Brightspace test

19 important questions on Brightspace test

What is the role of the type II cell in the lung?

1)
It produces mucus and secretes electrolytes in the conducting airways.
2)
It is the primary cell type that covers the alveolar surface to facilitate gas exchange.
3) It produces surfactant and functions as a progenitor cell.

4)
It expresses cilia that help in the mucociliary clearance of the lung.

It produces surfactant and functions as a progenitor cell.

Sensory nerves in the airways secrete tachykinins, including Substance P and Neurokinin A. Which of the following statements is correct?

1)
Substance P and Neurokinin A both mediate bronchoconstriction.
2)
Neurokinin A mediates brochoconstruction, whereas Substance P regulates plasma exudation and mucus secretion.

3)
Substance P mediates bronchoconstriction, whereas Neurokinin A regulates plasma exudation and mucus secretion.
4)
Substance P and Neurokinin A both mediate plasma exudation and mucus secretion.

Neurokinin A mediates brochoconstruction, whereas Substance P regulates plasma exudation and mucus secretion.

Which of the following drugs would you recommend as a controller medication for asthma?
Question 3 options:

1) Isoprenaline
2) Terbutaline
3) Salmeterol
4) Salbutamol

Salmeterol
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Why are PDE4 inhibitors better anti-inflammatory drugs then Beta2-agonists?

1) Inflammatory cells express high levels of GRKs, which lead to beta2-receptor desensitization, rendering beta2-agonists less effective.
  

2) Inflammatory cells do not express beta2-receptors, but do express PDE4.


3) PDE4 inhibition mainly induces cGMP accumulation, whereas beta2-agonists mainly induce cAMP accumulation. cGMP is more effective in suppressing inflammatory activity than cAMP.
   

  4) Clinically used PDE4 inhibitors have a much longer duration of action than clinically used beta2-agonists.

Inflammatory cells express high levels of GRKs, which lead to beta2-receptor desensitization, rendering beta2-agonists less effective.

How do cromoned work in allergic diseases?



1) Cromones inhibit IgE binding to the high affinity IgE receptor on mast cells.

  2) Cromones inhibit IP3 production by the high affinity IgE receptor. 
3) Cromones inhibit Ca2+-influx into the mast cell upon activation of the high affinity IgE receptor.

  4) Cromones interfere with the Ca2+ dependent degranulation process in the mast cell.



Cromones inhibit Ca2+-influx into the mast cell upon activation of the high affinity IgE receptor.

What is the mode of action of dupilumab?

An antibody targeting IgE
An antibody targeting  IL-4
An antibody targeting  IL-5R
An antibody targeting  IL-4R

An antibody targeting  IL-4R

What is the main side effect observed with inhaled corticosteroid?

1) Candida infections in the throat
2) Euphoria
3) Increased abdominal fat
4) Impaired wound healing

Candida infections in the throat

What is the main function of the parasympathetic nervous system in the nose in patients with allergic rhinitis?

1) It promotes sneezing
2) It promotes the activation of secretions
3) It promotes the activation vascular leakage (edema)
4) It promotes the activation of sensory nerves

It promotes the activation of secretions

Which of the following therapies would you not recommend in case of acute allergic rhinitis?

1) Beclomethasone.
2) Xylomethazoline.
3) Loratidine.
4) Cromoglycate.

Xylomethazoline.

Why do ACE inhibitors have cough as a side-effect?

1) Angiotensin I promotes cough and accumulates in response to ACE inhibitor therapy.

2) Angiotensin II represses cough and is reduced in response to ACE inhibitor therapy.

3) Substance P promotes cough and accumulates in response to ACE inhibitor therapy.
    
  4) Bradykinin promotes cough and accumulates in response to ACE inhibitor therapy.

Bradykinin promotes cough and accumulates in response to ACE inhibitor therapy.

Which of the following treatments would you recommend in a patient with non-productive dry cough?

1) Noscapine
2) Acetylcysteine
3) Tiotropium
4) Bromohexine

Noscapine

What is the mode of action of Nintedanib?

1) It is a broad-spectrum kinase inhibitor that interferes with the fibrotic process.

2) It is a broad-spectrum antibiotic that prevents bacterial colonization.
3) It is a novel antitussive agent that blocks the P2X3 receptor.
4) It specifically interferes with the PDE4 subtype of phosphodiesterases.

It is a broad-spectrum kinase inhibitor that interferes with the fibrotic process.

What is pepsin?

1) A hormone that regulates gastric acid secretion.
  
2) A plasma membrane protein responsible for pumping protons into the lumen of the stomach.

3) A protein that forms part of the gastric mucosa and protects against the effects of stomach acid on the stomach wall.
  
4) An enzyme that breaks down proteins in the food in the stomach.

An enzyme that breaks down proteins in the food in the stomach.

Which of the following drugs would you prescribe for nausea / vomiting?

1) Anticholinergic

2) Dopamine antagonists

3) 5-HT3 reuptake inhibitors

4) H2 antagonists

Dopamine antagonists

Which of the following would you not prescribe for diarrhea caused by an intestinal infection?

1) Loperamide
2) ORS
3) Antibiotics
4) Activated carbon (norit)

Loperamide

What is the use of the drug ivacaftor in cystic fibrosis based on?

1) Ivacaftor is a recombinant DNAse that breaks down the mucus.

2) Ivacaftor is an antibiotic that suppresses infections associated with cystic fibrosis.

3) Ivacaftor is a stimulant that promotes mucus production.

4) Ivacaftor is a drug that enhances the function of the CFTR.

Ivacaftor is a drug that enhances the function of the CFTR.

What is the basis for inflammatory bowel disease (IBD) treatment with sulfasalazine?

1) Inhibition of prostaglandic acid metabolism and inhibition of oxidative stress.

2) Inhibition of the neutrophil influx that excites sensory nerves.

3) Increased permeability of the intestinal epithelium due to inhibition of the enzyme NOS.
      
4) Suppression of T cell activity by inhibition of the cytokine TNF?.

Inhibition of prostaglandic acid metabolism and inhibition of oxidative stress.

Benzoyl peroxide and tretinoin are used in the treatment of acne, but never as a combination. Why is this?

1) The combination of these drugs causes damage to the hair follicle.

2) Benzoyl peroxide reacts with tretinoin to make it inactive.

3) The combination leads to the formation of allergens, to which an allergic reaction is possible.

4) The combination induces vasodilation causing redness.

Benzoyl peroxide reacts with tretinoin to make it inactive.

In addition to atopic eczema, we also know contact eczema (for example as a result of contact of nickel with the skin). How does this arise?

1)  By activating neutrophils, which secrete elastases and damage the skin.

2) Through the activation of Th2 cells that attract eosinophils, causing damage to the skin.

3) Due to the activation of mast cells, which after contact with the allergen cause an IgE dependent histamine release.

4) Due to the activation of Th1 cells, which activate cytotoxic CD8 + T cells, causing skin damage.

Due to the activation of Th1 cells, which activate cytotoxic CD8 + T cells, causing skin damage.

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