Respiratory Pharmacology and Support: Antihistamines, NSAIDs, and Physiotherapy

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Last updated 2:50 AM on 5/15/26
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65 Terms

1
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What are the three main categories of the 'Therapeutic Arsenal' in respiratory management?

Antihistamines, NSAIDs, and non-pharmacological support.

2
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Antihistamines are primarily used for management mediated by which antibody?

IgE (Immunoglobulin E).

3
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What is the primary pharmacological goal of NSAIDs in respiratory care?

Modulation of inflammation and pain.

4
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Non-pharmacological support focuses on which two physiological processes?

Mechanical ventilation and oxygenation.

5
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Which enzyme do NSAIDs inhibit to reduce prostaglandin synthesis?

Cyclooxygenase (COX).

6
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In the pathophysiology of histamine, which cells release histamine after encountering an antigen?

Mast cells and basophils.

7
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How does histamine release affect vascular diameter, and what is the clinical result?

It causes vasodilation, resulting in nasal congestion.

8
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What clinical symptom results from histamine-induced increased vascular permeability?

Rhinorrhea.

9
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Histamine stimulation of sensory nerves leads to which two primary symptoms?

Sneezing and pruritus (itching).

10
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What is the effect of histamine on bronchial smooth muscle?

Smooth muscle contraction (bronchospasm).

11
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What is the specific mechanism of action for antihistamines at the H₁ receptor?

They act as inverse agonists, stabilizing the inactive receptor conformation.

12
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Why do antihistamines have a 'highly limited effect' on acute asthma exacerbations?

They have minimal effect on established bronchospasm.

13
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Which specific vascular and capillary effects do antihistamines successfully attenuate?

Vasodilation and capillary permeability.

14
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List four examples of first-generation antihistamines.

Diphenhydramine, chlorpheniramine, hydroxyzine, and promethazine.

15
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What characteristic of first-generation antihistamines allows for high Blood-Brain Barrier (BBB) penetration?

They are lipophilic.

16
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First-generation antihistamines show low receptor selectivity, interacting with which three non-histamine systems?

Muscarinic, α-adrenergic, and serotonergic systems.

17
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What are the two primary safety concerns/side effects of first-generation antihistamines?

CNS depression and anticholinergic effects.

18
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List three examples of second-generation antihistamines.

Loratadine, cetirizine, and desloratadine.

19
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How does the Blood-Brain Barrier (BBB) penetration of second-generation antihistamines compare to the first generation?

It is minimal.

20
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What is the primary receptor focus of second-generation antihistamines?

Peripheral H₁ receptors.

21
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List three examples of third-generation antihistamines.

Fexofenadine, levocetirizine, and desloratadine.

22
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What is the level of Blood-Brain Barrier (BBB) penetration for third-generation antihistamines?

Negligible.

23
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What safety advantage do third-generation antihistamines have over previous generations regarding the heart?

Minimal cardiotoxic potential.

24
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What are the primary clinical indications for antihistamines?

Seasonal/perennial allergic rhinitis and allergic conjunctivitis.

25
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In what secondary respiratory condition is antihistamine use considered an 'adjunctive' therapy?

Mild allergic asthma.

26
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For which specific symptoms of allergic rhinitis are antihistamines highly effective?

Sneezing and rhinorrhea.

27
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How effective are antihistamines for treating nasal congestion?

They have limited efficacy.

28
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Which age group is at risk for 'paradoxical excitation' from antihistamines?

Pediatrics.

29
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Why must antihistamines be used with caution in the elderly?

Risk of CNS depression and impaired cognition leading to falls.

30
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Antihistamines are contraindicated in which specific ocular condition?

Narrow-angle glaucoma.

31
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What is the clinical term for the dry mouth caused by the anticholinergic burden of antihistamines?

Xerostomia.

32
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Caution is advised when using antihistamines in patients with which bladder-related condition?

Prostatic hyperplasia (due to urinary retention risk).

33
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What is the 'constitutive' or 'protective' role of the COX-1 enzyme?

Gastric mucosal protection, platelet aggregation, and renal blood flow regulation.

34
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What is the 'inducible' or 'inflammatory' role of the COX-2 enzyme?

Synthesis of prostaglandins mediating inflammation, pain sensitization, and fever.

35
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Which medication is an irreversible salicylate that inhibits COX enzymes for the lifespan of a platelet?

Aspirin (Acetylsalicylic acid).

36
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List four examples of traditional non-selective NSAIDs.

Ibuprofen, diclofenac, naproxen, and indomethacin.

37
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What is the primary toxicity risk associated with traditional non-selective NSAIDs?

Higher GI (gastrointestinal) toxicity risk.

38
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List two examples of preferential COX-2 inhibitors.

Meloxicam and etodolac.

39
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List two examples of selective COX-2 inhibitors (Coxibs).

Celecoxib and etoricoxib.

40
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Selective COX-2 inhibitors carry an increased risk for which type of adverse events?

Prothrombotic (cardiovascular) events.

41
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In NSAID toxicity, why does blocking COX-1 lead to peptic ulcer disease?

It reduces gastric mucosal protection.

42
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What is the renal consequence of NSAID-induced decreased perfusion?

Sodium/water retention and acute kidney injury risk.

43
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NSAIDs are generally contraindicated during which stage of pregnancy?

The third trimester.

44
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What does the acronym NERD stand for in the context of NSAID toxicity?

NSAID Exacerbated Respiratory Disease.

45
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What is the pathophysiology behind NERD-induced bronchospasm?

Inhibiting the COX pathway shunts arachidonic acid toward increased leukotriene production.

46
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List three interventions for nasal mucosal hydration.

Isotonic/hypertonic saline, nasal gels, and humidified air.

47
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How does nasal mucosal hydration assist in allergic rhinitis?

It removes allergens and mediators while improving mucociliary clearance.

48
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List four techniques used in respiratory physiotherapy.

Chest percussion, postural drainage, positive expiratory pressure (PEP) devices, and diaphragmatic breathing.

49
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Respiratory physiotherapy reduces the risk of _____ in patients with COPD or cystic fibrosis.

Atelectasis

50
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What is the primary goal of oxygen therapy?

To correct arterial oxygen deficiency (PaO₂) and improve tissue oxygen delivery.

51
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Which oxygen delivery device allows for the most precise FiO₂ control?

Venturi Mask.

52
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List the four oxygen delivery systems in order of typical clinical progression.

Nasal Cannula, Simple Face Mask, Venturi Mask, High-Flow Nasal Systems.

53
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In chronic CO₂ retention (COPD) patients, excessive oxygen can suppress the _____.

Hypoxic respiratory drive

54
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What core protocol is essential during oxygen therapy to prevent adverse outcomes?

Continuous monitoring of oxygen saturation and arterial blood gases.

55
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For uncomplicated seasonal allergic rhinitis, what generation of antihistamine is preferred?

Second or third generation.

56
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Why are antihistamines considered of limited utility in viral URIs?

The symptoms are not IgE-mediated.

57
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In a patient with asthma and nasal polyposis, NSAIDs should be _____.

Strictly avoided

58
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Why should first-generation antihistamines be avoided in severe COPD exacerbations?

They cause anticholinergic drying of secretions.

59
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Which non-pharmacological intervention is recommended for airway clearance in asthma patients with mucus retention?

Respiratory physiotherapy.

60
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In a severe COPD exacerbation with hypoxemia, which oxygen mask is preferred to avoid CO₂ retention?

Titrated Venturi Mask.

61
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How do NSAIDs affect blood pressure?

They can cause hypertension due to sodium and water retention.

62
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Which specific NSAID class is most associated with an imbalance between thromboxane and prostacyclin?

Selective COX-2 inhibitors.

63
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What is the mechanism of isotonic saline in managing allergic rhinitis?

It restores moisture and reduces epithelial microtrauma.

64
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What is the therapeutic window goal for oxygen therapy?

To stay within the 'Optimal Range' and avoid the 'Risk Zone' of toxicity or drive suppression.

65
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Identify the primary cardiovascular risks associated with NSAID toxicity.

Hypertension, MI (Myocardial Infarction), and stroke risk.