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MS-PA: Respiratory Diseases > Respiratory pharamacology > Flashcards

Respiratory pharamacology Flashcards

1
Q

What are the 4 types of HSRs ?

A

Type I = Anaphylactic and Atopic
Type II = AntiBody – mediated
Type III = Immune Complex
Type IV = Delayed

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2
Q

What is the mechanism of type 01 hypersensitivity reaction?

A

IgE antibodies bind to antigens of allergens. These allergen-bound IgE molecules interact with Fcε receptors on the surface of mast cells. Activation of mast cells following engagement of FcεR results in a process called degranulation.

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3
Q

What are the examples of type 01 IgE mediated HSR ?

A

Atopic dermatitis
Allergic rhinitis
Asthma
Anaphylaxis

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4
Q

What is the difference b/w Th1 and Th2 responses ?

A

The main difference between TH1 and TH2 helper cells is thatthe TH1 helper cells generate immune responses against intracellular parasites, including bacteria and viruses, whereas the TH2 helper cells generate immune responses against extracellular parasites including, helminths

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5
Q

What are the phases of type 01 response ?

A

Sensitisation phase: Initial encounter to allergen causes TH2 cells mediated IgE antibody production by the B cell to the allergen and the IgE binds to Fc receptors on Mast cells.
Effectors phase: The re-exposure to allergen causes acute IgE mediated mast cell degranulation leading to histamine and prostaglandine release.
Late phase: Increase in CK causes recruitment of inflammatory cells and Eosinophils.

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6
Q

How is histamine synthesized ?

A

Histamine is formed from the amino acid histidine with the help of the enzyme histidine decarboxylase.

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7
Q

What are the receptors of histamine ?

A

H1, H2, H3, H4 receptors (G coupled proteins)

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8
Q

What are the tissues and cells in which histamine concentration is high ?

A

*The lungs, skin and GI tract.
* Mast cells and Basophils in blood.
* Non adrenergic and non cholinergic systems of the brain.
* Histaminocytes in stomach.

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9
Q

What cause circulating histamine activation ?

A

It is found in an inactive bound form and released in response to physical trauma or IgE mediated activation.

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10
Q

What are the physiological effects of histaminergic resposne ?

A

*Smooth muscle contraction (except arterioles), *bronchoconstriction
*Arterioles dilation causing BP drop
* On the Skin causes itch
*Increases acid and pepsin content of gastric secretion

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11
Q

What are G protein coupled H2 receptors ?

A

They are located in gastric parietal cells and responsible for gastric acid secretion through adenylyl cyclase mediated cAMP up regulation.

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12
Q

What are G protein coupled H3 receptors ?

A

They are located in the presynaptic neurons in the brain and responsible for inhibiting the release of histamine, acetylcholine, norepinephrine, serotonin.

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13
Q

What are G protein coupled H4 receptors ?

A

They are located in Thymus, small intestine, spleen, colon, basophils and bone marrow. responsible for Leukocyte chemotaxis, through adenylate cyclase mediated cAMP upregulation. They are the drug target for pruritic dermatitis, asthma and arthritis

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14
Q

What are the methods of therapeutically targeting histamine function?

A
  • Competitive antagonism of H1 and H2.
  • Inhibition of degranulation of mast cells.
  • Physiologic non-competitive antagonism of histamine receptors using adrenalin and epinephrine.
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15
Q

What are the difference between first generation anti-histamines and second generation anti-histamines?

A
  • The first generation anti-histamines are not specific for H receptors alone. therefore they can block serotonin and muscaranic receptors also.
  • The second generation anti-histamines have high specificity for Histamine receptors and have lesser side effects.
  • First generation cross the blood brain barrier and causes sedation. It also causes blurred vision, dry mouth, constipation, urinary retention, seizures, agranulocytosis, topical agents can cause dermatitis.
  • The second generation anti histamines has poor blood brain barrier penetration and has minimal side effects.
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16
Q

What is the action,indication and side effects of Sodium cromoglycate ?

A

They inhibit histamine release from the mast cells and basophils and has to be taken 30 to 60 min before meals. They are indicated for allergic conjunctivitis, intranasal allergy and asthma. Side-effects are uncommon but may include nausea, joint pain, and skin rash

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17
Q

What is Samter’s triad

A

It is also known as Aspirin-exacerbated respiratory disease (AERD) and is a syndrome of airway inflammation characterized by rhinosinusitis with polyposis, asthma, and NSAID intolerance.

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18
Q

What are the causes of asthma

A

CD14 gene polymorphisms and environmental triggers.

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19
Q

What are the environmental triggers of asthma ?

A
  • Viral Infections
    *Allergens such as house dust, mite, animal fur
    *Environmental and air pollutants,
    *Occupational exposure to metal salts and industrial chemicals.
    *Pharmacological agents such as aspirin (Samter’s Triad), beta-blockers
  • Exercise and Emotional stress.
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20
Q

What are the risk factors for asthma ?

A

*Personal history of atopy
*Family history of asthma or atopy
*Inner city environment; *socio-economic deprivation
*Obesity
*Prematurity and low birth weight
*Viral infections in early childhood
* Smoking and Maternal smoking.
*Early exposure to broad-spectrum antibiotics

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21
Q

What are the protective factors for Asthma ?

A

*Vaginal birth
*Increasing siblings
*Farming environment

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22
Q

What is the pathophysiology of Asthma ?

A

Genetic and environmental triggers cause recruitment and/or activation of the inflammatory cells in the airways. Which release a variety of inflammatory mediators that cause acute bronchoconstriction, plasma leakage, vasodilatation, mucus secretion, sensory nerve activation and cholinergic reflex-induced bronchoconstriction. Together with structural changes such as subepithelial fibrosis, angiogenesis and increase in mucus-secreting cells, smooth muscle hyperplasia and hypertrophy leads to asthma

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23
Q

What is the parasympathetic effect seen in asthma ?

A

Increased mucus secretion and bronchonconstriction due to vagal stimulation mediated Ach- M3 signalling.

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24
Q

What are the beneficial and non beneficial non pharmacological interventions in Asthma ?

A

*Beneficial ones are Smoking cessation
Breathing exercises
Weight reduction
* Non-beneficial ones are Fish oils ,Antioxidants
Probiotics , Physical and chemical methods of reducing house dust mite levels in the home.

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25
Q

What are the controller drugs in Asthma ?

A

Controllers are medications taken daily on a long-term basis to keep asthma under clinical control, chiefly through their anti-inflammatory effects.

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26
Q

What are the types of controller medications in Asthma ?

A

*inhaled and oral corticosteroids
*Leukotriene receptor antagonists
*Long-acting β2-agonists in combination with inhaled steroids.
*Tiotropium and sustained-release theophylline.

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27
Q

What are the most effective controller medications currently available?

A

Inhaled corticosteroids

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28
Q

What is the action of reliever drugs in Asthma ?

A

Relievers are medications used on an as needed basis that act quickly to reverse bronchoconstriction and relieve its symptoms.

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29
Q

What are the types of reliever drugs in Asthma ?

A

*short-acting β2-agonists
*formoterol in a MART regimen
*inhaled short-acting anticholinergics
*immediate -release theophylline
*short-acting oral β2-agonists.

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30
Q

What are the aims of pharmacological treatment of Asthma ?

A

*Control symptoms, including nocturnal symptoms and those related to exercise.
*Prevent exacerbations and need for rescue medication.
*Achieve the best possible lung function (practically, FEV1 and/or PEFR >80% predicted or best).
*Minimise side-effects

31
Q

What is the approach to pharmacological treatment in Asthma ?

A
  • Start Tx at the level most appropriate to initial severity.
  • Achieve early control.
  • Maintain control by increasing treatment as necessary and decreasing when good control.
32
Q

What are the elements of stepwise approach in asthma management ?

A

Assess: Diagnose asthma, identify risk factors and co-morbidities, check inhaler technique and adherence, identify patient preference and goals.

Adjust: adjust modifiable risk factors and co-morbiditeis, and patient education and training on inhaler and titrate drugs based on clinical indications.

Review: Symptoms, exacerbations, side effects, lung function, and patient satisfaction.

33
Q

What is the step 01 in asthma pharmacotherapy?

A

Controller therapy.
* PRN low dose ICS-Formeterol ( preferred) or low dose ICS taken whenever SABA is taken.

Reliever therapy.
* PRN ICS- formeterol
( prefered) or PRN SABA.

34
Q

What is the step 02 in asthma pharmacotherapy?

A

Controller therapy.
* Daily low dose ICS preferred or PRN low dose ICS- Formeterol.
* Alternatively low dose ICS taken whenever SABA taken.

Reliever therapy.
* PRN ICS- formeterol
( prefered) or PRN SABA.

35
Q

What is the step 03 in asthma pharmacotherapy?

A

Controller
* Low dose ICS-LABA preferred.
* Medium dose ICS or low dose ICS + LTRA.

Reliever
* PRN ICS- formeterol for patients on maintenance and reliever therapy.
* PRN SABA

36
Q

What is the step 04 in asthma pharmacotherapy?

A

Controller
* Medium dose ICS-LABA preferred.
* High dose ICS with add-on Tiotropium or LTRA.

Reliever
*PRN ICS- formeterol for patients on maintenance and reliever therapy.
* PRN SABA

37
Q

What is the step 05 in asthma pharmacotherapy?

A

Controller
* High dose ICS-LABA and refer for phenotypic assessment +/- Add-on therapy with Anti-IgE, Anti IL-5 , Anti IL-4 ( preferred).
* Add low dose OCS based on risk factors.

reliever
*PRN ICS- formeterol for patients on maintenance and reliever therapy.
* PRN SABA

38
Q

What are the classes of bronchodilators used in Asthma ?

A

B2 adrenoreceptor agonists
Muscarinic antagonists
Xanthines

39
Q

What is the pharmacological action of beta two agonists ?

A

Bronchodilation by increasing cAMP and decreasing bronchoconstrictors such as Ca2+ and MLCK. They also inhibit mast cell degranulation and increase mucociliary clearance.

40
Q

What is the 1/2 life of SABA?

A

They have a half life of 2 to 3 hrs. example: salbutamole ( Ventolin), Terbutaline.

41
Q

What are LABA and its action?

A

They bind to exoreceptors beside the Beta 2 receptors causing repetitive activation the B2 receptors and has a 1/2 life > 15 hrs.
examples are Salmeterol / Formeterol / Indacaterol / Vilanterol.

42
Q

What are the routes of administration of beta two agonists ?

A

*Inhaled as powder or aerosol, neubuliser
*Rarely given orally (prophylaxis of allergen or exercise induced bronchospasm) or parenterally.

43
Q

What are the systemic side effects of beta two agonists ?

A

*tremor
*arrhythmias, hypokalemia
Palpitations.
*
*Bronchospasm paradoxical (rare)
*muscle cramps, (very rarely, rhabdomyolysis)
* BETA BLOCKERS CAN PRECIPITATE ASTHMA

44
Q

What is the impact of the overuse of SABA ?

A
  • It is the marker of uncontrolled asthma and asthma related deaths.
45
Q

What is the action of muscaranic antagonist Ipratropium Bromide ?

A

It is also called N-isopropylatropine. It Inhibits the action of acetyl choline at M1, M2, and M3 receptors thus producing bronchodilation and reducing mucous secretion. It is slower acting than B2 agonists.

46
Q

What is the action of muscaranic antagonist Tiotropium Bromide
?

A

Selective inhibition of M1 and M3 receptors

47
Q

What is the route of administration of muscaranic antagonist ?

A

Inhalation and is poorly absorbed into the systemic circulation, thus have fewer side effects.

48
Q

What are the indications for muscaranic antagonist ipratropium bromide?

A

Adults acute asthma: Nebulised ipratropium bromide (0.5 mg 4 to 6 hourly) should be added to β2agonist treatment for patients with acute severe or life-threatening asthma or those with a poor initial response to β2agonist therapy. Ipratropium bromide combined with a nebulised β2agonist produces significantly greater bronchodilation than a β2agonist alone resulting in faster recovery and a shortened duration of admission.

49
Q

What is the action of Xanthines in Asthma ?

A

bronchodilation by inhibiting phosphodiesterase resulting in increased cAMP and cGMP.

50
Q

What are oral xanthines ?

A

Caffeine and Theophylline and have short 1/2 life.

51
Q

What is the IV xanthine used in asthma?

A

Aminophylline

52
Q

What are the side effects of Xanthines ?

A

*Narrow therapeutic range (27-80 mciro mol/l).

*Side effects likely with concentrations >110 micro mol/l
*Gastrointestinal: nausea / anorexia
*Cardiovascular:arrhythmias can be fatal
*CNS: nervousness, tremor, seizures

53
Q

What is the pharmacokinetics of Xanthine ?

A

Metabolised in the liver and the 1/2 life is increased by liver disease, heart failure and
decreased by smoking and heavy drinking.

54
Q

What are the anti inflammatory drugs used in Asthma ?

A

*Glucocorticoids
*Cromones
*Leukotriene synthesis inhibitors & receptor antagonists

55
Q

What are the steroids used in the effective controller of asthma ?

A

Beclomethasone
Budesonide (extensive 1st pass metabolism in liver)
The current evidence suggests that in asthma the inhaled corticosteroids do not differ in efficacy or safety

56
Q

What is the most effective asthma reliever anti-inflammatory drugs ?

A

oral (Prednisolone) or IV (Hydrocortisone).

57
Q

What are the important side effects of ICS ?

A

Dysphonia due myopathy of laryngeal muscles and oral candidiasis.

58
Q

What are Leukotriene Receptor Antagonists and their indications?

A

they are add on therapy in Asthma
and they Improves lung function, cough and reduces airway inflammation. The side effects are GI upset and headache. example: Montelukast.

59
Q

What is the advantage of Maintenance and reliever therapy (MART) ?

A

Fixed dose ICS/LABA combination inhalers are
Convenient for patients.It
Improve adherence to drug treatment, as fewer inhalations and devices are needed. It
Can overcome the potential for over-reliance on bronchodilator therapy at the expense of ICS.

60
Q

What is Omalizumab and its indication ?

A

*Omalizumab (Xolair®) is a humanised monoclonal antibody that binds to circulating IgE, markedly reducing levels of free serum IgE and is given subcutaneously every 2 to 4 week.s

*It is licensed for adults and children over 6 years on high dose inhaled steroids and LABAs who have impaired lung function with frequent attacks and have allergy as an important cause of their asthma.

61
Q

What is the action of Sodium Cromoglycate ( Cormones) in Asthma ?

A

It’s anti-inflammatory effects are due
Mast cell stabilisation by inhibition of Ca+ influx.
It also Inhibits sensory neurons reducing exaggerated neuronal reflexes triggered by irritant stimuli such as sulfur dioxide.
It also causes Inhibition of eosinophil accumulation in lungs and Reduced IgE production.
It is a highly ionized inhalation agent poorly absorbed and not a reliever.It may cause Cough and wheeze transiently post administration.

62
Q

What is the acute management of asthmatic bronchospasm ?

A

2-4 puffs of inhaled SABA as required for symptoms.
If more severe – up to 3 treatments at 20 minute intervals, or single nebulizer treatment.

*A Course of oral prednisolone may be needed.

63
Q

what is the A&E management of severe asthma attack ?

A

*Ensure adequate hydration
*40-60% oxygen via face mask
*Nebulised b2 agonists (salbutamol)
*Nebulised ipratropium
*Oral prednisolone or IV hydrocortisone

64
Q

What is the management of life threatening asthma ?

A

*Magnesium sulphate 2gm IV over 20 mins (Bronchodilator/antiarrhythmic agent).

*IV aminophylline or salbutamol

*Intubation and Ventilation (ICU)

65
Q

What are the sages of COPD ?

A

Stage 01: mild symptoms with 80% of normal lung function preserved.

Stage 02: Moderate symptoms with 50 to 80% of normal lung function preserved.
Stage 03: It is severe COPD with difficulty breathing and frequent exacerbations. 30 to 50% of the lung function preserved.
Stage 04: This is the very serve stage of COPD with significant compromise of lung function FEV1 < 30 % of the normal lung function.

66
Q

What is the acute management of COPD attacks ?

A

*2-4 puffs of inhaled short acting b2 agonists as required for symptoms
*If more severe – up to 3 treatments at 20 minute intervals, or single nebulizer treatment
*Antibiotics for acute exacerbations with purulent sputum
* A course of oral prednisolone may be needed.

67
Q

What is the A& E management of acute severe COPD attack ?

A

*Ensure adequate hydration
*24-28% oxygen via face mask
*Antibiotics for acute exacerbations with purulent sputum
*Nebulised b2 agonists
*Nebulised ipratropium
*Oral or IV steroids

68
Q

What is the management of life threatening COPD attack ?

A

*IV aminophylline or salbutamol
*If persistently hypoxic or acidotic consider:
1) Nasal Intermittent Positive Pressure Ventilation (NIPPV)
2) Invasive ventilation

69
Q

What is the GOLD recommendation for considering ICS therapy in COPD ?

A

Use it only if the blood eosinophil levels > 300 other wise LABA or LAMA / LABA + LAMA in group D.

70
Q

What is the GOLD recommendation for SABA ( salbutamol, terbutaline ) and ipratropium (SAMA)
in COPD ?

A

GOLD states that rescue SABA should be prescribed to all patients for immediate symptom relief.

71
Q

What are theGOLD guidelines of LAMA and LABA in COPD ?

A

GOLD guidelines recommend treatment initiation with a single agent long-acting bronchodilator for patients in GOLD group A ( LABA). The Patients in groups B, C and D should be on combination bronchodilatory therapy (LAMA + LABA)

72
Q

What is Roflumilast ?

A

Roflumilast (Daxas®) is a phosphodiesterase type-4 inhibitor which act by inhibiting fibroblasts and slow fibrosis, bronchial smooth muscle relaxation. It also inhibit macrophages and down-regulate neutrophils.

73
Q

What is the action of carbocisteine?

A

It is mucolytic thought to reduce the viscosity of sputum and help patients to expectorate as overproduction of sputum is common in COPD.

MS-PA: Respiratory Diseases (15 decks)

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