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Medical Studies 1 > Week 6 Respiratory > Flashcards

Week 6 Respiratory Flashcards

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USMLE® Step 1 flashcards
1
Q

What is normal sleep architecture

A

-normal human sleep comprises two states (REM and NREM sleep
-clinical sleep staging is based on EEG , EOG and submental (EMG criteria)

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2
Q

what are the stages of NREM sleep

A

-N1,N2 and N3

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3
Q

what are alpha waves representative of

BATD

A

awake but resting, eyes closed, not mentally concentrating on any one subject or task

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4
Q

what are beta waves representative of

BATD

A

receiving sensory stimulation or engaged in concentrated mental activity

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5
Q

what are theta waves representative of

BATD

A

drowsy or sleepy state in adults, common in children

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6
Q

what are delta waves representative of

BATD

A

deep sleep

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7
Q

what are the stages of sleep

A

W, N1,N2,N3,REM

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8
Q

features of W stage of sleep

A

-alpha waves (8-13Hz)
*5% of sleep
-function=normal bodily activity

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9
Q

features of N1 stage of sleep

A

-theta waves (4-7Hz)
*5% of sleep
-function=cardiovascular rest

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10
Q

features of N2 stage of sleep

A

-sleep spindles and k complexes
*50% of sleep
-function=cardiovascular rest

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11
Q

features of N3 sleep

A

-delta waves (0.5-2Hz)
*15% of sleep
-function=cardiovascular rest

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12
Q

features of REM sleep

A

-sawtooth waves
*25% of sleep
-function=cardiovascular activation

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13
Q

Discuss the normal changes in ventilation during sleep

A

-drive to breathe is reduced during sleep
-upper airway resistance increases during sleep , reducing breathing capacity
-metabolic rate drops by 10-15% during sleep
-PCO2 increases and PO2 decreases
-hypoventilation occurs in sleep

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14
Q

Define obstructive sleep apnoea

A

disordered breathing during sleep in which the airway is mechanically obstructed, leading to cessation of airflow

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15
Q

what are the clinical features of OSA

A

-daytime somnolence
-nocturia
-cognitive impairment
-dry mouth
-large neck (risk factor)
-witnessed apnoea
-insomnia
-morning headaches
-high BMI
-crowded oropharynx

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16
Q

what is the mallampati score

A

-clinical assessment tool
-pt sits upright with mouth open and tongue protruded
-based to visualisation of uvula,softpalate,pillars

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17
Q

Class I of mallampati score

A

complete visualisation of uvula, soft palate and fauces

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18
Q

Class II of mallampati score

A

visibility of soft palate and part of uvula

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19
Q

Class III of mallampati score

A

only see soft palate

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20
Q

Class IV of mallampati score

A

only can see hard palate

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21
Q

How is OSA diagnosed

A

polysomnography
blood oxygen
home sleep apnoea testing

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22
Q

How is polysomnography used to diagnose OSA

A

comprehensive overnight sleep study recording multiple physiological parameters

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23
Q

how is blood oxygen used to diagnose OSA

A

measurement of oxygen saturation levels in blood

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24
Q

how is home sleep apnoea testing used to diagnose OSA

A

portable assessment for detecting sleep disordered breathing at home

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25
Q

what are the features of polysomnography

A

pulse oximetry
electroencephalogram
electrooculogram
electromyogram
ECG
nasal pressure canula
thermocouple
microphone
thoraco-abdominal bands

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26
Q

function of pulse oximetry in polysomnograph

A

measures oxygen levels in blood (attached to index finger)

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27
Q

function of EEG in polysomnograph

A

records brains electrical activity (attached to forehead)

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28
Q

function of EOG in polysomnograph

A

tracks eye movements during sleep (attached to next to eyes)

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29
Q

function of EMG in polysomnograph

A

monitors muscle activity (attached to neck)

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30
Q

function of ECG in polysomnograph

A

monitors hearts electrical activity (attached to chest)

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31
Q

function of nasal pressure canala in polysomnograph

A

measures airflow through the nostrils (attached to nose)

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32
Q
A
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33
Q

function of microphone in polysomnograph

A

records sounds like snoring during sleep (attached to above sternum)

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34
Q

function of thoraco-abdominal bands in polysomnograph

A

monitor chest and abdominal movements to assess breathing (attached around chest)

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35
Q

define apnoea

A

complete cessation of airflow

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36
Q

Contrast OSA and central apnoea

A

OSA = Complete cessation of airflow due to upper airway resistance and obstruction, characterised by effort to breathe against resistance

CA=Complete cessation of airflow due to lack of control from brainstem respiratory centres; caused by medications, cardiac failure, brainstem disease, or idiopathic in nature.

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37
Q

define mixed apnoea

A

combination of central and obstructive apnoea

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38
Q

define hypopnea

A

Significant reduction in airflow, associated arousal during sleep, or oxygen desaturation; definitions can vary.

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39
Q

define ‘unsures’

A

Reduction in airflow, not reaching any of the above criteria.

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40
Q

what is respiratory disturbance index

A

-number of apnoeas and ‘unsures’ are measured per hour

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41
Q

identify the acute consequences of sleep disordered breathing

A

-excessive solomnence
-inappropriate falling asleep
-psychological consequences
-snoring

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42
Q

identify the chronic complications of sleep disorders breathing

A

-pulmonary HTN
-CVD
-CVA
-uncontrolled HTN

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43
Q

identify the treatments for OSA

A

CPAP
Mandibular splint
surgery
lifestyle modification
sleeping on side

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44
Q

describe the use of CPAP for OSA

A

high efficacy, low risk, pressure is set based on body habits, blows air into nose/mouth to splint open upper airway; provides major benefit

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45
Q

describe the use of mandibular splint for OSA

A

moulded mouthpiece that pries open the airway (not effective for obese patients)

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46
Q

describe the use of surgery for OSA

A

variable results, generally, this is a second line option due to invasiveness and associated costs

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47
Q
A
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48
Q

describe the use of sleeping on side for OSA

A

positional changes may be sufficient to provide symptomatic relief, easy method

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49
Q

what are some reasons why pt with OSA don’t go on CPAP

A

-uncomfortable
-xanthostoma (dry mouth)
-aesthetic
-cost
-claustraphobia
-lack of symptomatic response

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50
Q

what is pulmonary ventilation

A

process of moving air into and out of the lungs, allowing for the continuous supply of oxygen and removal of carbon dioxide

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51
Q

what is pulmonary gas exchange

A

occurs in the alveoli, where oxygen from the inhaled air diffuses into the bloodstream and carbon dioxide from the blood diffuses into the alveoli to be exhaled

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52
Q

what is type 1 respiratory failure

A

failure of oxygenation with low PaO2 and normal/low CO2

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53
Q

what is type 2 respiratory failure

A

ventilatory failure with low PaO2 and elevated PaCO2

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54
Q

Examples of type 1 respiratory failure

A

impaired ability to exchange oxygen (pneumonia, pulmonary oedema)

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55
Q

Examples of type 2 respiratory failure

A

hypoxia (PaO2 <60mmHg) and hypercapnia (PaCO2 > 50mmHg)
-cant remove CO2 adequately
-COPD, obesity, neuromuscular disorders

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56
Q

identify the common causes of respiratory failure

A

pulmonary ventilation failure and gas exchange failure

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57
Q

Describe pulmonary ventilation failure

A

-lungs can not effectively move air in and out, leading to inadequate alveolar ventilation
-this leads to respiratory acidosis and tissue hypoxia

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58
Q

Describe gas exchange failure

A

-lungs are unable to effectively transfer oxygen from the alveoli to the blood due to issues in the alveolar compartment, ventilation, perfusion
-does not typically lead to CO2 retention

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59
Q

what is hypoxia

A

state where tissues and organs are deprived of adequate oxygen, affecting cellular function

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60
Q

what is hypoxaemia

A

low oxygen levels in the blood

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61
Q

what is hypercapnia

A

condition of elevated CO2 in blood, (due to inadequate ventilation)

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62
Q

identify the physiological consequences of hypoxemia and hypercapnia

A

cellular hypoxia
sympathetic discharge
lactic acidosis
chronic effects
cerebral autoregulation
cardiorespiratory effects
respiratory acidosis
physiologic changes

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63
Q

what is cellular hypoxia

A

inflammatory cascade and oxygen radical release, cases irreversible damage to the brain, lung,heart,liver,renal and GI cells

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64
Q

what is sympathetic discharge

A

can lead to uncontrolled tachycardia and hypertension

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65
Q

what is lactic acidosis

A

accumulation of lactic acid in the blood, leading to decreased blood pH

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66
Q

what are chronic effects of hypoxemia and hypercapnia

A

impaired cough reflex, depressed asthma symptom perception

67
Q

what is cerebral auto regulation as a result of hypoxemia and hypercapnia

A

-cerebral autoregulation involves the vasodilation of cerebral arteries to increase blood flow and oxygen (o₂) delivery to the brain.
-this enhanced blood flow can help with the absorption and excretion of carbon dioxide (co₂) in the lungs.
-however, high co₂ levels in the brain can lead to headaches and confusion due to increased intracranial pressure.
-additionally, prolonged exposure to elevated co₂ can result in co₂ narcosis, which may cause cognitive impairment and other neurological effects.

68
Q

what are the cardiorespiratory effects of hypoxemia and hypercapnia

A

decreases myocardial and diaphragmatic contractility, arrhythmia, cardiorespiratory arrest

69
Q

what is respiratory acidosis

A

breathing causing accumulation of acidic products in the blood, with metabolic compensation if renal function intact

70
Q

what are the physiologic effects of hypoxaemia and hypercapnia

A

stimulates Bohr effect on Hg-O2 dissociation curve

71
Q

what are the implications on hypoxic drive in respiratory failure

A

-redistributed blood flow: the body naturally redirects blood to well-ventilated lung areas for effective co₂ clearance.
-high oxygen interference: excessive oxygen disrupts this redistribution, causing more blood to flow to poorly ventilated areas (alveolar deadspace) reducing co₂ elimination.
-haldane effect: high oxygen levels increase blood co₂ by displacing it from hemoglobin.
-blunted hypoxic drive: high oxygen reduces the breathing stimulus in COPD patients, worsening co₂ retention due to slower, shallower breathing.

72
Q

how does hypoxemia impact acid-base levels

A

-lowered oxygen in cells and tissues
-increased anaerobic metabolism
-lactic acid produced
-causes lactic acidosis

73
Q

how does hypercapnic (type 2 respiratory failure) impact acid base levels

A

-elevated CO2 levels lead to development of primary respiratory acidosis
-kidneys attempt to counteract this by increasing HCO3- retention (kidneys need to be functional)

74
Q

changes to PaCO2,pH, HCO3- in T2RF

A

Acute T2RF:
PaCO2: Elevated
pH: Decreased significantly (severe acidosis)
HCO3-: Normal (no time for compensation)

Chronic T2RF:
PaCO2: Elevated
pH: Slightly decreased or near-normal (due to compensation)
HCO3-: Elevated (due to renal compensation)

75
Q

when is oxygen therapy used for respiratory failure

A

-primary/reversible conditions should always be treated with oxygen therapy
-vital in T1RF; however, oxygen therapy can correct hypoxemia in T2RF but can worsen hypercapnia

76
Q

list the main types of oxygen therapy

A

HFNOT
CPAP
BPAP
Intubation
ECMO

77
Q

what does HFNOT stand for

A

high flow nasal oxygen therapy

78
Q

describe use of HFNOT

A

provides high-flow, humidified oxygen through nasal prongs to improve oxygenation and breathing comfort

79
Q

what does CPAP stand for

A

Continuous positive airway pressure

80
Q

describe the use of CPAP

A

A device that delivers a steady flow of air through a mask to keep the airways open
during sleep

81
Q

what does BPAP stand for

A

bi-level positive airway pressure

82
Q

describe the use of BPAP/Bipap

A

offers two levels of pressure (inhalation and exhalation) to assist with breathing, often used fro patients with respiratory issues

83
Q

describe the use of intubation

A

insertion of tube into airway to maintain an open airway and assist with ventilation

84
Q

what does ECMO stand for

A

Extra-corporal Membrane Oxygenation

85
Q

describe the use of ECMO

A

machine that provides long term support for patients with severe HF or lung failure by oxygenating blood outside the ovoid

86
Q

how do ABG’s work

A

-assesses pulmonary gas exchange by analysing partial pressures of oxygen and CO2, reflecting the efficiency of gas transfer in the lungs
-can also measure acid base balance and lactate + electrolytes

87
Q

list the parameters measured in ABGs

A

PaO2
PaCO2
bicarbonate
pH
electrolytes
lactate

88
Q

normal blood pH

A

7.35-7.45

89
Q

normal PaCO2

A

45-35

90
Q

normal HCO3-

A

22-26

91
Q

acronym for hypersensitivity reactions

A

ACID

92
Q

describe type 1 hypersensitivity reaction

A

(A)
IgE mediated (Allergic) responses eg anaphylaxis and atopic tetrad

93
Q

describe type 2 hypersensitivity reactions

A

(C)
antibody dependent cellular cytoxicity

94
Q

describe 3 hypersensitivity reaction

A

(I)
immune mediated responses involving IgG and IgM

95
Q

describe type 4 hypersensitivity reaction

A

(D)
delayed or cell mediated responses

96
Q

define atopy

A

describes genetic predisposition to develop IgE mediated hypersensitivity reactions, manifesting as things such as allergic rhinitis, asthma, atopic dermatitis

97
Q

define allergy

A

exaggerated immune response to specific antigens that typically involve the activation of mast cells and basophils, symptoms range from urticaria to anaphylaxis

98
Q

what is allergic rhinitis

A

inflammation of the nasal mucosa due to IgE-mediated response to airborne allergens, leading to symptoms such as sneezing, nasal congestion and itching

99
Q

what is asthma

A

a chronic inflammatory disorder of airways with bronchial hyper-reactivity, leading to recurrent wheezing, SOB and cough

100
Q

what is eczema

A

chronic skin condition marked by intense itching, erythema, dry, scaly patches often associated with FHx of atopy

101
Q

what is a food allergy

A

immune mediated adverse reaction to specific food proteins, resulting in a spectrum of symptoms, ranging from mild urticaria to severe anaphylaxis

102
Q

Outline a mechanism for atopic disorders

A

-Genetic and Environmental Triggers: Genetic predisposition and environmental allergens lead to an immune response.

-Th2 Cell Activation: Allergen exposure activates antigen-presenting cells, which stimulate naïve T cells to differentiate into Th2 cells.

-Cytokine Release: Th2 cells release cytokines (IL-4, IL-5, IL-13) that:
Promote IgE production by B cells.
Recruit and activate eosinophils.

-IgE and Mast Cell Activation: IgE binds to mast cells, which, upon re-exposure to the allergen, release histamine and other mediators.

-Chronic Inflammation: Eosinophils and other inflammatory cells cause ongoing inflammation and tissue damage.

103
Q

what are the risk factors for atopic disorders

A

maternal exposures
C section birth
Skin epithelium dysfunction
Lung epithelium dysfunction
Gut epithelium dysfunction

104
Q

what maternal exposures can make it a risk factor for atopic triad

A

pollutants, smoking, soaps/detergents, antibiotics, microplastics

105
Q

function of Th1 cells

A

traditional immune responses to viral/bacterial pathogen

106
Q

function of Th2 cells

A

immune responses to environmental allergens

107
Q

function of T reg cells

A

regulate immune responses (remove responses to NONharmful antigens)

108
Q

Outline Th1/Th2 skewing

A

-in western counties (small family size, affluent homes, high antibiotic use, good sanitation) skew direction of an overactive Th2 response
-In developing countries, large family sizes, rural homes, low antibiotic use, and poor sanitation lead to a skew
in the direction of an underactive Th2 response (Th1 skew)

109
Q

how does diet influence atopy development

A

-diets high in sat fats, low fibre, less fresh food reduce efficacy of immunological response
-diet high in VD, folate and fish oils improve resistance to allergy
-probiotics and prebiotics support development of Treg cells

110
Q

causes of allergic rhinitis

A

mostly driven by IgE

111
Q

causes of eczema

A

epithelial danger signs
IgE mediation
allergic inflammation

112
Q

causes of asthma

A

epithelial danger signs
IgE mediation
allergic inflammation

113
Q

list the management of atopy

A

corticosteroids
anti-alarmin therapy
anti-Th2 therapy
immunosuppressants
anti-IgE

114
Q

how does anti-alarmin therapy treat atopy

A

inhibits differentiation of naive T cells into th2 cells

115
Q

how do corticosteroids treat atopy

A

anti-inflammatory properties, suppresses Dc, Tc,Bc

116
Q

how do immunosuppressants treat atopy

A

anti-inflammatory properties, suppresses Dc, Tc,Bc

117
Q

how does anti-Th2 therapy treat atopy

A

blocks cytokine receptor signalling

118
Q

how does anti-IgE therapy treat atopy

A

binds to IgE, prevents IgE binding to mast cells

119
Q

define anaphylaxis

A

any acute onset illness with typical skin features (urticarial/rash/erythema/flushing/angiodema) plus the involvement of respiratory and/or cardiovascular and/or severe GI symptoms

120
Q

what are the causes of IgE allergic reactions

A

food
medications
latex
cold temperature
insects
airborne allergens
exercise
idiopathic

121
Q

outline a clinical allergic reaction

A

-allergen contacts the integument
-allergen detected by APC
-antigen is processed
-Th cells promote the activation of B cells
-B cells produce IgE
-IgE binds to mast cell
-IgE cross-linking on mast cells
-release of chemical mediators
-production of clinical signs

122
Q

what are the integument signs of allergy

A

hives, allergy

123
Q

what are the GI signs of allergy

A

emesis, abdominal pain

124
Q

what are the respiratory signs of allergy

A

tongue swelling, cough, wheeze, dysarthria

125
Q

what are the CV signs of allergy

A

hypotension
pre syncope
pale and floppy appearance

126
Q

what are the neurological signs of allergy

A

anxiety
headache
seizures

127
Q

Describe the pathophysiology of acute bronchoconstriction

A

-Triggering Agents: Allergens or irritants cause mast cells and immune cells to release mediators like histamine, leukotrienes, and prostaglandins.
-Mediator Action: These mediators bind to receptors on bronchial smooth muscle.
Calcium Influx: This binding increases intracellular calcium levels.
-Smooth Muscle Contraction: Elevated calcium causes bronchial smooth muscle contraction, narrowing the airways.
-Parasympathetic Activation: The vagus nerve releases acetylcholine, which stimulates muscarinic receptors on the smooth muscle, worsening bronchoconstriction.
-Symptoms: Narrowed airways impair airflow, leading to wheezing, shortness of breath, and chest tightness.

128
Q

identify the role of airway inflammation in asthma

A
  • Airway Hyperresponsiveness: Inflammation increases bronchial smooth muscle sensitivity, leading to excessive airway constriction in response to stimuli.
  • Airway Remodeling: Chronic inflammation causes structural changes like thickened airway walls and increased mucus production, resulting in persistent airway narrowing and obstructed airflow.
129
Q

list the characteristics of asthma

A

-lung inflammation
-airway hyper-responsiveness
-airway remodelling
-mucous hypersecretion
-increased eosinophils and/or -neutrophils in airway lumen

130
Q

describe lung inflammation as a characteristic of asthma

A

chronic inflammation of the airways in response to various triggers, leading to airway constriction and other asthma symptoms

131
Q

describe airway hyper-responsiveness as a characteristic of asthma

A

exaggerated and excessive narrowing of the airways in response to irritants or allergens, a hallmark of asthma

132
Q

describe airway remodelling as a characteristic of asthma

A

structural changes in the airways walls, including thickening and increased smooth muscle, which occur over time in asthma

133
Q

describe mucous secretion as a characteristic of asthma

A

overproduction of mucous in the airways, leading to congestion and difficulty breathing

134
Q

describe increased eosinophils and/or neutrophils in airway lumen

A

elevated levels of WBC’s in the airways, which contribute to inflammation and airway obstruction in asthma

135
Q

contrast type 2 asthma and non type 2 asthma

A

-T2=more common vs NT2=less common
-T2=more severe vs NT2=less severe
-T2=airways/systemic eosinophilia vs NT2=no airways/systemic eosinophilia
-T2=responsiveness to corticosteroids vs NT2=lack of responsiveness to corticosteroids

136
Q

List the clinical features of asthma

A

wheezing
cough
dyspnoea
chest tightness

137
Q

what is a wheeze

A

high pitched, whistling sound during breathing, especially on exhalation

138
Q

what is a cough

A

persistent, often dry or mucous-producing, typically worsening at night or early morning

139
Q

what is dyspnoea

A

shortness of breath or difficulty breathing, especially noticeable during exertion

140
Q

what is chest tightness

A

a sensation of pressure or constriction in the chest, often described as feeling squeezed

141
Q

define chronic bronchitis

A

chronic inflammation of the bronchi, resulting in mucous hyper secretion and goblet cell hypertrophy, chronic cough, and airway narrowing

142
Q

define emphysema

A

destruction of alveolar walls, leading to loss of elastic recoil and impaired gas exchange

143
Q

Outline a mechanism for the pathophysiology of COPD

A

-Exposure to Noxious Particles:
-Trigger: Long-term exposure to irritants, especially cigarette smoke.
-Chronic Inflammation:
Response: Inflammatory cells infiltrate the airways and lung tissue, releasing mediators that worsen inflammation.
-Oxidative Stress:
Damage: Increased reactive oxygen species (ROS) from smoke exacerbate inflammation and damage lung tissue.
-Airway Changes:
Chronic Bronchitis: Mucus hypersecretion and airway narrowing cause a persistent cough due to increased mast cell activty
-Emphysema: Destruction of alveolar walls leads to loss of elastic recoil due to release of proteolytic enzymes from inflammation
-Airflow Obstruction:
Mechanisms: Excessive mucus, airway narrowing, and loss of elastic recoil impair airflow.
-Impaired Gas Exchange:
Effect: Damaged alveoli reduce gas exchange efficiency, leading to low oxygen and high carbon dioxide levels.
-Exacerbation by Cigarette Smoke:
Impact: Increases oxidative stress and inflammation, worsening COPD symptoms.

144
Q

list the clinical features of COPD

A

-persistent cough (with thick, mucoid sputum)
-wheezing
-chest tightness

145
Q

contrast the clinical features of asthma and COPD

A

-chronic sputum production in COPD, rarer in asthma
-COPD worsens at morning time whereas asthma worsens in the night
-COPD exacerbated by infections of environment vs asthma is exacerbated by allergens or infections
-COPD has barrel chest and cyanosis whereas asthma doesn’t

146
Q

how is history used to diagnose COPD

A

pt presents with chest tightness, dyspnoea, cough

147
Q

how is examination used to diagnose COPD

A

barrel chest, expiratory wheeze, crackles, breath sounds

148
Q

how is spirometery used to diagnose COPD

A

confirms COPD by measuring airflow limitation, specifically a reduced FEV1/FVC ratio and bronchodilator to rule out asthma

149
Q

how is chest x ray used to diagnose COPD

A

identifies hyperinflation and other structural lung changes consistent with COPD, ruling out alternative diagnoses

150
Q

how are bloods used to diagnose COPD

A

assesses for polycythaemia or anaemia and screens for comorbid conditions

151
Q

describe the role of infection in acute exacerbation of COPD

A

-infection increases airway inflammation and mucous production, leading to worsened airflow obstruction
-most common organisms include (H.influenzae, S.pneumoniae,M,catarrhalis)

152
Q

identify pharmacoligical options for management of COPD

A

SABA
LABA
SAMA
LAMA
ICS

153
Q

how do SABA work

A

stimulate beta-2-adrenergic receptors in the bronchial smooth muscle, leading to bronchodilator

154
Q

how do LABA work

A

activate beta-2-adrenergic receptors in the bronchial smooth muscle for pre longed bronchodilator, typically lasting 12-24 hours

155
Q

how do SAMA work

A

block muscarinic M3 receptors in the bronchial smooth muscle, reducing bronchoconstriction and mucous secretion

156
Q

how do LAMA work

A

block muscarinic M3 receptors in the bronchial smooth muscle, providing extended bronchoconstriction and reduced mucous secretion

157
Q

how do ICS work

A

reduce airway inflammation and oedema by inhibiting the release of inflammatory mediators and suppressing the activty of inflammatory cells

158
Q

what are the non pharmacological management of asthma

A

avoid known triggers
inhaler technique
breathing exercises
physical active
adhere to medications
healthy diets

159
Q

explain the concept of preventer vs reliever in terms of asthma

A

Preventers such as ICS are used daily to reduce airway inflammation and prevent asthma symptoms by
decreasing the production of inflammatory mediators and suppressing inflammatory cells.
Relievers, such
as (SABA), provide rapid bronchodilation by stimulating beta-2 adrenergic
receptors in the bronchial smooth muscle, offering immediate relief of acute symptoms like wheezing and
shortness of breath.

160
Q

principles of bronchodilator use

A

-Bronchodilators for asthma and COPD management can act via two principal mechanisms; agonising beta-2
receptors (SABA, LABA) or antagonising muscarinic-3 receptors (SAMA, LAMA).
-ICS is gold standard

161
Q

describe use of mucolytics for asthma

A

-Mucolytics are used in asthma and COPD to reduce mucus viscosity and enhance mucus clearance from the
airways
-less common in asthma

162
Q

Describe potential use of oxygen therapy amongst patients with COPD.

A

-Manages chronic hypoxemia, preventing complications like pulmonary hypertension and heart failure.
-Increases blood oxygen levels, reducing shortness of breath and improving exercise tolerance.
-Recommended for severe COPD with resting hypoxemia.
-Long-term use can improve survival and quality of life.
-Administered via nasal cannulas or masks, suitable for hospital or home use.
-Smoking cessation is crucial to avoid risks like explosions during home oxygen therapy.

163
Q

Outline the use of monoclonal antibodies for severe, chronic airway disease

A

Target specific inflammatory pathways or cytokines to reduce chronic
inflammation and exacerbations in severe COPD.

164
Q

Outline the use of bronchial thermoplasty for severe, chronic airway disease

A

Uses controlled thermal energy to reduce airway smooth muscle mass and
decrease excessive bronchoconstriction.

Medical Studies 1 (15 decks)

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