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12. respa Flashcards

1
Q

Cough is

A

a useful physiological mechanism
Is a protective reflex
Clear the respiratory passages of foreign material and excess secretions.
May be annoying and prevent rest and sleep.
Chronic cough can contribute to fatigue, especially in elderly patients.

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2
Q

Involves the………. and ………….., as well as the……… of the bronchial tree

A

cns pns and smooth muscle

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3
Q

pathogenesis of cough

A

Irritation of the bronchial mucosa  bronchoconstriction  stimulates cough receptors (stretch receptor) in tracheobronchial passages  afferent fibers of the vagus nerve  cough centers in the CNS (medulla)

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4
Q

cough occurs due to stimulation of …………. receptor in throat, respiratory passage or ………. receptors in the lungs.

A

mechanic- or chemoreceptor
stretch

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5
Q

Stimulation of sensory nerves in the epithelium by

A

secretions, foreign bodies, cigarette smoke and tumors

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6
Q

Sensitization of the cough reflex in which there is an abnormal increase in the sensitivity of the cough receptors demonstrable by inhalation of

A

capsaicin or hypotonic chloride solutions

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7
Q

Sensitization of the cough reflex presents clinically as a ………………………………………………………………………………….

A

persistent tickling sensation in the throat with paroxysms of coughing induced by changes in air temperature, aerosol sprays, perfumes and cigarette smoke.

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8
Q

sensitization associated with

A

association with viral infections, oesophageal reflux, postnasal drip, cough- variant asthma, idiopathic cough, and in 15% of patients taking ACE inhibitors.

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9
Q

Useless (non productive) cough:
stimulated by

A

Stimulated by inflammation in the respiratory tract or by neoplasia.
Should be suppressed to reduce frequency

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10
Q

Peripheral antitussives
MOA plus include

A

They suppress the irritated sensory nerve endings which initiates the cough reflex
They include:
Pharyngeal demulcents
Steam inhalation
Local anaesthetic

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10
Q

Dry cough is treated by antitussive drugs which are classified into :

A

Peripheral antitussives.
Central antitussives

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11
Q

Steam inhalation

A

e.g. tincture benzoin
One teaspoonful is added to a litre of boiling water and inhaled with the steam
It promotes the secretion of protective mucous

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11
Q

Pharyngeal demulcents
relieve cough due to?
MOA
include

A

e.g. liquorice lozenges
Relieve cough due to sore throat and pharyngitis
Smooth the throat (directly as well as promoting salivation) and Reduce afferent impulses from the inflamed irritated pharyngeal mucosa.
Thus provide symptomatic relief in dry cough arising from throat.

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12
Q

Drugs with local anaesthetic action

A

Benzonatate

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13
Q

Benzonatate isrelated to the local anesthethic

A

tetracaine

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14
Q

……….. anesthetizes the stretch receptors in the lungs, thereby reducing coughing.

A
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15
Q

Adverse reactions of benzonatate

A

include hypersensitivity, sedation, dizziness, and nausea.

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15
Q

Central antitussives
define moa plus includes

A

Act in the CNS to raise the threshold of cough center
Suppress the symptom without influencing the underlying condition.
opoids
non opoids
antihistamines

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16
Q

central antituissives Can cause harmful

A

sputum thickening and retention
They should not be used for the cough associated with asthma

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17
Q

Opioids
include
why these

A

Codeine, Pholcodeine
Less addiction liability than the main opioid analgesics and is an effective cough suppressant.

It also decreases secretions in the bronchioles, which thickens sputum and inhibits ciliary activity

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18
Q

drying action on the respiratory mucosa may be ………………..or ………………………….

A

useful (eg, in bronchorrhea) or deleterious (eg, when bronchial secretions are already viscous)

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18
Q

opoids excretes its action through

A

mu opioid receptors in the brain.

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19
Q

side effects of opiods

A

constipation
drowsiness
respiratory depression

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20
Q

codeine metabolism

A

codein prodrug
to
codeine 6 glucoronide by UGT2B7
Morphine CYP2D6

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21
Q

Non opioids
include
moa
potency with codein
but makes it better by

A

Dextromethorphan
Has selective antitussive action (raises threshold of cough center) by blocking NMDA receptors
Its antitussive potency is equivalent to that of codeine and it produces only marginally less constipation and inhibition of mucociliary clearance

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22
Q

side effects of dextrometrophan

A

Has got side effect like, dizziness, nausea, drowsiness, and ataxia.

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23
Q

dextrometrophan metabolism

A

by hepatic first pass to dextrophan whic has less effect on CNS

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24
Q

Antihistamines include
receptor type?
moa
which generation

A

Many H1 antihistamines have been conventionally added to antitussive (expectorant) formulation.
They offered relief in cough due to their sedative and anticholinergic action, but lack selectivity for cough center.
first generation

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25
Q

Useful (productive) cough:

A

Serves to drain the air way
Its suppression is not desirable, may be even harmful, except if the amount of expectoration achieved is small compared to the effort of continuous coughing

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26
Q

Expectorants are used for

A

They increase bronchial secretion or reduce its viscosity, facilitating its removal by coughing.
They are believed to “loosen” cough which becomes less tiring and more productive.

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27
Q

types of expectorants

A

direct acting
stimulant
mucolytic

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28
Q

Directly acting:

include
MOA

A

Sodium and Potassium citrate or acetate, potassium iodide, Guanacol, and
Guaifenesin

They increase bronchial secretion by salt action.

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29
Q

Stimulant expectorants
include
MOA

A

They stimulate healing and repair of chronically inflammed respiratory mucosa.
They decrease the amount of sputum and have mild antiseptic action .
They include:
- Creosote 0.1 - 0.6 Tid
- Terpene hydrate 0.3 g. Tid

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29
Q

side effects of mucolytics

A

lachrymator, gastric irritant and hypertensive action

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29
Q

Mucolytics
include
moa

A

Bromhexine, Carbocisteine, Acetyl cytokine and Ambroxol

they depolymerizes monopoly saccharine directly as well as liberating lysosome enzymes – net work of fibers in tenacious sputum is broken.

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29
Q

Rhinitis
plus type

A

iswhen a reaction occurs that causes nasal congestion, runny nose, sneezing, and itching
seasonal
perennial

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29
Q

seasonal rhinitis
symptoms
may develop

A

This is often called ‘hayfever’ and is the most common of all allergic diseases.
Nasal irritation, sneezing and watery rhinorrhoea are the most troublesome symptoms
asthma

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30
Q

in rhinitis itching of the eyes and soft palate and occasionally even itching of the ears because

A

of the common innervation of the pharyngeal mucosa and the ear.

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30
Q

Patients with perennial rhinitis rarely have symptoms that affect the ………..

A

eyes or throat.

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30
Q

Half have symptoms predominantly of sneezing and watery rhinorrhoea, whilst the other half complain mostly of nasal blockage.
The patient may lose the sense of smell and taste.

A
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31
Q

A swollen mucosa can obstruct drainage from the sinuses, causing

A

sinusitis in half of the patients.

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32
Q

Pathogenesis of perennial rhinitis

A

Sneezing, increased secretion and changes in mucosal blood flow are mediated both by efferent nerve fibres and by released mediators

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33
Q

Mucus production results largely from ………..stimulation, while blood vessels are under ……………..

A

parasympathetic

both sympathetic and parasympathetic control.

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34
Q

Sneezing, largely caused by histamine, results from stimulation of ………nerve endings and begins within minutes of the allergen entering the nose.

A

afferent

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34
Q

Allergic rhinitis develops as a result of interaction between the inhaled allergen and adjacent molecules of IgE antibody present on the surface of mast cells found in increased numbers in nasal secretions and within the nasal epithelium.

A
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34
Q

Release of preformed mediators, in particular histamine, causes an increase in permeability of the epithelium, allowing allergen to reach IgE-primed mast cells in the lamina propria.

A
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34
Q

drugs for rhinitis

A

antihistamins
decongestans
corticosteriods

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34
Q

The……………. and ……………..released from mast cells, eosinophils and macrophages are especially potent in causing nasal blockage.

A

cysteinyl leukotrienes and vasodilator prostaglandins (PGD2, PGE2 and PGI2)

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34
Q

anti histamins
best for which symptom and less effective for which symptom

A

Antihistamines remain the most common therapy for rhinitis
They are particularly effective against sneezing
Less effective against rhinorrhoea and have little influence on nasal blockage.
The first-generation antihistamines cause sedation.

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34
Q

Second-generation drugs

A

cetirizine (10 mg once daily), loratadine (10 mg once daily), desloratadine (5 mg daily) and fexofenadine (120 mg daily) are highly specific for H1, receptors

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34
Q

Fatal cardiac arrhythmias (torsades de pointes) have been described with

A

terfenadine and astemizole.

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35
Q

Antihistamines also control

A

Antihistamines also control itching in the eyes and palate.

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36
Q

Decongestants
moa
work well with combination with

A

Decongestants are sympathomimetic agents that act on adrenergic receptors in the nasal mucosa, producing vasoconstriction.
Decongestants shrink swollen mucosa and improve ventilation.
When nasal congestion is part of the clinical picture, decongestants work well in combination with antihistamines.

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37
Q

types of decongestants

A

topical
and
systemic

38
Q

topical decongestants
include

A

are applied directly to swollen nasal mucosa via drops or sprays.
Short-acting
Phenylephrine hydrochloride
Intermediate-acting
Naphazoline hydrochloride
Tetrahydrozoline hydrochloride
Long-acting
Oxymetazoline hydrochloride
Xylometazoline hydrochloride

39
Q

Prolonged use of these agents (for more than 3 to 5 days) can result in a condition known as

A

rhinitis medicamentosa, or rebound vasodilation, with associated congestion.

40
Q

Combining the weaning process with ………… is useful.

A

nasal steroids

41
Q

Systemic Decongestants.
types

A

pseudoephedrin and oral form of phenylephrine

and

Sodium cromoglicate and nedocromil sodium

41
Q

Adverse effects
of topical decongestants

A

include burning, stinging, sneezing, and dryness of the nasal mucosa.

42
Q

pseudoephedrin and oral form of phenylephrine
effectiveness
lasts?
safe?

A

Are not as effective on an immediate basis as the topical agents
Their effects last longer and they cause less local irritation.

43
Q

Pseudoephedrine can cause mild central nervous system stimulation
why

A
43
Q

Doses of …. mg pseudoephedrin have been shown to produce no measurable change in blood pressure or heart rate.
In higher doses (…….), pseudoephedrine has raised both blood pressure and heart rate.

A

180
210-240

44
Q

Sodium cromoglicate and nedocromil sodium
moa

A

They act by blocking an intracellular chloride channel and preventing cell activation.
Sodium cromoglicate applied topically

45
Q

The most effective treatment for rhinitis is to use small doses of

A

topically administered corticosteroid preparations (e.g. beclometasone spray twice daily or fluticasone propionate spray once daily).

46
Q

The amount used is insufficient to cause systemic effects and the effect is

A

primarily anti-inflammatory.

47
Q

Bronchial asthma
is

A

Is characterized by hyperresponsiveness of tracheo-bronchial smooth muscle to variety of stimuli

47
Q

when should we start corticosteroids

A

Preparations should be started prior to the beginning of seasonal symptoms.

48
Q

The combination of a………………………………………………………………………………. taken regularly is particularly effective.

A

topical corticosteroid with a non-sedative antihistamine

48
Q

If other therapy has failed, seasonal and perennial rhinitis respond readily to a short course (2 weeks) of treatment with

A

oral prednisolone 5-10 mg daily..

49
Q

It may be necessary to use an …………………………………….. to decongest the nose prior to taking the topical corticosteroid.

A

alpha-1 adrenergic agonist

49
Q

Results in narrowing of air tubes, often accompanied by increased secretion, mucosal edema and mucus plugging.

A
50
Q

athsma patients present with

A

It causes shortness of breath, cough, chest tightness, wheezing and rapid respirations.

50
Q

In addition to airway obstruction, cardinal features of asthma include

A

inflammation and hyperreactivity of the airway.

51
Q

Bronchial asthma

A

Is characterized by hyperresponsiveness of tracheo-bronchial smooth muscle to variety of stimuli

51
Q

Factors that contribute to airway obstruction in asthma

A

Contraction of the smooth muscle that surrounds the airways
Excessive secretion of mucus and in some, secretion of thick, tenacious mucus that adheres to the walls of the airways

52
Q

Based on the underlying pathophysiology of the disease, anti-inflammatory therapy must be used in conjunction with bronchodilators in all but…..,..

A

the mildest asthmatics

52
Q

Primary classes of antiasthma drugs are

A

bronchodilators and antiinflammatory agents.

53
Q

Drug groups in Asthma
7

A

-adrenergic receptor agonists
Anticholinergics
Methylxanthines
Glucocorticoids
Leukotriene inhibitors
Chromones mast cell stabilizer
Anti-immunoglobulin E (IgE)

53
Q

Sympathomimetic, Methylxanthines and Anticholinegics are commonly called

A

bronchodilators

53
Q

Approaches to Treatment 7

A

Prevention of AB:AG reaction
Avoidance of antigen, hyposensitization if antigen can be identified.

Suppression of inflammation and bronchial hyperactivity.
Corticosteroids

Prevention of release of mediators.
Mast cell stabilizers
E.g. Sodium cromoglycate (Cromolyn sod.)

Antagonism of released mediators.
leukotriene antagonist
E.g. Montelukast and Zafirlukast
Antihistamines

Blockade of constrictor neurotransmitter
Anticholinergics
E.g. Atropine, Ipratropium

Mimicking dilator neurotransmitter
Sympathomimetics
E.g. Adrenaline, Ephedrine, Salbutamol, Terbutaline, Bambuterol, Salmeterol, Formoterol.

Directly acting bronchiodilators
Methylxathines
E.g. Theophylline

53
Q

The sympathomimetics have several pharmacologic actions that are important in the treatment of asthma.
like
3

A

They relax airway smooth muscle
Inhibit release of bronchoconstricting mediators from mast cells.
They inhibit microvascular leakage and increase mucociliary transport by increasing ciliary activity.

54
Q

B-adrenergic receptor agonists
selectivity?
classification

A

Selective 2-receptor agonists
They are mostly delivered directly to the airways via inhalation.
Classified as
Short-acting agonists: used only for symptomatic relief of asthma
Long-acting agonists: used prophylactically in the treatment of the disease.

55
Q

MOA of B2 AR agonists

A

activates adenylate cyclase consequently increasing cytosolic cAMP  bronchial relaxation

56
Q

Long-term exposure to 2-agonists may desensitize some of these receptor-response pathways

A
57
Q

β-Adrenoceptor-mediated airway smooth muscle relaxation. Rho-kinase normally phosphorylates and thus inhibits myosin phosphatase, favoring contraction. In
the presence of β-adrenoceptor agonists, increased cyclic adenosine monophosphate (cAMP) and protein kinase A (PKA) inhibit RhoA, which inhibits Rho-kinase, increasing
the activity of myosin phosphatase. The net result is dephosphorylation of myosin light chain20 and relaxation.

A
58
Q

Short-Acting 2-AR Agonists
include
route
onset
duration

A

Drugs in this class include albuterol, levalbuterol, metaproterenol, terbutaline, and pirbuterol.
Used for acute inhalational treatment of bronchospasm, though some are also used orally.
Inhalation drugs has rapid onset of bronchodialation (1-5 min) which lasts for about 2 to 6 hours

59
Q

…………………….Are the preferred treatment for rapid symptomatic relief of dyspnea associated with asthmatic bronchoconstriction.

A

short term b agonist

60
Q

Long-Acting B2-AR Agonists
include
dilation last how many hours?
and why

A

Drugs in this class include Salmeterol and formoterol
Bronchodilation lasts over 12 h with inhalation salmeterol
The higher lipophilicity of the drugs may be responsible for the extended effect
Chronic use leads to receptor desensitization and a diminution of effect

61
Q

long term B2 agonist More pronounced in -AR on ……………………than that on ………………………….

A

inflammatory cells
bronchial smooth muscle.

62
Q

Oral Therapy with B-AR Agonists
is used in 2 situations
plus the drus

A

In children (< 5 yrs) who can not manipulate metered-dose inhalers (albuterol or metaproterenol syrups)
In some severe asthma exacerbations, aerosols can worsen cough and wheezing by causing local irritation

63
Q

Methylxanthines
include
MOA

A

Theophylline, ……. tea,
Theobromine, …….. cocoa
Caffeine. …… coffee
At high concentrations, they inhibit several members of the phosphodiesterase (PDE) enzyme.

64
Q

methylxanthines inhibit which PDE
plus what

A

The inhibition of PDE4 in inflammatory cells reduces the release of cytokines and chemokines
decrease in immune cell migration and activation

The inhibition of PDE4 in inflammatory cells reduces the release of cytokines and chemokines
decrease in immune cell migration and activation

65
Q

margin of safety of methylxanthines
plus side effects

A

narrow margin of safety
Adverse effect is primarily to GIT, CNS and CVS.

66
Q

CNS effects of methylxanthines in differents doses

A

In low and moderate doses;
mild cortical arousal with increased alertness and deferral of fatigue.

The larger doses
cause nervousness and tremor in some patients ( dose that is necessary for bronchodiltion).

Very high doses,
cause medullary stimulation and convulsions

67
Q

CVS effects of methylxanthines
plus viscosity

A

Have positive chronotropic and inotropic effects.
The clinical expression of these effects on cardiovascular function varies among individuals.
In sensitive individuals, consumption of a few cups of coffee may result in arrhythmias.
Methylxanthines decrease blood viscosity and may improve blood flow under certain conditions.

68
Q

methylxanthine effects on GIT and kidney

A

Stimulate secretion of both gastric acid and digestive enzymes.
However, even decaffeinated coffee has a potent stimulant effect on secretion, which means that the primary secretagogue in coffee is not caffeine.

are weak diuretics.
This effect may involve both increased glomerular filtration and reduced tubular sodium reabsorption.

69
Q

In addition to their effect on airway smooth muscle, these agents - in sufficient concentration - inhibit antigen-induced release of histamine from lung tissue

A

methylxanthines

70
Q

Effects on skeletal muscles
methyl xanthine

A

Strengthen the contractions of isolated skeletal muscle in vitro and improve contractility and reverse fatigue of the diaphragm in patients with COPD.

71
Q

theophylline Improvement in pulmonary function is correlated with plasma concentration in the range of

A

5_20 mg/L.

72
Q

Anorexia, nausea, vomiting, abdominal discomfort, headache, and anxiety occur at concentrations of …..mg/L in some patients and become common at concentrations greater than…….. mg/L.

A

15
20

73
Q

Higher levels (40 mg/L) may cause :
theophylline

A

seizures or arrhythmias;
These may not be preceded by gastrointestinal or neurologic warning symptoms.

74
Q

anticholinergic include

A

Muscarinic antagonists competitively inhibit the effect of acetylcholine at muscarinic receptors.
M3
Atropine
Ipratropium bromide

75
Q

Leukotriene antagonists include:

A

Inhibition of 5-lipoxygenase, thereby preventing leukotriene synthesis;
Zileuton, a 5-lipoxygenase inhibitor

Inhibition of the binding of LTD4 to its receptor on target tissues, thereby preventing its action.
Zafirlukast and Montelukast

76
Q

Adverse effects of leukotriene inhibitors

A

Zafirlukast and Montelukast
Rare incidences of systemic eosinophilia and a vasculitis

Zileuton
Liver enzymes elevated, generally within the first 2 months of therapy.
Decreases clearance of theophylline and warfarin clearance.

77
Q

Pharmacokinetics of leukotriene inhibitors
absorbtion
bioavailability
proteinbound
half life

A

Pharmacokinetics

Zafirlukast
absorbed rapidly, with greater than 90% bioavailability.
Over 99% protein-bound
Its half-life is approximately 10 hours.

Montelukast
is absorbed rapidly, with about 60% to 70% bioavailability.
It is highly protein-bound (99%).
Its half-life is between 3 and 6 hours.

Zileuton
is absorbed rapidly on oral administration.
It is a short-acting drug with a half-life of approximately 2.5 hours
is highly protein-bound (93%).

77
Q

Their principal advantage is that they are taken orally; some patients - especially children - comply poorly with inhaled therapies.

A
78
Q

Chromones define plus include

A

mast cell stabilizer
Cromolyn Sodium (Disodium Cromoglycate) and Nedocromil sodium.

79
Q

what effectively inhibit both antigen-and exercise-induced asthma

A

chromones

79
Q

cromolyn…….
medocromil………
how takes

A

Cromolyn ……..must be inhaled as a microfine powder or aerosolized solution.
Nedocromil ..….is available only in metered-dose aerosol form.

79
Q

Cromolyn solution is also useful in reducing symptoms of

A

allergic rhinoconjunctivitis

80
Q

chromones inhibit what

A

Release of Histamine, LTS, Interlukines e.t.c. from mast cells as well as other inflammatory cell is prevented and Chemotaxis of inflammatory cells is inhibited.

80
Q

when are chromones takes

A

prophylactically

81
Q

side effects of chromones include

A

Include such as throat irritation, cough, and mouth dryness, and, rarely, chest tightness, and wheezing.
Serious adverse effects are rare.
Reversible dermatitis, myositis, or gastroenteritis, pulmonary infiltration with eosinophilia and anaphylaxis have been reported.

82
Q

lack of toxicity of chromones accounts for

A

cromolyn’s widespread use in children, especially those at ages of rapid growth.

83
Q

MoA of glucocorticoids in Asthma

A

The antiinflammatory effects of glucocorticoids in asthma include
Modulation of cytokine and chemokine production
Inhibition of eicosanoid synthesis
Marked inhibition of accumulation leukocytes in lung tissue
Decreased vascular permeability
Upregulation of -adrenoceptor number

84
Q

glucocorticoids effect on airway obstruction may be due in part;-

A

Contraction of engorged vessels in the bronchial mucosa

Potentiate the effects of β-receptor agonists,

Inhibit the lymphocytic, eosinophilic mucosal inflammation of asthmatic airways.

85
Q

types of corticosteroids for asthama

A

oral
predinisone and methylpredinison

86
Q

oral corticosteroids
parentral
inhatd

A
87
Q

Inhaled corticosteroids are used for maintenance treatment of asthma as……………
because

A

prophylactic therapy
Inhaled corticosteroids are not effective for relief of acute episodes of severe bronchospasm

88
Q

An average daily dose of four puffs twice daily of beclomethasone (400 mcg/d) is equivalent to about 10-15 mg/d of oral prednisone , with far fewer systemic effects.

A
89
Q

one of the cautions in switching patients from oral to inhaled corticosteroid therapy is to taper oral therapy slowly to avoid

A

precipitation of adrenal insufficiency.

90
Q

Adverse Effects and Contraindications
Systemic administration of the corticosteroids

A

Adrenal suppression, cushingoid changes, CNS effects and behavioral disturbances , increase susceptibility to infection
Increase the risks of osteoporosis and cataracts over the long term
In children, growth retardation, but this effect appears to be transient

91
Q

……………………Are either poorly absorbed or rapidly metabolized and inactivated and thus have greatly diminished systemic effects relative to oral agents.

A

inhaled corticosteroids

92
Q

adverse effects of inhaled corticosteroids

A

Oropharyngeal candidiasis.
hoarseness of the vocal cords.
sore throat and throat irritation,
and coughing.

93
Q

The risk of this complication of oropharyngeal candidiasis can be reduced by

A

having patients gargle water and spit after each inhaled treatment.

94
Q

solution for side effect of inhaled -hoareness

A

Special delivery systems (e.g., devices with spacers) can minimize these side effects.

95
Q

Anti-IgE therapy name

A

omalizumab

96
Q

Pharmacokinetics and Metabolism
route
every what days
bioavailabilty
halflife
where eliminated

A

Delivered as a single subcutaneous injection every 2 to 4 weeks.
It has a bioavailability of about 60%.
The serum elimination half-life is 26 days.
The elimination of omalizumab-IgE complexes occurs in the liver.
Some intact omalizumab is also excreted in the bile.

97
Q

Adverse effects
of omalizumab

A

Generally well tolerated.
Most frequent adverse effects: injection-site reactions (e.g., redness, stinging, bruising, and induration), anaphylaxis was seen in 0.1% of treated patients.
Possibly malignancies

98
Q

treatment for quick relief of asthma

A

1.adreneregic stimulants
Catecholamines(E,NE,isopretenol)

Resorcinols(terbutaline)
Saligenins(albuterol) respiratory selective, less cardiac effect

G-protein/cAMP→↓release of mediators/increased mucocilliary
Short acting-30-90 min

  1. Mythylxanthines
    Theophylline-medium potency, aminophylline

3.Anticolinergics iprathropium-in CHF(others contraindicated, but slow 60-90 min

99
Q

Long term treatment
of asthma

A

For long term treatment two cases of medicine are required:
- inhaled corticosteroids
- short acting B2-agonists
Inhaled medicine most conveniently administered using metered-dose inhalers

100
Q

Components of COPD

A

Chronic Bronchitis
Emphysema
Asthma (?)
Although not strictly a COPD disorder asthma is often
linked with being a COPD disorder.

101
Q

Risk factors
for COPD

A

Cigarette smoking-pack year(dose X years) ↓FEV1 faster
Airway responsive as in asthma(genetic predisposition)
Respiratory infections-childhood(initiate/exacerbate)
Occupational exposure-dust,gold,↓FEV1
Air pollution town>rural,↑Women( indoor pollution)
+/_ genetic /environmental+passive
Genetic –α1 antitrypsin deficiency(emphysema)

Pharma (7 decks)

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