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RS > Lecture 13 > Flashcards

Lecture 13 Flashcards

1
Q

What are the goals of asthma treatment?

A
  1. Control chronic symptoms.
  2. Maintain normal activity levels and exercise.
  3. Maintain near-normal lung functions.
  4. Prevent exacerbation of asthma.
  5. Minimise emergency department (ED) visits and hospitalisations.
  6. Avoid adverse effects of asthma medications.
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2
Q

What are the types of treatment of asthma?

A
  1. Relievers.
  2. Preventers.
  3. Others.
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3
Q

Describe reliever treatments?

A

Drugs that provide relief from a asthma symptoms. Normally paid onset but short duration, cause airway smooth-muslce relaxation. Only take during attack.

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4
Q

Describe preventer treatments?

A

Do not provide relief for an acute asthma attack. Still need to take even if there are no symptoms.

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5
Q

What are the benefits for using inhaled beta-agonist in the management of asthma?

A
  1. Relief of broncho-constriction due to smooth-muscle relaxation.
  2. marked protection against all nonspecific constrictor stimuli, such as cold air, metacholine and exercise.
  3. Reduced vascular permeability and edema.
  4. Increased mucociliary clearance due to increased ciliary beat frequency.
  5. May reduce inflammation due to inhibition of mediator release from inflammatory cells and priming of glucocorticoid receptors.
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6
Q

Describe the mechanism of relaxation of bronchial smooth muscle?

A

Beta 2 stimulant will bind to the Beta 2 receptor on the cell membrane. It will activate the Gs which activates AC. AC will convert ATP to cAMP. cAMP increases which increases PKA. This will activate:

  • Calcium and Potassium channels which will cause Potassium release.
  • Sodium/Potassium ATPAse.
  • Decrease in PI hydrolysis.
  • Sodium/Calcium exchange.
  • Decrease in MLCK.
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7
Q

What is the route of administration of asthma treatment?

A
  1. Inhalation.
  2. Oral - use oral when you cannot use inhalation.
  3. Direct endotracheal instilaltion.
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8
Q

What are the types of inhalers?

A
  1. Metered dose inhalers - aerosol spray.

2. Dry powder device.

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9
Q

Why use a spacer with an inhaler?

A

Allows you to deliver more of the drug to the lung. Largely reduce the chance of systemic adverse effects.

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10
Q

What are nebulisers?

A

Warm and moisture can comfort the airway. usually combine 2 or 3 medications together. Need a machine to do ti.

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11
Q

Describe short acting Beta-2-adrenoreceptor aganoists?

A

Rapid onset but short duration - maximum effect occurs within 30 minutes and the duration is around 4-6 hours. Effective in preventing - exercise induced asthma, cold air and allergen triggered asthma. Also used for acute severe asthma. use on an “As needed” basis.

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12
Q

What are the adverse effects of the Beta2 agonists?

A
  1. tremor.
  2. Tolerance (tachyphylaxis) due to down-regulation of beta-2 receptors.
  3. Hypokalemia.
  4. Tachycardia.
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13
Q

Describe Long-acting beta2 agonists (LABA)?

A

The duration of action is longer than 12 hours. Use on a regular basis. Used to prevent bronchospasm in patients requiring long-term bronchodilator therapy. Inhaled corticosteroid (ICS) and LABA can be used as combined therapy.

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14
Q

What are the FDA recommendations for asthma treatment?

A
  1. LABAs should not be used as the first line medicine to treat asthma.
  2. LABAs should be added to the asthma treatment plan only if other medicines do not control asthma, including the use of low or medium does corticosteroids.
  3. LABAs do not relieve sudden wheezing. Always have a short acting bronchodilator medicine with you to treat sudden wheezing.
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15
Q

What are anticholinergic agents?

A

Each can cause broncho-constriction and mucus secretion. Currently available are non-selective.

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16
Q

Describe ipratropium bromide?

A

Slow onset (60-90minute) and a shorter duration (6-8h). use on a regular basis. Low side effect, less tachyphylaxis. Problems - reduced mucocillary clearance.

17
Q

Describe tiotropium bromide?

A

Long lasting muscarinic antagonist (>25 hours). Equal affinity for M1, M2 and M3 receptors. Dissociates rapidly from m2 receptors. Approximately 10-fold more potent than ipratropium bromide. Problems with dry mouth in 10-15% (systemic absorption of the drug is low but sufficient to cause it). Can cause constipation, blurred vision and urinary retention.

18
Q

Describe Xanthine drug?

A

It is non-selective inhibition of phosphodiesterase - cause broncho-dilation. Activation of histone deacetylases (HDAC): related to anti-inflammatory effects. Non-selective antagonism of adenosine receptors.

19
Q

what does theophylline do?

A

Prevents PDE3,4,7 from converting cAMP to AMP.

20
Q

what does theophylline do?

A

Prevents PDE3,4,7 from converting cAMP to AMP. Increase in cAMP will increase broncho-dilation.

21
Q

What are the side effects of theophylline?

A

Narrow therapeutic range (10-20microgram/mL). Toxicity can occur within the therapeutic range.
Serum level monitoring is the only reliable method of preventing toxicity.

22
Q

What are the side effects of theophylline?

A 
Narrow therapeutic range (10-20microgram/mL).  Toxicity can occur within the therapeutic range.  
Serum level monitoring is the only reliable method of preventing toxicity.  
-Nausea/vomiting.
-Headache.
-Diarrhoea.
-Insomnia.
-Hyperglycaemia (from overdose).
-Seizures (from overdose).
-Arrhythmias (from overdose).
23
Q

Describe the clearance of theophylline?

A

Heart failure, erythromycin, beta blocker, CYP1A2 polymorphism and ciprofloaxcin will decrease clearance.
smoking and phenytoin will increase clearance.

24
Q

Describe glucocorticoids (GCs)?

A

They reduce inflammation and immune responses. Used clinically since 1948 and the market size in the US per year is around $10,000,000,000.

25
Q

What are GCs?

A

Are a class of steroid hormones that bind to the glucocorticoid receptor (GCR). The name glucocorticoid (glucose + cortex + steroid) derives from their role in the regulation of the metabolism of glucose, their synthesis in the adrenal cortex and their steroidal structure.

26
Q

What are the physiological effects of GCs?

A
  1. regulation of carbohydrate, protein and lipid metabolism.
  2. Maintenance of fluid and electrolyte balance.
  3. Preservation of normal function of the cardiovascular system, the immune system, the kidney, skeletal muscle, the endocrine system and the nervous system.
  4. Preservation of organism homeostasis.
27
Q

Describe the pharmacokinetics of GC?

A

Ideal GCs should have:

  1. Increased lung deposition and pulmonary retention.
  2. Increased residence time and high receptor-binding affinity.
  3. Rapid clearance, and have an on-site activation of the pro-drug to promote safety.
28
Q

How do GCs work?

A

The GC receptor is in the cytoplasm. The GC will travel through to the nucleus. Once at the nucleus will have gene activation and gene repression.

29
Q

Describe the cellular and molecular effects of GCs?

A

GCs suppress circulating eosinophils, basophils, monocytes, mast cells, dendritic cells and to a smaller degree lymphocytes (particularly T lymphocytes). The principal effects: Inhibit the synthesis, release, and expression of cytokines, inflammatory peptides, chemokine, growth factors, adhesion molecules, and lipid mediators involved int he inflammatory response. Reduce the inflammatory cell numbers including inhibition of recruitment or migration, activation, survival, and proliferation of cells. Up-regualtion of beta-adrenergic receptors on airway smooth muscle cells.

30
Q

Describe prednisone?

A

Inactive oral pro-drug and it is metabolised in liver to form prednisolone. The drug has less mineralocorticoid effects, so decreases swelling of ankle, retaining of water and salt.

31
Q

Describe GCs in chronic asthma treatment?

A

Inhaled GCs Treatment can decrease asthma symptoms, number of uses of bronchodilator, and frequency of acute asthma symptoms; and can improve lung function and bronchial hyper responsiveness. Onset of response: improvement in lung function may be within 1 month; improvement in airway inflammatory markers can be seen as early as 2 weeks.

32
Q

Describe the adverse effect of GCs?

A

Inhaled GCs: around 20% of the drug is inhaled to the lung while 80% is deposited in the mouth and swallowed, reaching the systemic circuit and metabolised by liver.

33
Q

What is crushing syndrome?

A

Hypercortisolims promotes distribution of body to trunk, back of neck (buffalo hump) and also face (moon-face) i.e. central obesity with thin arms and legs.

34
Q

If you use GCs in long term dose what will happen?

A

Increase in gluconeogenesis with high glucose level; cause diabetes and protein/muscle breakdown; cause proximal weakness. Osteoporosis with loss of collagens and increased risk of fracture. Increase BP and affect CNS which decrease depression but become happy. Maybe verbally psychotic, increase risk of cataract. Increase chance to have TB and salt water retention.

35
Q

What are the local adverse effects of GCs?

A

Hoarseness or dysphonia, cough, and oral candidiasis (thrush) are the most commonly reported problems associated with inhaled GCs, due to immunosuppressant effect and myopathy of the vocal cords.

36
Q

How do we prevent local adverse effects?

A

Rinse mouth to prevent thrush. Use a spacer (easier administration of drug).

37
Q

Describe outgrow of asthma?

A

Only 6% of kids fully outgrew their asthma. This means no asthma symptoms for at least one year. An additional 39% of kids had improvement in their asthma. Effects of ICS treatment on % of the outgrowing of asthma are still not very clear.

38
Q

Describe leukotriene receptor antagonists?

A

Inhibit LT4 can reverse all the effects of pro-inflammatory release. It can prevent:
-Aspirin induced asthma.
-Exercise induced asthma.
-Decrease both early and late responses to inhaled allergen.
Relax airway in mild asthma:
-Bronchodialtor effect = 1/3 salbutamol.
-Additive bronchodilation effect with Beta2-agonist.

39
Q

What are the side effects of leukotriene?

A

Headache, GI disturbances and reversible hepatitis and hyperbilirubinemia.

RS (24 decks)

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