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Pulmonology > OHS and OSAHS > Flashcards

OHS and OSAHS Flashcards

1
Q

Diagnosis of OHS. (Harrison’s 19th edition, pp 1723)

A

BMI >/= 30kg/m2

PaCO2 >/= 45mmHg in the absence of other known causes of hypercapnia

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2
Q

Number of apneas plus hypopneas per hour of sleep. (Harrison’s 19th edition, pp 1725)

A

Apnea-Hypopanea Index (AHI)

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3
Q

Number of apneas plus hypopneas plus RERAs per hour of sleep. (Harrison’s 19th edition, pp 1725)

A

Respiratory Disturbance Index (RDI)

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4
Q

A partially obstructed breath that does not meet the criteria for hypoapnea but provides evidence of increasing inspiratory effort (usually through pleural pressure monitoring) puncturated by an arousal. (Harrison’s 19th edition, pp 1725)

A

Respiratory Effort-Related Arousal (RERA)

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5
Q

Cessation of airflow for >/= 10 sec during sleep. (Harrison’s 19th edition, pp 1725)

A

Apnea
Obstructive = with persistence respiratory effort
Central = absence of respiratory effort

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6
Q

Mild OSAHS. (Harrison’s 19th edition, pp 1725)

A

AHI of 5-14 events/hr

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7
Q

Moderate OSAHS. (Harrison’s 19th edition, pp 1725)

A

AHI of 15-29 events/hr

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8
Q

Severe OSAHS. (Harrison’s 19th edition, pp 1725)

A

AHI of >/= 30 events/hr

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9
Q

A partially obstructed breath, typically within a hypopnea or RERA, identified by a flattened or “scooped-out” inspiratory flow shape. (Harrison’s 19th edition, pp 1725)

A

Flow limited breath

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10
Q

A 30% reduction in airflow for at least 10 sec during sleep that is accompanied by either a 3% desaturation or an arousal. (Harrison’s 19th edition, pp 1725)

A

Hypopnea

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11
Q

Standard medical therapy with the highest level of evidence for efficacy. (Harrison’s 19th edition, pp 1727)

A

CPAP

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12
Q

Side effects of Continuous Positive Airway Pressure (CPAP). (Harrison’s 19th edition, pp 1727)

A 
Nasal Congestion
Claustrophobia
Difficulty exhaling
Bruised nasal ridge
Aerophagia
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13
Q

Risk for cardiovascular, cerebrovascular and metabolic diseases that OSAHS significantly increases. (Harrison’s 19th edition, pp 1726)

A 
Coronary artery disease
Heart failure (with or without reduced ejection fraction)
Atrial and ventricular arrhythmias
Atherosclerosis
Stroke
Diabetes
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14
Q

Treatment for nasal congestion due to CPAP. (Harrison’s 19th edition, pp 1727)

A

Provide heated humidification

Administer saline/steroid nasal sprays

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15
Q

Treatment for claustrophobia due to CPAP. (Harrison’s 19th edition, pp 1727)

A 
Change mask interface (to nasal prongs)
Promote habituation (practice breathing on CPAP while awake)
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16
Q

Factors for residual sleepiness. (Harrison’s 19th edition, pp 1726)

A

Suboptimal treatment adherence
Insufficient sleep time
Other sleep disorders
Prior hypoxic-mediated damage in the brain (areas involved in alertness)
Somnogenic cytokines (from visceral adipose tissue)

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17
Q

Treatment for difficulty of exhaling due to CPAP. (Harrison’s 19th edition, pp 1727)

A

Temporarily reduce pressure

Provide bilevel positive airway pressure

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18
Q

Treatment for bruised nasal ridge due to CPAP. (Harrison’s 19th edition, pp 1727)

A

Change mask interface

Provide protective padding

19
Q

Treatment for aerophagia due to CPAP. (Harrison’s 19th edition, pp 1727)

A

Administer antacids

20
Q

Proportion of patients with moderate to severe OSAHS that report daytime sleepiness. (Harrison’s 19th edition, pp 1726)

A

50%

21
Q

Incidence of accidents due to OSAHS. (Harrison’s 19th edition, pp 1726)

A

2 fold increased risk of occupational accidents

7 times more often involved in motor vehicular accidents

22
Q

Most common complaint in OSAHS. (Harrison’s 19th edition, pp 1724)

A

Snoring

23
Q

Most common daytime symptom in OSAHS. (Harrison’s 19th edition, pp 1724)

A

Sleepiness

24
Q

Major risk factors for OSAHS. (Harrison’s 19th edition, pp 1724)

A

Obesity

Male gender

25
Q

Risk factors for OSAHS. (Harrison’s 19th edition, pp 1724)

A 
Obesity
Male gender
Variation in craniofacial morphology
Genetic
Age (elderly)
Diabetes
Hypertension
Race (Asian)
26
Q

The Gold standard for diagnosis of OSAHS. (Harrison’s 19th edition, pp 1725)

A

Overnight polysomnogram (PSG)

27
Q

A cost-effective alternative means for diagnosing patients without significant comorbidity who have a high pretest probability of OSAHS. (Harrison’s 19th edition, pp 1725)

A

Home sleep tests

28
Q

A ____ weight gain associated with a ____ increase in AHI. (Harrison’s 19th edition, pp 1724)

A

10%, > 30%

29
Q

Absence of the following does not exclude the diagnosis of OSAHS. (Harrison’s 19th edition, pp 1724)

A

Snoring

Obesity

30
Q

The most common medical cause of daytime sleepiness and negatively influences quality of life. (Harrison’s 19th edition, pp 1725)

A

Obstructive Sleep Apnea/Hypopnea Syndrome (OSAHS)

31
Q

The major contributor to cardiac, cerebrovascular and metabolic disorders as well as to premature death. (Harrison’s 19th edition, pp 1725)

A

Obstructive Sleep Apnea/Hypopnea Syndrome (OSAHS)

32
Q

Consequences of Hypoxemia in OSAHS. (Harrison’s 19th edition, pp 1725)

A

Stimulate release of acute-phase proteins and reactive oxygen species
Exacerbate insulin resistance and lipolysis
Augment prothrombotic and proinflammatory state
Electrical remodeling of the heart
Myocyte injury

33
Q

Consequences of Sympathetic-parasympathetic imbalance. (Harrison’s 19th edition, pp 1725)

A

Electrical remodeling of the heart

Myocyte injury

34
Q

Consequences of inspiratory effort against an occluded airway. (Harrison’s 19th edition, pp 1725)

A

Large intrathoracic negative pressure swings
Altering cardiac preload and afterload
Cardiac remodeling
Reduced cardiac function

35
Q

Consequences of OSAHS-related respiratory events. (Harrison’s 19th edition, pp 1725)

A

Stimulate sympathetic overactivity
Acute blood pressure surges during sleep
Endothelial damage
Nocturnal as well as daytime hypertension

36
Q

Effect of CPAP therapy regarding hypertension in patients with OSAHS. (Harrison’s 19th edition, pp 1725)

A

Modest reduction in 24h ambulatory blood pressure (averaging 2-4mmHg)
Larger improvements observed if with high AHIs and sleepiness

37
Q

Causes of elevated blood pressure in OSAHS. (Harrison’s 19th edition, pp 1725)

A

Augmented sympathetic nervous system activation
Alterations in the rennin-angiotensin-aldosterone system (RAAS)
Alterations in the fluid balance

38
Q

Effect of OSAHS in the blood pressure. (Harrison’s 19th edition, pp 1725)

A

Raise BP to prehypertensive to hypertensive ranges
Increase prevalence of a non-dipping overnight blood pressure pattern
Increase risk of resistant hypertension

39
Q

Absence of the typical 10-mmHg fall during sleep from blood pressure while awake. (Harrison’s 19th edition, pp 1725)

A

“Non dipping” pattern of overnight blood pressure

40
Q

Evaluation and screening for OSAHS should be done to the following patients. (Harrison’s 19th edition, pp 1724)

A

Symptoms of OSAHS

One or more risk factors

41
Q

Basis for the definition of OSAHS. (Harrison’s 19th edition, pp 1723)

A

Nocturnal and daytime symptoms

Sleep study findings

42
Q

Diagnosis of OSAHS requires the following. (Harrison’s 19th edition, pp 1723)

A

(1) Symptoms of nocturnal breathing disturbances or daytime sleepiness/fatigue that occurs despite sufficient opportunities to sleep and is unexplained by the other medical problems
(2) >/= 5 episodes of Apnea/Hypopnea Index (AHI)
(may also be diagnosed in the absence of symptoms if AHI > 15)

43
Q

Most common level in which airway may collapse. (Harrison’s 19th edition, pp 1723)

A

Soft palate

44
Q

Various levels in which airway may collapse. (Harrison’s 19th edition, pp 1723)

A

Soft palate
Tongue base
Lateral pharyngeal walls
Epiglottis

Pulmonology (16 decks)

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