Class 7 Respiratory 3 Flashcards

1
Q

Allergic Rhinitis

A

A group of signs and symptoms, mainly in the nose and eyes, triggered by inhaling allergens

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2
Q

Names for allergic rhinitis

A
  • Hay fever
  • Seasonal allergies
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3
Q

Allergic Rhinitis common comorbidities

A
  • Asthma
  • Atopic dermatitis - Atopy
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4
Q

Allergic Rhinitis Pathogenesis

A

An acute vasomotor response caused by histamine and related substances released locally in the nose from IgE-coated mast cells.

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5
Q

Allergic Rhinitis Clinical Manifestations

A

Itchy nose and mouth, conjunctivitis, sneezing, sinus and nasal obstruction, coughing, wheezing, and coryza.

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6
Q

Allergic Rhinitis Diagnosis

A

History, symptoms, and skin test.

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7
Q

Allergic Rhinitis Treatments

A

Avoid triggers, antihistamines, decongestants, and injections.

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8
Q

Asthma

A
  • Increased bronchial responsiveness to stimuli, classified as reversible COPD
  • chronic inflammatory condition with acute exacerbations
  • complex disorder involving biochemical, autonomic, immunologic, infectious, endocrine, and psychological factors.
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9
Q

Asthma Incidence

A

The most common chronic disease in adults and children, more prevalent in males (2:1)

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10
Q

Extrinsic Asthma

A

Results from an allergy to specific triggers, primarily affecting children and young adults, and classified as hypersensitivity disorders.

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11
Q

Intrinsic Asthma

A

No known triggers, adult onset, possibly related to viral exposure, and referred to as post-viral asthma

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12
Q

Occupational Asthma

A

Narrowing of the airways caused by workplace exposure

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13
Q

Exercise-Induced Asthma

A

Bronchoconstriction can occur in individuals without other forms of asthma, affecting up to 20% of the healthy population, and is more common in cold temperatures.

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14
Q

Asthma Pathogenesis
An inflammatory response in the airway causes:

A

Cellular infiltration, epithelial disruption, mucosal edema, and mucous plugging

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15
Q

Asthma Pathogenesis
The inflammatory mediators produce:

A

Smooth muscle spasm, vascular congestion, increased vascular permeability, edema formation, production of thick mucous, and impaired mucociliary function

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16
Q

Asthma Pathogenesis
Mediators also cause

A
  • Thickening of airway walls
  • Increased contractile response of bronchial smooth muscle
17
Q

Asthma Pathogenesis:
Airway hyper-responsiveness, swollen airways, and mucous plugs lead to distal air trapping, resulting in:

A

Hypoxemia, obstructed airflow, and increased work of breathing.

18
Q

Asthma Clinical Manifestations
⬧Variation

A

Variation in presentation, cough, shortness of breath (SOB), wheezing, degree (mild, moderate, severe), and frequency.

19
Q

Asthma Clinical Manifestations Duration

A
  • Most attacks are short-lived with asymptomatic periods in between.
  • Repeated episodes may lead to barrel chest, elevated shoulders, and hypertonicity of accessory muscles.
  • Acute severe asthma (formerly status asthmaticus) is an unresponsive attack requiring emergency care and can be fatal.
20
Q

Asthma Diagnosis

A

History, clinical manifestation, and pulmonary function tests (FEV-1).

21
Q

Asthma Treatment

A

Identify and avoid specific triggers, and use medications such as corticosteroids and bronchodilators.

22
Q

Asthma Prognosis

A
  • Asthma may resolve in many children, but for about one in four, wheezing persists into adulthood or relapses later.
  • Approximately 4,000 deaths per year in the U.S. are asthma-related, most of which are preventable with treatment, leading to a good prognosis with proper access and adherence.
  • Over time, some patients may experience permanent airway remodeling, hindering normal lung function; early aggressive use of anti-inflammatory drugs may help prevent this
23
Q

PNEUMOCONIOSES

A

Restrictive lung diseases caused by inhalation of mineral dusts and inorganic particulates, resulting in permanent deposition of substantial amounts of particles in the lungs, particularly from inorganic dust like iron ore or coal.

24
Q

PNEUMOCONIOSES Classification

A

Most are classified as occupational diseases resulting from long-term workplace exposure, with the most common being coal worker’s pneumoconiosis (anthracosis), silicosis, and asbestosis.

25
Q

PNEUMOCONIOSES
⬧ Lung injury caused by mineral particles depends on

A

duration and concentration of exposure, as well as the size, shape, and solubility of the particles. Large dust particles are retained in nasal mucus and do not reach the lower respiratory tract.

26
Q

PNEUMOCONIOSES
⬧ Biochemical composition of the inhaled dust

A

Inert particles, such as coal, are less reactive;

silica particles are more reactive and cause greater tissue injury;

and asbestos particles are insoluble, remaining lodged in the lungs permanently.

27
Q

PNEUMOCONIOSES
Incidence and Etiology

A

Most commonly occurs in miners, sandblasters, stonecutters, asbestos workers, and insulators. Incidence increases with age due to cumulative exposure, though overall incidence is decreasing.

28
Q

Coal worker’s pneumoconiosis

A

Amorphous carbon particles are retained in the nasal mucosa. Inhaled coal dust is ingested by alveolar macrophages and later expectorated, leading to black lung

29
Q

PNEUMOCONIOSES
Silicosis

A

Macrophage cell membranes are destroyed, leading to their death and the release of silica, which is then ingested by other macrophages. Dead macrophages release substances that stimulate collagenous nodule formation. Confluent nodules destroy lung parenchyma, causing massive pulmonary fibrosis, with tuberculosis as a common complication.

If caused by volcanic ash, it is referred to as pneumonoultramicroscopicsilicovolcanoconiosis.

30
Q

PNEUMOCONIOSES
Asbestosis

A

Asbestos particles are engulfed by macrophages, which are activated to release inflammatory mediators, leading to an increased risk of lung cancer.

31
Q

PNEUMOCONIOSES
Clinical Manifestations

A

Progressive dyspnea, chest pain, chronic cough, and expectoration of mucus.

32
Q

PNEUMOCONIOSES
Management

A

Diagnosis is based on workplace exposure, chest X-ray, clinical manifestation, and pulmonary function tests. Prevention and safety measures are crucial, but there is no standard treatment, and the prognosis is generally poor.

33
Q

HYPERSENSITIVITY
PNEUMONITIS

A

Hypersensitivity reaction in the alveoli to inhaled organic particulates, considered an occupational pathology similar to pneumoconiosis, resulting in restrictive lung disease.

34
Q

HYPERSENSITIVITY
PNEUMONITIS Symptoms

A

Fever, cough, dyspnea, headache, pleuritis, clubbing, honeycomb lungs, bronchiolitis, and crackles

35
Q

HYPERSENSITIVITY
PNEUMONITIS Diagnosis

A

History, blood tests, X-ray, biopsy, and pulmonary function tests (PFT).

36
Q

HYPERSENSITIVITY
PNEUMONITIS Treatment

A

Avoid triggers and use anti-inflammatories.