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Pathopharm Exam 3 > Module 8: Part 3 (53-79) > Flashcards

Module 8: Part 3 (53-79) Flashcards

1
Q

Late asthmatic response (6)

A

Begins 4 to 8 hours after the early response
Chemotactic recruitment of lymphocytes, eosinophils, and neutrophils occurs
Air trapping
Hyperinflation distal to obstructions
Increased work of breathing
Hypoxemia

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2
Q

Chemotactic recruitment of lymphocytes, eosinophils, and neutrophils occurs in late asthmatic response causes… (5)

A

Prolonged smooth muscle contraction
Airway scarring
Increased bronchial hyperresponsiveness
Impaired mucociliary function with accumulation of mucous and cellular debris, forming plugs in the airways
Leads to airway remodeling if left untreated

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3
Q

clinical manifestations of asthma (8)

A

Asymptomatic between attacks
Chest constriction, expiratory wheezing, dyspnea, nonproductive coughing, prolonged expiration, tachycardia, tachypnea
Pulsus paradoxus
Status asthmaticus
Ominous signs of impending death

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4
Q

status asthmaticus

A

Bronchospasm not reversed by usual measures
Life threatening

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5
Q

What treatment is indicated for severe asthma and can potentially worsen asthma in some individuals?

A

Long-acting beta agonists

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6
Q

Ominous signs of impending death

A

Silent chest (no audible air movement) and a Paco2greater than 70 mm Hg

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7
Q

Asthma TX (5)

A

Immediate administration of O2 & inhaled beta-agonist bronchodilators
Oral corticosteroids administration early
Careful monitoring of gas exchange & airway obstruction in response to therapy
Antibiotics are not indicated for acute asthma unless a bacterial infection is documented
Education over allergens and irritants and peak flow meters

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8
Q

asthma Pharmacologic treatments (6)

A

Mildest form of asthma (intermittent): Short-acting beta-agonist inhalers
Persistent asthma: Antiinflammatory medications and inhaled corticosteroids—the mainstay of therapy
Not adequately controlled on inhaled corticosteroids: Leukotriene antagonists
Severe asthma: Long-acting beta agonists (can actually worsen asthma in some individuals)
Reduction of asthma exacerbations: Immunotherapy
Monoclonal antibodies to IgE

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9
Q

What are the ominous signs of impending death in status asthmaticus?

A

Silent chest (no audible air movement) and a PaCO2 greater than 70 mm Hg

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10
Q

Which medication is used as the mainstay of therapy for persistent asthma?

A

Inhaled corticosteroids​

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11
Q

Airflow limitation that is not fully reversible

A

COPD

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12
Q

Usually progressive and a/w an abnormal inflammatory response of the lung to noxious particles or gases

A

COPD

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13
Q

3rd leading cause of death in the US and the 6th leading cause of death worldwide

A

COPD

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14
Q

Chronic bronchitis plus emphysema

A

COPD

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15
Q

Air trapping

A
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16
Q

COPD risk factors (8)

A

Tobacco smoke
Occupational dusts and chemicals
Indoor air pollution from biomass fuel used for cooking and heating
Outdoor air pollution
Any factor that affects lung growth during gestation and childhood
Genetic susceptibilities

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17
Q

Which genetic mutation is associated with the development of emphysema even in nonsmokers?

A

Inherited mutation in the alpha-1 antitrypsin gene​

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18
Q

Inherited mutation in the alpha-1 antitrypsin gene results in the development of emphysema even in nonsmokers

A

Genetic susceptibilities of COPD

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19
Q

Hypersecretion of mucus &chronic productive cough that lasts at least 3 months of the year & for at least 2 consecutive years

A

Chronic Bronchitis

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20
Q

Chronic Bronchitis (4)

A

Inspired irritants increase mucous production, size & number of mucous glands, & bronchial edema; mucus is thicker than normal
Hypertrophied bronchial smooth muscle
Hypoxemia & hypercapnia
Airways collapse early in expiration, trapping gas in the lung

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21
Q

Chronic Bronchitis Clinical manifestations (5)

A

Decreased exercise tolerance
Wheezing and shortness of breath
Productive cough (“smoker’s cough”) becomes copious
Polycythemia
Decreased FEV1

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22
Q

Chronic Bronchitis TX (8)

A

Smoking cessation: Disease progression can be halted
Bronchodilators
Expectorants
Chest physical therapy
Antibiotics
Steroids
Mechanical ventilation, if needed
Oxygen therapy

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23
Q

Chronic Bronchitis teaching (4)

A

Nutritional counseling
Respiratory hygiene
Recognition of the early signs of infection
Techniques that relieve dyspnea, such as pursed-lip breathing

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24
Q

Abnormal permanent enlargement of thegas-exchange airways accompanied by the destruction of the alveolar walls w/out obvious fibrosis

A

Emphysema

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25
Q

Loss of elastic recoil

A

Emphysema

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26
Q

Inherited deficiency of the enzyme α1-antitrypsin

A

Primary emphysema

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27
Q

Secondary emphysema

A

Cigarette smoke: Main cause
Air pollution, occupational exposures, and childhood respiratory infections: Possible contributors

28
Q

Centriacinar (centrilobular) pathophysiology

A

Septal destruction occurs in the respiratory bronchioles and alveolar ducts, usually in the upper lobes.
Alveolar sac (alveoli distal to the respiratory bronchiole) remains intact.
Tends to occur in smokers with chronic bronchitis.

29
Q

Panacinar (Panlobular) pathophisiology

A

Involves the entire acinus.
Damage is more randomly distributed.
Involves lower lobes of the lung

30
Q

Emphysema Pathophysiology

A

Destruction of the alveoli occurs thru breakdown of elastin in the septa as a result of an imbalance between proteases and antiproteases, oxidative stress, and apoptosis of the lung’s structural cells.
Alveolar destruction also produces large air spaces within the lung parenchyma (bullae) and air spaces adjacent to pleurae (blebs).

31
Q

emphysema Clinical manifestations (7)

A

Dyspnea on exertion
Later progresses to marked dyspnea, even at rest
Little coughing and very little sputum
Thin
Tachypnea with prolonged expiration; use of accessory muscles for ventilation; pursed lips
Increased anteroposterior diameter of the chest (barrel chest)
To increase lung capacity: Leans forward with arms extended and braced on knees when sitting

32
Q

emphysema treatment (9)

A

Oxygen; may require noninvasive positive pressure ventilation or mechanical ventilation
Inhaled bronchodilators by either an inhaler or a nebulizer
Immediate administration of oral corticosteroids and antibiotics
Inhaled anticholinergic agents and beta agonists
Inhaled corticosteroids can be added
Smoking cessation
Pulmonary rehabilitation
Improved nutrition
Breathing techniques

33
Q

Infection of the lower respiratory tract

A

Pneumonia

34
Q

Responsible for more disease and death than any other infection

A

Pneumonia

35
Q

Community-acquired pneumonia strain

A

Streptococcus pneumoniae

36
Q

PNA Routes of infection (4)

A

Aspiration
Inhalation
Endotracheal tubes and suctioning
Respiratory defenses cannot destroy the microorganism

37
Q

Pneumococcal pneumonia
Four phases

A

Consolidation
Red hepatization
Gray hepatization
Resolution

38
Q

ALI, resulting in inflammatory cytokines and cells, causes alveolar edema

A

Pneumococcal pneumonia

39
Q

Edema creates a medium for the multiplication of bacteria and aids in the spread of infection into adjacent portions of the lung

A

Pneumococcal pneumonia

40
Q

Involved lobe undergoes consolidation

A

Pneumococcal pneumonia

41
Q

Is seasonal; usually mild and self-limiting & can set the stage for a secondary bacterial infxn

A

Viral pneumonia

42
Q

Most common form of viral PNA:

A

Influenza

43
Q

T/F
Community-acquired pneumonia is commonly caused by Streptococcus pneumoniae

A

True

44
Q

T/F Viral pneumonia is typically severe and requires intensive treatment

A

False
(Viral pneumonia is usually mild and self-limiting)​

45
Q

T/F
Secondary emphysema is primarily caused by an inherited deficiency of the enzyme α1-antitrypsin

A

False
(Primary emphysema is caused by the inherited deficiency, while secondary is mainly due to cigarette smoke)​

46
Q

T/F
Pneumonia can be transmitted through inhalation, aspiration, and endotracheal tubes

A

True

47
Q

T/F
Emphysema treatment does not include the use of inhaled corticosteroids

A

False
(Inhaled corticosteroids can be used in the treatment of emphysema)

48
Q

T/F
Pulsus paradoxus is a decrease in systolic blood pressure during inspiration seen in severe asthma attacks

A

True

49
Q

T/F
In emphysema, centriacinar (centrilobular) destruction occurs in the lower lobes of the lungs.

A

False (Centriacinar destruction usually occurs in the upper lobes)

50
Q

T/F
Air trapping and increased work of breathing are common features in COPD

A

True

51
Q

T/F
Indoor air pollution from biomass fuel used for cooking and heating is not a significant risk factor for COPD

A

False
(It is a significant risk factor)​

52
Q

T/F
Chronic bronchitis is characterized by increased FEV1 (Forced Expiratory Volume in 1 second)

A

False
caused by decreased FEV1 (Forced Expiratory Volume in 1 second)

53
Q

T/F
Pursed-lip breathing is a technique that can help individuals with emphysema increase their lung capacity

A

True

54
Q

T/F
Nosocomial pneumonia refers to pneumonia acquired outside of healthcare settings

A

False
(Nosocomial pneumonia is hospital-acquired)​

55
Q

T/F
Viral pneumonia is always a primary infection and does not predispose individuals to secondary bacterial infections

A

False
(It can set the stage for secondary bacterial infections)​

56
Q

T/F
The late asthmatic response begins 4 to 8 hours after the early response

A

True

57
Q

T/F
The early asthmatic response typically begins 12 to 24 hours after allergen exposure

A

False
(The early response begins within minutes)

58
Q

T/F
Occupational dusts and chemicals are not considered significant risk factors for COPD

A

False
False (They are significant risk factors)

59
Q

T/F
The main symptom of chronic bronchitis is a dry cough with little to no sputum production

A

False
(The main symptom is a productive cough with copious sputum production)

59
Q
A
60
Q

T/F
Polycythemia is not a common clinical manifestation of chronic bronchitis

A

False
(Polycythemia is a common manifestation due to chronic hypoxemia)

61
Q

How long must symptoms persist for a diagnosis of chronic bronchitis?

A

At least 3 months of the year and for at least 2 consecutive years​

61
Q

What physical posture is often adopted by individuals with emphysema to increase lung capacity?

A

Leaning forward with arms extended and braced on knees when sitting

61
Q

What respiratory hygiene technique can help relieve dyspnea in chronic bronchitis patients?

A

Pursed-lip breathing​

61
Q

T/F
Pneumococcal pneumonia resolves without progressing through distinct phases

A

False
(Pneumococcal pneumonia typically progresses through phases of consolidation, red hepatization, gray hepatization, and resolution)

62
Q

T/F
Community-acquired pneumonia is most commonly caused by viruses rather than bacteria

A

False
(Community-acquired pneumonia is most commonly caused by bacteria, such as Streptococcus pneumoniae)

Pathopharm Exam 3 (18 decks)

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