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3 Cardiopulmonary > Respiratory pathophys > Flashcards

Respiratory pathophys Flashcards

1
Q

Upper respiratory

A

above the larynx
pharyngitis, otitis media, sinusitis

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2
Q

Lower respiratory tract

A

below the larynx
acute bronchitis, chronic bronchitis, pneumonia, TB

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3
Q

Defense mechanisms against infections, URT

A

nasal hairs, gag reflex, epiglottis, mucosal lymphoid tissue, secretory immunoglobulins

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4
Q

Defense mechanisms against infection, LRT

A

secretory IGA, ciliated epithelium, bronchospasm, cough reflex, alveolar macrophages

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5
Q

Conditions that impair host defenses

A

Cigarette smoking
Intubation
Recurrent laryngeal nerve damage
Absent gag reflex
Cystic fibrosis
Congenital absence of IgA
Oversedation

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6
Q

Cigarette smoking

A

paralyzes cilia, destroys epithelium, decreases number of macrophages, decreases macrophages’ activity

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7
Q

Intubation

A

impairment of host defenses, bypasses upper respiratory tract

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8
Q

Recurrent laryngeal nerve damage

A

at risk during surgeries
speech, swallowing, coughing

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9
Q

Absent gag reflex

A

1/3 individuals don’t have it, increased risk for aspiration

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10
Q

Cystic fibrosis

A

overproduction of thick sputum, risk for increased infection

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11
Q

Congenital absence of IgA

A

increased risk for infection

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12
Q

Oversedation

A

decreases ability to cough
usually occurs was opiates or other CNS depressants

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13
Q

Pathogenesis of lower respiratory tract infections

A
  1. nasopharyngeal colonization with the organism and subsequent aspiration of nasopharyngeal secretions
  2. reflux of GI bacteria and aspiration of contents in presence of antacid use
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14
Q

Acute bronchitis

A

D: inflammation of bronchial mucosa and increased endobronchial mucus production, due to infection
E: viral and seasonal
CP: dry cough or cough with purulent or mucoid sputum. myalgias, sore throat
T: no antibiotics

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15
Q

Pneumonias

A

inflammation of lungs with consolidation (something in lungs besides air

can be bacterial (community, nosocomial, aspiration), viral, mycoplasma

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16
Q

Atelectasis

A

partial or complete collapse of lung

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17
Q

_____ can lead to aspiration pneumonia

A

dysphagia

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18
Q

Dysphagia

A

difficulty swallowing, can lead to aspiration pneumonia

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19
Q

How can we prevent aspiration?

A

NPO
Positioning, semiupright in bed with HOB >30 (semi-fowler and fowler’s)

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20
Q

Clinical Presentation of Bacterial pneumonia

A

abrupt onset of high fever
chills, cough with purulent sputum
chest pain, dyspnea, myalgias, malaise, tachycardia
altered mental status in elderly

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21
Q

Diagnosis and Treatment of Bacterial Pneumonia

A

DX: hx, physical exam, chest xray, blood cultures, sputum culture, WBC count
Treatment: ABX, bronchodilators, airway clearance techniques

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22
Q

Outcome of bacterial pneumonias

A

Good in young and middle-aged, little or no permanent defect

elderly can die, 30-50% in bacteremic pneumonia. Harder to diagnose

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23
Q

Clinical presentation & Diagnosis of Viral pneumonia

A

S/S: fever, dry cough, myalgias, tachypnea, flu-like symptoms, scattered crackles, hypoxemia
DX: History, PE, CXR

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24
Q

Treatment and Outcome Viral Pneumonias

A

Treatment: symptomatic, no ACTs

Outcome: usually resolvles w/out complications or lasting damage, mortality <5%.

Covid-19 is an example

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25
Q

Pleurisy

A

inflammation of pleural lining of the lung with exudate formation into pleural cavity (pleural effusion)

secondary to pneumonia
pleural infection w/TB or influenza
Secondary to other systemic illnesses

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26
Q

Pleurisy Clinical Presentation

A

Chest pain due to edema
referred to chest wall, abdomen, upper trap, shoulder
Cough, fever, tachypnea

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27
Q

Diagnosis and Treatment of Pleurisy

A

Dx: History & PE
pleural friction rub. splinting area of pain may decrease discomfort

Tx: time, NSAIDs, other analgesics

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28
Q

TB Etiology

A

acquired by inhalation of m. tuberculosis in aerosols & dusts

airborne transmission extremely efficient, droplets are sprayed by infectious individuals

thrives in crowding, poverty, poor nutrition

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29
Q

Primary Infection of TB

A

latent TB infection

-transient bacteremic phase brought under control by host immune system
-mild symptoms or asymptomatic
-lung lesion and enlarged lymph nodes walled off (granuloma)

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30
Q

Secondary active TB infection clinical presentation

A

TB disease, active TB

lapse in immune competence allows reactivation of dormant mycobacteria

any organ can be affected, lungs are the most due to high PO2

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31
Q

Dx and Tx of TB

A

DX = history, PE, CXR, sputum

Tx: anti-TB drug combo (isoniaxid, rifampin, ethambutol

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32
Q

Outcome and Prevention of TB

A

Outcome: modern cure rates are high. Development of multi-drug resistant TB (low compliance), TB is leading cause of people with HIV

Prevention: improved social conditions, immunizations, wear appropriate PPE

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33
Q

Tuberculosis Risk Factors

A

HIV
Diabetes
Substance abuse
Homelessness
Migrant workers
healthcare workers
jails
nursing homes

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34
Q

COPD

A

preventable and treatable disease
airflow limitation that is progressive
reaction to noxious particles or gases

chronic airflow limitation caused by mixture of small airway disease and parenchymal destruction

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35
Q

How does airflow obstruction occur in COPD?

A

Inflammation within airways
Mucus obstructs airways
Remodeling/scarring
airways collapse due to damaged parenchyma

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36
Q

How is COPD diagnosed?

A

S/S: shortness of breath, chronic cough, sputum
RF: host factors, tobacco, occupation, pollution

Spirometery: required to establish dx
other tests: CXR, ABGs, CBC/increased HcT

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37
Q

Clinical Features of COPD

A

40s to 50s with cough or acute chest illness
dyspnea on exertion
Hx of episodic wheezing and dyspnea

CXR: hyperinflated lungs, flat diaphragm, enlarged right ventricle

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38
Q

Risk factors for COPD

A

Environment
Host

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39
Q

Environment for COPD

A

Tobacco smoke
Occupational exposure
Indoor/outdoor air pollution
infections
poverty

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40
Q

Pack-year

A

1 pack per day x 40 years
2 packs per day x 20 years

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41
Q

Host and COPD

A

Genetic predisposition
specific gene abnormality (antitrupsin deficiency)
aging (increased
females
early lung development

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42
Q

____ is required to make a diagnosis of COPD

A

spirometry

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43
Q

FEV levels and COPD

A

FEV1/FVC <.70 confirms persistent airflow limitations

44
Q

COPD Treatment Goals

A

Reduce Symptoms = reduce airflow obstruction, improve ex tolerance, improve QOL

Limit disease progression = prevent and treat exacerbations, reduce mortality

45
Q

5 As of smoking cessation

A

Ask = identify tobacco users
Advise = 3 minute counseling session
Assess = determine willingness to quit
Assist = aid pt in quitting
Arrange = schedule f/u contact

46
Q

5 Rs of smoking cessation

A

Relevance–help pt identify why quitting is relevant now
Risks–encourage them saying negative outcomes
Rewards–help pt identify benefits
Roadblocks–help identify obstacles in quitting
Repetitions–take more than 1 time to quit

47
Q

Medications for COPD

A

does not stop long term decline in lung function

goals are instead to prevent/control symptoms, reduce frequency of exacerbations, improve ex tolerance

48
Q

Drug classes for COPD

A

Bronchodilators
Glucocorticoids
Supplemental O2

49
Q

Bronchodilators

A

prn or regular use reduce airflow obstruction

B2 adrenergic agonists, anticholinergics, methylxanthines

50
Q

Glucocorticoids

A

short-term use only
prednisone

51
Q

Supplemental O2

A

improve hemodynamics, lung mechanics and survival
usually for severe COPD pts with PaO2 thats less than 55

52
Q

Treatment Options for COPD

A

Reduce risk factors
Drug classes for COPD
Surgery for COPD
Pulmonary Rehab

53
Q

Surgery for COPD

A

Bullectomy = removal of large distended portion of lung
Lung transplantation = only in very advanced and select cases

54
Q

Pulmonary Rehab

A

for improvement in dyspnea, health status, and QOL in stable pts, reducing symptoms of anxiety and depression

55
Q

COPD Prognosis

A

w/out smoking cessation, lungs will continue to lose function

peripheral skeletal muscle dysfunction, muscle wasting, osteoporosis are also possible conditions.

be cautious with positioning and spinal mobs

56
Q

Blue bloater is known as

A

chronic bronchitis

57
Q

Pink puffer is known as

A

emphysema

58
Q

Barrel-chested

A

describes the rounded, bulging chest that resembles shape of barrel
not a disease, may indicate underlying condition

59
Q

Chronic bronchitis

A

chronic inflammation of bronchi/bronchioles. increased tracheobronchial mucus production sufficient to cause a cough producing sputum on most days for 3 months during consecutive years

blue bloater

60
Q

Pathogenesis of chronic bronchitis

A

increased size of tracheobronchial mucus glands and increased mucus production

decreased # of cilia

bronchoconstriction due to irritation in tracheobronchial tree

61
Q

How to improve exercise tolerance in chronic bronchitis

A

hydration
airway clearance techniques
ventilatory strategies
smoking cessation
prevention of infections
maintain healthy immune system

62
Q

Emphysema

A

abnormal permanent enlargement of airspaces distal to terminal bronchioles accompanied by destruction of alveolar walls

can be centrilobular (more common) or panlobular

pink puffer

63
Q

Pathogenesis of emphysema

A

inflammation, edema, thickened bronchiolar walls

lungs become hyperinflated, enlarged air space in parenchyma

bullae = spaces greater than 1 cm form that allow air in but not out

64
Q

How to improve exercise tolerance for emphysema

A

ventilatory strategies
teach energy conservation techniques
teach breath control (pursed lip breathing)
infection control
flu shots
hydration and nutrition

65
Q

Pores of Kohn

A

interalveolar connections
pausing at top of breath allows for air to disperse through alveoli

66
Q

Cor pulmonale

A

right ventricular failure. causes edema (blue bloater)

67
Q

Summary of Emphysema

A

60 yr old+
severe dyspnea
scanty/mucoid sputum
not frequent infections
hyperinflation, bullae
normal PaCO2, low PaO2, low hematocrit
rare for cor pulmonale
severely decreased elastic recoil

68
Q

Summary of Chronic Bronchitis

A

+50 yr olds
mild dyspnea
copious, purulent sputum
frequent infections
large heart
increased PaCO2, low PaO2, increased hematocrit
common cor pulmonale
normal elastic recoil

69
Q

Bronchiectasis

A

abnormal dilation and anatomical distortion of medium sized bronchi and bronchioles, associated with previous chronic necrotizing infection

w/intervention, pts can expect normal life expectancy

70
Q

Pathogenesis of bronchiectasis

A

obstruction of airways and recurrent respiratory infections

mucosa destroyed, replaced by scar

damaged bronchi become permanently dilated and distorted

recurrent infections, cystic fibrosis, TB, fungal infections, kung abscesses, pneumonia

71
Q

Clinical Presentation of Bronchiectasis

A

chronic productive cough
dyspnea and tachypnea
increased PCO2, decreased PO2
FINGER CLUBBING

72
Q

Treatment Bronchiectasis

A

IV fluids
IV/oral ABX
hydration
Chest PT and other ACTs
education

73
Q

Strategies to improve ex tolerance, Bronchiectasis

A

Hydration
ACTs
proper medication use, frequent ABX use
surgical lung resection

74
Q

Cystic Fibrosis

A

genetic disorder inherited in autosomal recessive pattern. characterized by widespread abnormalities of all exocrine glands w/pathology in bronchial mucus glands, exocrine glands of pancreas, sweat glands

75
Q

Clinical Presentation of CF

A

productive cough
proliferative sputum production
decreased ex tolerance
recurrent hemoptysis (bloody cough)
steatorrhea (oily stools)

76
Q

Dx of CF

A

New born genetic screening test
sweat chloride test
hypoxemia, respiratory acidosis, mixed obstructive/restrictive pattern on labs
eval at CF care center

77
Q

Treatment options for CF

A

ideal place to receive treatment is at a CF care center

education, bronchodilators, ACTs, exercise, pancreatic enzyme replacement, nutritional support, antibiotics, mucus thinners, modulators, lung transplantation

78
Q

Prognosis of CF

A

highly variable presentation and severity
life expectancy has begun to increase

79
Q

Strategies to improve exercise tolerance, CF

A

hydration
pancreatic enzymes to promote fat digestion and improve nutrition
aggressive ACTs
respiratory muscle training
strength and endurance ex

80
Q

Asthma

A

chronic inflammatory disorder of airways, characterized by increased responsiveness of airway smooth muscle to various stimuli. narrowing of airways reverses either spontaneously or due to treatment

81
Q

Epidemiology of Asthma

A

higher in boys, higher in women
african americans have more attacks
low income families
higher and worst incomes in rural

82
Q

Asthma triggers

A

Allergic: pollen, animal dander, feathers, molds, dust, food

Nonallergic: air pollution, weather, infections, medications, emotions, exercise

83
Q

Pathogenesis of Asthma

A

1.some stimulus triggers cascade inflammatory cell migration, activation.
2.process is multicellular–> mast cells, eosinophils, t-lymph, macrophages, neutrophils
3.repetitive inflammation increases bronchial hyper-reactivity
4.during acute asthma attack, lumens of airways are narrowed by combo of muscle spasm, inflammation, mucus overproduction

84
Q

3 S’s of asthma

A

spasm
swelling
secretions

85
Q

Presentation of acute asthma attack

A

increased work of breathing and use of accessory muscles
tachypnea
audible wheezing in expiratory phase
dry cough
chest tightness
waking at night

86
Q

Dx of asthma

A

no single universally accepted test
history, spirometry (improvement in FEV1 by 12-15%), peak expiratory flow rate

87
Q

Exercise-induced asthma

A

transient airway obstruction occurring. also called bronchospasm. during or after exercise. usually does not involve inflammation and mucus formation

symptoms include wheezing, coughing, SOB, chest discomfort

88
Q

Pathophysiology of EIB

A
  1. bronchial hyper-reactivity most likely initiated by loss of airway surface liquid
    2.air are humidified in conducting zone, results in cells losing water. after exercise is done, influx of water restores osmolarity
    3.bronchospasm is triggered by loss of heat/water from airway
89
Q

Diagnosis of EIB

A

pt self-reported symptoms
spirometry (pre and post exercise PFT)
10-15% decrease in post-exercise FEV1

90
Q

Triggers for EIB

A

hyperventilation
respiratory heat loss (cold air)
increased osmolarity caused by respiratory water loss (dry air)

91
Q

RF for EIB

A

80-90% of those diagnosed with asthma
winter sport athletes

92
Q

Prevention of EIB

A

Good control of asthma
Pre-exercise prevention
gentle, intermittent warm-up
promote nasal breathing
vary exercise duration
incorporate proper cool down
ex in warm humid environment

93
Q

Good control of asthma

A

controller medications may not prevent EIB

peak flow meter to measure amount of air flow in one fast, hard exhalation (peak expiratory flow rate)

94
Q

Pre-exercise prevention for EIB

A

take 20-30 minutes before exercise to take short-acting bronchodilator. mast cell stabilizer, prevents histamine release

95
Q

What to do during an asthma attack?

A

stop an activity
use rescue inhaler = short acting bronchodilator
sit up
call 911
continue to use rescue inhaler if S/S improve

96
Q

Goals for asthma treatment

A

-Control for chronic respiratory S/S
-appropriate medication intervention, Controllers & Relievers

-minimize use of rescue inhalers
-patient education
-ex symptom-free
-review status frequently

97
Q

Asthma Action Plan

A

everyone with asthma needs their own action plan
goal is to prevent and control asthma attacks, HCP works w/pt to create plan. Typically has a green, yellow, red level

98
Q

Relievers

A

relieve acute bronchoconstriction
taken on as needed basis
may supplement controllers
relaxes smooth muscle increase airflow

types: 1. short acting beta adrenergic agonists (albuterol) 2. oral glucocorticoids (at hospital)

99
Q

Controllers

A

provide long-term control by decreasing inflammation. taken daily, foundation for asthma management

types: inhaled glucocorticoids, leukotriene modifiers, long-acting Beta adrenergic agonists (salmetrol)

100
Q

Short-acting relievers

A

albuterol
prednisolone
prednisone

101
Q

Long-acting anti-inflammatory controller

A

salmeterol, beta 2 agonist

102
Q

Inhaled glucocorticoid

A

CONTROLLER
most effective, potent, and frequently used anti-inflammatory asthma meds

fewer ADRs and shorter onset of action time than oral form
improves pulmonary function w/long term use.

103
Q

Actions of Inhaled glucocrticoid

A

inhibit multiple segments of asthmatic cascade
suppress generation of cytokines
decrease population of airway eosinophils
prevent inflammatory mediator release

104
Q

Leukotriene modifiers

A

oral
long-term control and prevention of symptoms
protect against EIB
decrease needed dose of inhaled glucocorticoid

anti-inflammatory
block leukotriene receptors in airways which are involved in inflammatory

105
Q

Long acting Beta agonists

A

decrease frequency and intensity of asthma exacerbations

may be used as supplement to inhaled glucocorticoids

some provide prophylaxis against EIB for up to 8 hr

actions: bronchodilation–effective up to 12 hours, increase expiratory flow rate

106
Q

Strategies we can teach to improve ex tolerance and asthma

A

coordinate activities w/inhalers
evaluate and instruct in proper use of MDIs
warm-up and stretch active muscles and chest wall
slow initiation and pacing, energy conservation
ventilatory strategies
incorporate cool down
hydration

107
Q

Prognosis of asthma

A

variable disease course
reversible w/meds and respiratory therapy
untreated = damage
early detection is imperative

3 Cardiopulmonary (9 decks)

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