition

adrenal suppression

79
Q

what are some examples of targeted monoclonal antibody therapy?

A

end with mab

omalizumab

mepolizumab

80
Q

whats the function of the antibodies?

A

they bind to igE stopping them from binding to mast cells and release of histamine and what not

81
Q

on which phases do the antibodies work on?

A

both phases immediate and delayed

82
Q

how are the antibodies administered?

A

subcutaneously at 2-4 weeks

require expert administration

83
Q

whats the clinical uses of the antibodies?

A

persistent allergic asthma that is not controlled by laba or corticosteroids

84
Q

what are the adverse effects of the antibodies?

A

hypersensitivity reactions

85
Q

what does omalizumab bind to?

A

igE

86
Q

what does dupilumab bind to?

A

IL4 and IL3 receptors ( antagonist )

87
Q

what does reslizumab bind to?

A

bind to IL-5 directly

88
Q

what does mepolizumab bind to?

A

similar to reslizumab, binds to IL-5

89
Q

what does benralizumab bind to?

A

IL-5 receptor

90
Q

what are the uses of IL-5 inhibitors?

A

reslizumab and mepolizumab and benralizumab

they are used in refractory eosinophilic asthma

91
Q

what are the adverse effects of IL-5 inhibitors?

A

headache
injection site reactions
back pain
myalgia

92
Q

what are examples of mast cell inhibitors ?

A

cromolyn

nedocromil

93
Q

whats the function of cromolyn / nedocromil ?

A

they stabilize the mast cells and prevent their degranulation

94
Q

how are cromolyn/nedocromil administered?

A

powder inhalation

95
Q

when are the mast cell inhibitors used?

A

prophylaxis of asthma mainly in older children to reduce symptoms of allergic rhinitis

96
Q

what are the adverse effects of mast cell inhibitors?

A

irritation of throat by powder

97
Q

whats the best initial drug choice in acute bronchospasm?

A

Selective SABA –> albuterol
terbutaline
metaproterenol
pirbuterol

98
Q

whats the most useful drug in long term management of COPD?

A

SAMA –> ipratropium

but its ineffective in acute bronchospasm but it aids the beta agonists تفضي الملعب

99
Q

whats the 2nd line drug in COPD?

A

theophylline ( methylxanthine )

orally

100
Q

which drugs are used prophylactically ?

A

cromolyn and nedocromil

101
Q

which anti inflammatory drug is given in acute episodes of bronchoconstrictions?

A

corticosteroid –> orally or IV

102
Q

whats the common regimen for moderate asthma?

A

inhaled corticosteroid + SABA

103
Q

whats the common regimen for severe asthma?

A

inhaled corticosteroid + SABA + LABA

leukotriene inhibitor can be added if needed

104
Q

whats the common regimen for severe asthma in children?

A

leukotriene inhibitor + saba and laba

leukotriene inhibitor replaced corticosteroids

105
Q

whats the advantage of multi regimens than single regimen?

A

you will give smaller doses of multiple drugs than js large doses of single drugs

106
Q

whats combivent?

A

albuterol ( saba ) + ipratropium ( sama ) combination in inhaler

107
Q

whats advair?

A

salmeterol ( laba ) + fluticasone ( corticosteroid ) in combined inhaler

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