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Medical Studies 1 > Resp Week 6 > Flashcards

Resp Week 6 Flashcards

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USMLE® Step 1 flashcards
1
Q

what are the two states of normal human sleep

A

REM

non-REM

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2
Q

what is clinical sleep staging based on

A

EEG

EOG

EMG

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3
Q

what are the subdivisions of NREM sleep

A

N1, N2, N3 (going from lighter to deeper sleep )

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4
Q

describe EEG waves, percentage of time, and function during the different stages of sleep

A

stage W (awake but resting) = alpha waves, 5%, normal bodily activity

stage N1 = theta waves, 5%, cardiovascular rest

stage N2 = sleep spindles and K complexes, 50%, cardiovascular rest

stage N3 = delta waves, 15%, cardiovascular rest

stage REM = sawtooth waves, 25%, cardiovascular activation

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5
Q

describe the normal changes in ventilation during sleep

A

drive to breathe is reduced during sleep

upper airway resistance increases during sleep, therefore reduced breathing capacity

metabolic rate decreases by 10-15% during sleep, decreasing breathing drive

PCO2 increases and PO2 decreases

as a result, hypoventilation occurs during sleep

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6
Q

describe obstructive sleep apnoea

A

disordered breathing during sleep in which the airway is mechanically obstructed, leading to a cessation of airflow, resulting in intermittent hypoxia and fragmented sleep

has CV and cerebrovascular impacts

several risk factors e.g obesity, alcohol use, upper airway abnormalities

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7
Q

what are 10 clinical features of OSA

A

daytime somnolence

nocturia

cognitive impairment

dry mouth

large neck

witnessed apnoeas

insomnia

morning headaches

high BMI

crowded oropharynx

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8
Q

what is the mallampati score

A

clinical assessment tool used to evaluate the visibility of the oral structures and predict the difficulty of intubation

determined by having patient sit upright with their mouth open and tongue protruded

score is based on visualisation of oropharynx

a higher score indicates a higher likelihood of difficult intubation

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9
Q

what are the 4 classes of the mallampati score and what can be seen in each

A

class 1 - full visibility of uvula, soft palate and fauces

class 2 - visibility of soft palate and part of uvula

class 3 - only soft palate seen

class 4 - only shows hard palate

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10
Q

what are 3 diagnostic methods of OSA

A

polysomnography

blood O2

home sleep apnoea testing

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11
Q

describe polysomnography

A

comprehensive overnight sleep study recording multiple physiological parameters

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12
Q

what are 9 measurements taken during polysomnography

A

pulse ox - O2 in blood

EEG - brain electrical activity

EOG - tracks eye movement

EMG - monitors muscle activity

ECG - heart electrical activity

nasal pressure cannula - measure airflow through nostrils

thermocouple - measures airflow by detecting temp changes

microphone - records sounds like snoring during sleep

thoraco-abdominal bands - monitor chest/ab mvmt to assess breathing

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13
Q

describe home sleep apnoea testing

A

portable assessment for detecting sleep-disordered breathing at home

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14
Q

what is the difference between obstructive and central apnoea

A

obstructive apnoea is complete cessation of airflow due to upper airway resistance and obstruction, whereas central apnoea is complete cessation of airflow due to lack of control from brainstem respiratory centres

central apnoea is much less common than obstructive (10:1)

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15
Q

what is mixed apnoea

A

combination of central and obstructive apnoea

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16
Q

what is hypopnea

A

significant reduction in airflow, associated arousal during sleep, or oxygen desaturation

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17
Q

what is the respiratory disturbance index (RDI)

A

number of apnoeas, hypopneas, and ‘unsures’ (reduction in airflow not reaching any of the criteria) per hour

this info forms basis of RDI

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18
Q

what are 4 acute complications of sleep disorder breathing

A

excessive somnolence

inappropriate falling asleep

psychosocial consequences

snoring

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19
Q

what are 4 chronic complications of sleep disordered breathing

A

pulmonary HTN

CVD

cerebrovascular accident

uncontrolled HTN

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20
Q

what is the importance of early referral

A

indicated for individuals w cerebrovascular co-morbidities or risk factors, patients who are drowsy driving, and patients who operate heavy machinery

OSA must be reported to the DMV in all instances

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21
Q

what are 5 Rx options for sleep apnoea

A

CPAP

mandibular splint

surgery

lifestyle modification

sleeping on side

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22
Q

describe CPAP as a Rx for sleep apnoea

A

high efficacy

low risk

pressure is set based on body habitus

blows air into nose/mouth to splint open upper airway

provides major benefit

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23
Q

describe mandibular splint as a Rx for sleep apnoea

A

moulded mouthpiece that pries open the airway

not effective for obese patients

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24
Q

describe surgery as a Rx for sleep apnoea

A

variable results

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

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25
Q

describe lifestyle modification as a Rx for sleep apnoea

A

reduced EtOH, sedatives, cigarettes, weight loss

has implications for other body systems e.g CV and GI

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26
Q

describe sleeping on side as a Rx for sleep apnoea

A

positional changes may be sufficient to provide symptomatic relief

easy method

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27
Q

what are 6 reasons for non-compliance with CPAP as a Rx for sleep apnoea

A

comfort - can be tight

xanthostoma - dry mouth due to airflow

aesthetic - may appear unattractive

claustrophobia - mask can be restricting in nature

cost - it is expensive

lack of symptomatic response - no immediate response, meaning less inclined to keep using

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28
Q

what is type 1 respiratory failure

A

lungs cannot move enough O2 into the blood, leading to hypoxaemia (PaO2 < 60mmHg)

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29
Q

what is type 2 respiratory failure

A

lungs cannot remove enough CO2 from the blood, leading to hypercapnia (PaCO2 > 45mmHg; often coexists w hypoxaemia)

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30
Q

compare and contrast pulse ox with ABG

A

pulse ox reflects tissue O2 supply by measuring the percentage of Hb saturated w O2 but does not measure blood CO2 or O2 level

whereas

arterial blood gas sample provides accurate assessment of hypoxaemia and hypercapnia, acid-base status, and extended parameters such as lactate

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31
Q

what are 2 key mechanisms of respiratory failure

A

failure of pulmonary ventilation

failure of pulmonary gas exchange

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32
Q

describe failure of pulmonary ventilation in regards to respiratory failure

define, cause, impact

A

this is the failure to physically move air in and out of lungs, resulting in alveolar hypoventilation (smaller, slower breathing)

caused by extrapulmonary factors such as CNS depression and respiratory pump failure

this leads to hypercapnia and hypoxaemia

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33
Q

what are 3 things that can lead to CNS depression (extrapulmonary cause of failure of pulmonary ventilation)

A

drugs e.g opioids

structural abnormalities e.g stroke

raised ICP e.g tumour

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34
Q

what are 3 things that can lead to respiratory pump failure (extrapulmonary cause of failure of pulmonary ventilation)

A

phrenic nerve dysfunction e.g due to direct damage

neuromuscular weakness e.g diseases such as MND

chest cage restriction e.g kyphoscoliosis

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35
Q

describe failure of pulmonary gas exchange in regards to respiratory failure

cause, impact

A

caused by pulmonary factors such as problems with the lungs or blood vessels

results in reduced O2 delivery from lung to blood

it does not usually cause CO2 retention except for in severe COPD where there is severely reduced lung reserve

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36
Q

what are 4 causes of pulmonary gas exchange failure and name one dominant mechanism for each with an example

A

diffusion limitation = thickened interstitium and alveolar-capillary membrane e.g interstitial lung disease

ventilatory defect (intrapulmonary shunt) = alveolar collapse e.g pneumothorax

perfusion defect (dead space) = pulmonary vascular narrowing or obstruction e.g PE

right to left anatomic shunt = de-O2 blood re-entering systemic circulation e.g intracardiac shunt

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37
Q

what are 4 major consequences of hypoxaemia

A

damage to vital organs and tissues via cellular hypoxia

increased sympathetic discharge, leading to tachycardia and HTN

lactic acidosis

chronic effects, such as impaired cough reflex and depressed asthma symptom perception

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38
Q

what are 4 major consequences of hypercapnia

A

cerebral autoregulation problems - there is an initial increase in inspiratory drive, but then due to an increase in cerebral blood flow there is increased ICP leading to headache, and decreased inspiratory drive, then there is CO2 narcosis and eventual seizure, coma or death

direct cardiorespiratory effects e.g arrthymia and cardioresp arrest

respiratory acidosis

physiologic responses e.g increase release of O2 to tissues

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39
Q

what are implications of O2 induced hypercapnia

A

increased alveolar dead space - normal compensatory mechanisms in chronic severe COPD act to redistribute pulmonary blood flow to better ventilated areas of the lung, but excessive O2 therapy will reverse this protective effect which leads to reduced CO2 clearance

haldane effect - excessive O2 will displace CO2 bound to Hb, thus raising blood CO2 retention

blunting of hypoxic ventilatory drive

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40
Q

what are 3 general principles for O2 therapy

A

always treat primary/reversible problems e.g pneumonia, HF

O2 therapy is vital for T1RF

O2 therapy can correct hypoxaemia in T2RF but does not correct hypercapnia, and may in fact make it worse

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41
Q

what are 5 treatment options for respiratory failure

A

high flow nasal O2 therapy (HFNOT)

continuous positive airway pressure (CPAP)

bi-level ventilation (BPAP)/non-invasive ventilation (NIV)

intubation and mechanical ventilation

extracorporeal membrane oxygenation (ECMO)

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42
Q

what are 2 acid-base consequences of respiratory failure

A

lactic acidosis in severe hypoxaemia

primary respiratory acidosis in hypercapnic respiratory failure (T2RF)

43
Q

describe how lactic acidosis in severe hypoxaemia can occur due to respiratory failure

A

tissue hypoxia leads to an increased in anaerobic respiration, which produces lactic acid as a byproduct

this is compensated for by an increased respiratory drive in an attempt to blow off CO2 to normalise pH

44
Q

describe how primary respiratory acidosis in hypercapnic respiratory failure can occur

A

an excess CO2 results in increased renal retention of bicarbonate ion to buffer in order to attempt to normalise pH

for metabolic compensation to occur to oppose this, you need to have normally functioning kidneys

45
Q

what are 4 assessments that can be made by measuring ABG

A

pulmonary gas exchange

acid-base balance

lactate

co-oximetry

46
Q

what is the normal range of PaO2

A

75-100mmHg, depending on age

47
Q

what is normal range of pH

A

7.35-7.45

48
Q

what is normal range of PaCO2

A

35-45mmHg

49
Q

what is normal range of bicarbonate ion

A

22-28mmol/L

50
Q

what is normal range of lactate

A

0.2-2.0mmol/L

51
Q

what is the difference between hyperlactatemia and lactic acidosis

A

lactate >2mmol/L is hyperlactatemia

lactate >4mmol/L is lactic acidosis

52
Q

what is type A lactic acidosis

A

severe tissue hypoxia or hypoperfusion eg hypovolemia or cardiac failure

53
Q

what is type B lactic acidosis

A

impaired cellular metabolism or regional ischemia without severe hypoxia or hypoperfusion e.g high dose inhaled beta antagonists such as salbutamol

54
Q

what are the four types of hypersensitivity reactions

A

type 1

type 2

type 3

type 4

55
Q

outline type 1 hypersensitivity reaction

A

IgE mediated (Allergic) response e.g anaphylaxis

56
Q

outline type 2 hypersensitivity reaction

A

antibody-dependent cellular cytotoxicity

57
Q

outline type 3 hypersensitivity reaction

A

immune mediated responses involving IgG and IgM

58
Q

outline type 4 hypersensitivity reaction

A

delayed or cell mediated response

59
Q

define atopy

A

genetic predisposition to develop IgE mediated hypersensitivity reactions, manifesting as conditions such as asthma, allergic rhinitis, and atopic dermatitis (atopic triad)

often involves a heightened immune response to environmental allergens leading to chronic inflammation

60
Q

define allergy

A

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

clinical manifestations include respiratory, cutaneous, and GI symptoms

61
Q

describe the pathophysiology of atopic disorders

A

exposure to allergens

leads to, antigen presenting cells activating naive t cells to differentiate into Th2 cells, which release cytokines e.g IL3, IL4, IL5

then, these promote IgE production by B cells and the recruitment of eosinophils causing chronic inflammation and tissue damage

62
Q

what are 5 risk factors for atopic disorders

A

maternal exposures - pollutants, smoking, antibiotics etc

type of birth - C-section

skin epithelial dysfunction - pollutants, smoke exposure, vitamin D deficiency etc

lung epithelium dysfunction - bacterial pathogens, viral pathogens, genetic influence etc

gut epithelium - formula feeding, increased antibiotic use, food allergen etc

63
Q

what are 5 causes of atopy

A

Th1/Th2 responses - responsible for immune responses by activating B cells and leading to the production of IgE

Th1/Th2 skewing - in western countries w smaller family sizes and good sanitation there is a skew in overactive Th2 whereas in developing countries w larger families and poor sanitation lead to a skew in Th1

dietary considerations - dietary profile changes likelihood of developing allergic responses due to the nutrients provided

genetic considerations - heritability is observed in atopic and allergic conditions

epigenetic considerations - biochemical changes to DNA that do not alter the gene sequence but instead modify expression / driven by environmental factors / e.g DNA methylation

64
Q

outline allergic rhinitis

A

nasal congestion, sneezing and itching due to airborne allergens and asthma leading to recurrent episodes of wheezing and breathlessness

65
Q

outline atopic dermatitis (eczema)

A

chronic, itchy, and inflamed skin lesions, often exacerbated by environmental triggers and skin barrier dysfunction

66
Q

what are 5 Rx methods for management of atopy

A

corticosteroids - anti-inflammatory properties/suppress dendritic cells, t cells, b cells

anti-alarmin therapy - inhibits differentiation of naive t cells into Th2 cells

anti-Th2 therapy - blocks cytokine receptor signalling

immunosuppressants - same as corticosteroids

anti-IgE - binds to IgE and prevents IgE binding to mast cells

67
Q

define anaphylaxis

A

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

first line of Rx is intramuscular injection of adrenaline

68
Q

what are 8 causes of IgE-mediated allergic reactions

A

food

meds

latex

cold temp

insects

airborne allergens

exercise

idiopathic

69
Q

outline the pathophysiology of clinical allergic reaction

A

allergen contacts the integument

then, allergen detected by antigen presenting cell

then, allergen is processed

then, Th cells promote the activation of B cells

then, B cells produce IgE

then, IgE binds to mast cells

then, IgE cross linking on mast cells

then, release of chemical mediators

then, production of clinical signs

70
Q

what are integumentary clinical signs of allergy

A

hives

swelling

71
Q

what are GI clinical signs of allergy

A

emesis

abdominal pain

72
Q

what are respiratory clinical signs of allergy

A

tongue swelling

cough

wheeze

dysarthria

73
Q

what are CV clinical signs of allergy

A

hTN

pre-syncope

pale and floppy

74
Q

what are neurological clinical signs of allergy

A

anxiety

headache

seizures

75
Q

describe the pathophysiology of acute bronchoconstriction

A

release of mediators such as histamine, leukotrienes, prostaglandins from mast cells and other immune cells in response to allergens or irritants

then, these mediators bind to specific receptors on bronchial smooth muscle, initiating a cascade that increases intracellular calcium levels resulting in muscle contraction

then, parasympathetic NS activation via the vagus nerve can exacerbate bronchoconstriction by increasing acetylcholine release, which further stimulates muscarinic receptors on the smooth muscle within the bronchial wall

then, the reduced airway diameter impairs airflow leading to symptoms such as wheezing, shortness of breath and chest tightness

76
Q

outline the role of airway inflammation in asthma

A

inflammatory cells release cytokines and other mediators that perpetuate inflammation and tissue damage, which leads to airway hyperresponsiveness where the bronchial smooth muscle reacts excessively to various stimuli resulting in bronchoconstriction

chronic inflammation also causes structural changes which further narrows airways

these give rise to recurrent symptoms

77
Q

what are 5 characteristics of asthma

A

lung inflammation

airway hyper-responsiveness

airway remodelling

mucus hyper secretion

increased eosinophils and/or neutrophils in airway lumen

78
Q

describe type 2 asthma

A

characterised by elevated levels of type 2 Th cell cytokines such as IL4, IL5, IL3 leading to eosinophilic inflammation and increased IgE production

commonly associated w atopy and allergic triggers and patients often respond well to corticosteroids and other anti-inflammatory treatments

79
Q

describe non-type 2 asthma

A

associated w neutrophilic inflammation and lacks Th-2 driven inflammation

may not respond well to traditional corticosteroid Rx and is more commonly linked to environmental factors

80
Q

what are 4 clinical features of asthma

A

wheezing

cough

dyspnoea

chest tightness

81
Q

describe clinical features of COPD

A

persistent cough often accompanied by the production of thick, mucoid sputum

dyspnea that worsens w physical exertion

wheezing

chest tightness

potential cyanosis and peripheral oedema

82
Q

compare and contrast clinical features of COPD and asthma

A

both have wheeze, chronic cough, dyspnea, chest tightness

COPD has chronic sputum production, whereas it is rarer in asthma

asthma worsens at night whereas COPD does not

acute exacerbations of COPD are triggered by infections or environmental pollutants whereas it is triggered by allergens or respiratory infections in asthma

COPD has cyanosis in advanced stage whereas there is no cyanosis in asthma

COPD has barrel chest whereas asthma doesn’t

83
Q

what would you find in a history in the diagnosis of COPD

A

dyspnea

chest tightness

cough

84
Q

what would you find in examination in the diagnosis of COPD

A

barrel chest

expiratory wheeze

crackles

breath sounds adventitious

85
Q

what would you find in a spirometry in the diagnosis of COPD

A

reduced FEV1/FVC ratio

present bronchodilator response to rule out asthma

86
Q

what would you find in chest X-ray in the diagnosis of COPD

A

hyperinflation

other structural lung changes consistent w COPD ruling out alternative diagnoses

87
Q

what would you find in bloods done in the diagnosis of COPD

A

assesses for polycythaemia or anaemia and screens for comorbid conditions such as infection or metabolic imbalances that may complicate COPD

88
Q

describe the role of infection in acute exacerbation of COPD

A

increases airway inflammation and mucus production which leads to worsened airflow obstruction

89
Q

what are some common organisms involved in the acute exacerbation of COPD

A

Haemophilus influenzae

Streptococcus pneumoniae

Moraxella catarrhalis

rhinoviruses

90
Q

what is SABA, give example, what is is used for and how does it work

A

short acting beta agonist (e.g albuterol) which are used as rescue inhalers to provide quick relief from acute bronchospasm

stimulates beta-2 adrenergic receptors in the bronchial smooth muscle, leading to bronchodilation

91
Q

what is LABA, give example, what is is used for and how does it work

A

long acting beta agonist (e.g salmeterol) which are used for sustained bronchodilation in asthma and COPD but are typically combined w inhaled corticosteroids for long term control

activates beta-2 adrenergic receptors in the bronchial smooth muscle for prolonged bronchodilation, typically lasting 12-24 hrs

92
Q

what is LAMA, give example, what is is used for and how does it work

A

long acting muscarinic antagonists (e.g tiotropium) which are employed mainly in COPD to achieve long term bronchodilation and improve lung function

block muscarinic M3 receptors in the bronchial smooth muscle, providing extended bronchodilation and mucus reduction

93
Q

what is SAMA, give example, what it is used for and how does it work

A

short acting muscarinic antagonist (e.g ipratropium) which are used a lot less frequently but can provide additional relief for acute symptoms and exacerbations of asthma

block muscarinic M3 receptors in the bronchial smooth muscle, reducing bronchorestriction and mucus secretion

94
Q

how do inhaled corticosteroids work

A

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

95
Q

what are 6 non-pharmacological management methods of asthma

A

avoid known triggers

inhaler technique

breathing exercises

physical activity

adhere to medications

healthy diet

96
Q

describe the role of the multidisciplinary team in the management of COPD as a model of chronic disease

A

key role in delivering comprehensive care

pulmonologists/resp physicians lead the clinical management, treatments etc.

resp therapists give education on inhaler techniques, breathing exercises and support w rehab

nurses offer ongoing patient education, symptom management, and coordinate care b/w specialists

dietitians and psychologists address nutritional needs and mental health

97
Q

outline the concept of a preventer

A

e.g ICS are used daily to reduce airway inflammation and prevent asthma symptoms by decreasing the production of inflammatory mediators and suppressing inflammatory cells

they aim to control chronic inflammation and reduce the frequency of asthma exacerbations

98
Q

outline the concept of relievers

A

e.g 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

99
Q

describe oral glucocorticoids

A

steroids e.g ICS are used to manage asthma and COPD by reducing chronic airway inflammation and swelling

in asthma, decrease frequency and severity of exacerbations

in COPD, used during acute exacerbations to quickly reduce inflammation

100
Q

describe mucolytics

A

used in asthma and COPD to reduce mucus viscosity and enhance mucus clearance from the airways

work by breaking down mucus, making it less sticky and easier to expel through coughing

in COPD< they have manage chronic productive cough

for asthma, less commonly used but may be prescribe to alleviate symptoms associated w excessive mucus production

101
Q

describe the potential use of oxygen therapy amongst patients w COPD

A

manage chronic hypoxemia which can lead to complications such as pulmonary HTN and RHS-HF

supplemental O2 helps increase blood O2 level, alleviating symptoms like shortness of breath and improving exercise tolerance

recommended for patients w severe COPD who have resting hypoxemia

home O2 therapy requires them to quit smoking cos if you smoke near O2 therapy machine it may explode

102
Q

outline the concept of self management in COPD

A

Pt taking active role in own care e.g monitoring symptoms, recognising early signs of exacerbation, adhering to prescribed Rx etc.

Pt encouraged to engage in regular physical activity, follow proper diet, avoid smoking etc.

103
Q

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

A

in asthma, monoclonal antibodies (e.g omalizumab) inhibit IgE thereby reducing allergen-induced exacerbations / mepolizamub target IL5 to decrease eosinophilic inflammation

in COPD, benralizumab is used to target IL5 to manage eosinophilic COPD

monoclonal antibodies are typically for Pt that do not respond adequately to standard Rx

104
Q

outline use of bronchial thermoplasty

A

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

Medical Studies 1 (16 decks)

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