Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Clinical Physiology > Respiratory > Flashcards

Respiratory Flashcards

1
Q

accessory inspiratory muscles

A

sternocleidomastoid,
thescalenusanterior, medius, and posterior, thepectoralis majorandminor,
the inferior fibres ofserratus anteriorandlatissimus dorsi,
theserratus posterior superiormay help in inspiration also theiliocostalis cervicis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

accessory expiratory muscles

A

theabdominal muscles:rectus abdominis,external oblique,internal oblique, andtransversus abdominis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

layers before alveoli out to in

A

capillary endothelium, RBC’S, capillary endothelium, surfactant, alveolar membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

diffusion barrier

A

alveolar membrane, surfactant, capillary endothelium, cell membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Lung Volumes

A

inspiratory reserve volume
tidal volume
expiratory reserve volume
residual volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

inspiratory capacity

A

inspiratory reserve volume + tidal volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

functional residual capacity

A

expiratory reserve volume + residual volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

vital capacity

A

inspiratory reserve volume + tidal volume + expiratory reserve volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

why are lung volumes calculated?

A

assessment of the mechanical condition of the lungs, musculature, airway resistance and effectiveness of gas exchange at the alveolar membrane.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

why should ventilation and perfusion of the lungs be adequately matched?

A

ensuring continuous delivery of oxygen
and removal of carbon dioxide from the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

ventilation rate

A

volume of gas inhaled and exhaled
from the lungs in a given time period`

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

perfusion

A

total volume of blood reaching the pulmonary capillaries in the same time period

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

ideal V/Q ratio

A

1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

how can a mismatch in ventilation and perfusion occur?

A

reduced ventilation of part of the lung or reduced perfusion,
and clinically manifests in several respiratory conditions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

differential diagnosis of breathlessness

A

asthma, COPD, cystic fibrosis, PE, iron deficient anaemia, anything causing issues with perfusion or ventilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

asthma

A

chronic inflammatory disorder of the airways characterized by bronchial wall hyper-reactivity and airway obstruction which is reversible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

risk factor for asthma

A

family history,
prematurity (& low birth weight), tobacco smoke exposure,
obesity and exposure to allergens in the case of atopic asthma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

types of asthma

A
  1. extrinsic/atopic asthma
  2. intrinsic/ non atopic asthma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

extrinsic asthma

A

known cause
Airway inflammation in this type
of asthma is due to allergen exposure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

atopy

A

Atopy is a group of disorders that typically occur together and includes rhinitis, eczema, hay-fever and asthma. It is associated with the ADAM33 and PHF11 genes, and as such, typically runs in families

atopic individuals have type 1 hypersensitivity reactions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

intrinsic asthma

A

no identified cause
airway inflammation not due to allergen exposure
patient specific triggers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

features of an asthmatic airway

A

increased mucus,
immune cells,
goblet cells,
thicker basement membrane,
muscle layer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Characteristic features of asthma

A

airflow limitation
airway hyper responsiveness
airway inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

asthma pathway

A
  1. asthmatic individual inhales allergen
  2. stimulates immune response CD4 differentiates into t helper 2
  3. th2 release cytokines interleukin 4 and 5
    • b cells diff into plasma
    • interleukin 4 recruits eosinophils
  4. plasma releases IgE
  5. igE binds to mast cells - mast cell IgE complexes
  6. allergen binds to complex
  7. causes mast cell degranulation
    • causes inflammatory mediators histamine, leukotrienes, prostaglandins release
    • causes airway inflammation and bronchostriction → clinical symptoms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

histamine

A

amine which causes inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

stridor

A

sound obstruction of in upper airway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

intrinsic asthma triggers

A
  1. emotion
  2. viral infection
  3. smoking
  4. occupational allergens
  5. drugs
  6. cold air
  7. exercise
  8. atmospheric pollution
  9. NSAIDs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

spirometry

A

gold-standard test to diagnose asthma, and is a method of assessing lung function by measuring the volume of air that the patient is able to expel from the lungs after a maximal inspiration. It is a reliable method of differentiating between obstructive airways disorders and restrictive diseases and to monitor disease severity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

key measures in spirometry

A

– FEV1; Volume of air forcibly exhaled after deep inspiration in 1 second.
– FVC; Total volume of air forcibly exhaled in one breath.
– FEV1/FVC ratio

– FEV1 and FVC are expressed as percentages of a ‘predicted normal’ based on
aged, gender and height.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

normal ranges for fev1, fvc, fev1/fvc ratio

A
  • FEV1: >80% predicted
  • FVC: >80% predicted
  • FEV1/FVC ratio: >0.7
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

typical spirometry findings in obstructive lung disease

A

– Reduced FEV1 (<80% of the predicted normal).
– Reduced FVC (but to a lesser extent than FEV1).
– FEV1/FVC ratio reduced (<0.7).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

airway inflammation pharmacological management

A

corticosteroids
leukotriene receptor antagonists
monoclonal antibody therapies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

corticosteroid examples

A

beclometasone, budenoside, fluticasone, prednisolone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

side effects of corticosteroids

A

Dysphonia, Oral Candida, Hyperglycaemia, Osteoporosis, Cushing’s
Syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

mechanism of action of corticosteroids

A

bind to intracellular glucocorticoid within bronchial smooth cells to form receptor complexes

complexes interfere in gene transcription
formation of PLA2 inhibited

result - decreased prostaglandin and leukotriene formation → decreased inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

mechanism of action of leukotriene receptor agonists

A

bind to leukotriene receptors on mast cells, eosinophils and alveolar macrophages

prevent leukotrienes from binding

reduced bronchostriction, reduced cytokine release, overall reduced airway oedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

side effects of leukotriene receptor agonists

A

headache, GI disturbance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

examples of leukotriene receptor agonists

A

montelukast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

mechanism of action of monoclonal antibody therapies

A

binds to IL5 and prevents this from binding to eosinophils

reduces inflammation and subsequent cytokine release

40
Q

examples of monoclonal antibody therapies

A

mepoluzimab benraluzimab

41
Q

airway obstruction pharmacological management

A

beta 2 agonists
muscarinic antagonists
theophyllines

42
Q

beta 2 agonists mechanism of action

A

bind to beta 2 receptors on bronchial smooth muscle
adenylyl cyclase activated and generation of cAMP
PKA activated
bronchial smooth muscle relaxation via potentiation of the SNS

43
Q

side effects of monoclonal antibody therapies

A

Abdominal pain, fever, headache, hypersensitivity

44
Q

side effects of beta 2 agonists

A

fine tremor
palpitations
hyperkalaemia
arrhythmia

45
Q

examples of beta 2 agonists

A

salbutamol, formoterol, tertubuline

46
Q

mechanism of action of muscarinic antagonists

A

bind to M2 receptors on bronchial smooth muscle

prevent Ach from binding

minimises activation of PNS, reduced bronchoconstriction

47
Q

side effects of muscarinic antagonists

A

dry mouth/eyes

48
Q

examples of muscarinic antagonists

A

Ipratropium Bromide, Tiotropium Bromide

49
Q

mechanism of action of theophyllines

A

inhibit phosphodiesterase enzyme (normally breaks down cAMP to AMP)
this means more cAMP remains within bronchial smooth muscle and can
go on to activate PKA and induce bronchial smooth muscle relaxation (potentiating SNS)

50
Q

side effect of theophyllines

A

arrhythmia, GI disturbance, seizures, hypokalaemia

51
Q

what is COPD?

A

an obstructive airways disease that is most commonly the result of a combination of chronic bronchitis and emphysema and characterised by airflow limitation

52
Q

chronic bronchitis

A

productive cough for more than 3 months each year for 2 or more consecutive years

53
Q

emphysema

A

destruction of the alveolar wall with dilation of airspaces

54
Q

risk factors for COPD

A

cigarettes
chemical dust
exposure to atmospheric pollution including biofuels
low birth weight
genetic - alpha-1-antitrypsin deficiency

55
Q

difference in a cross section of the airway for COPD

A

increased mucus
damaged cilia
extra goblet cells

56
Q

impact of COPD on ventilation/perfusion

A

abnormal V/Q resulting in respiratory acidosis - low O2 high CO2

57
Q

what is used to stage COPD?

A

spirometry

58
Q

stage 1 mild copd

A

fev1/fvc<0.7
fev1> 80% predicted

59
Q

stage 2 moderate copd

A

fev1/fvc<0.7
fev1 50-80% predicted

60
Q

stage 3 severe copd

A

fev1/fvc<0.7
fev1 30-50% predicted

61
Q

stage 4 very severe copd

A

fev1/fvc<0.7
fev1<30% predicted

62
Q

pharmacological management in copd

A

airway obstruction - beta agonists, muscarinic antagonists, theophyllines

airway inflammation - corticosteroids

63
Q

non pharmacological management in copd

A

smoking cessation/nicotine replacement
pulmonary rehab
long term oxygen therapy
non invasive ventilation
occasional lung surgery

64
Q

why does cor pulmonale occur?

A

increased right ventricular filling pressures from longterm pulmonary hypertension
pulmonary arterial pressure >20mmHg

65
Q

pathophysiology of cor pulmonale

A
  1. COPD and other diseases damage the lungs
  2. low oxygen leads to hypoxic pulmonary vasoconstriction - limits blood flow to hypoxic alveoli
  3. vascular remodelling
  4. increased pulmonary arterial pressure
  5. increased right ventricular afterload leading to RV dysfunction and failure
66
Q

diagnosis of cor pulmonale

A

ECHO - RV enlargement with tricuspid valve regurgitation
CXR - cardiomegaly (enlarged heart), chunky vessels, signs consistent with COPD
V/Q scan - rule out other causes of pulmonary hypertension
right heart catheterisation findings - pulmonary artery pressure >20mmHg

67
Q

management of cor pulmonale

A

optimise COPD treatment
long term oxygen treatment
some cases - heart-lung transplant

68
Q

differences between asthma and COPD

A
  1. AGE - asthma any, COPD typically older
  2. COUGH - asthma dry + night, COPD productive + anytime
  3. VARIATION OF SYMPTOMS - asthma diurnal variation, COPD consistent and progressive
  4. REVERSIBILITY OF AIRWAY OBSTRUCTION - asthma yes, COPD no
  5. CELL INVOLVEMENT - asthma eosinophils and CD4, copd - neutrophils, macrophages and CD8
  6. SMOKING HISTORY - asthma smoker or non smoker, COPD - typically smoking historu
69
Q

Pneumonia

A

type of lower respiratory tract infection, characterized by inflammation of lung tissue due to bacterial, viral, or fungal lung infection

70
Q

risk factors for pneumonia

A

smoking
underlying lung disease
immunocompromised
malnourished
underlying cardiovascular disease

71
Q

types of pneumonia

A
  1. community acquired pneumonia
  2. hospital acquired pneumonia
  3. aspiration pneumonia
72
Q

Pathophysiology of bacterial pneumonia

A
  1. bacteria is inhaled and uncontrollably replicates and colonises alveolus
  2. macrophages release cytokines
  3. vasodilation of pulmonary capillaries - vascular permeability
  4. more neutrophils recruited which go through leakt junction
  5. cell debris + neutrophils form pus
  6. improper ventilation - ventilation perfusion mismatch
  7. back flow of pus into other alveoli
73
Q

pathophysiology of viral pneumonia

A
  1. virus inhaled and enters cells in alveolar membrane and replicates in alveolar epithelium cell
  2. cell swells and bursts - cell lysis
  3. virus infects other cells lining alveoli
  4. inflammatory mediators and cytokines released during lysis - attracts macrophages
  5. macrophages release more cytokines - vascular permeability
  6. lymphocytes attracted and leak into alveoli
  7. pus build up
  8. ventilation perfusion mismatch and backflow
74
Q

key difference between viral and bacterial pneumonia?

A

viral - lymphocytes
bacterial - neutrophils

expect coryzal symptoms in viral

75
Q

alveolar congestion presents as:

A

chest pain, productive cough, breathlessness

clinical symptom: reduced air entry, bronchial breathing, dull to percussion, coarse crackles

76
Q

cytokines entering systemic circulation presents as:

A

fevers/rigors, fatigue, confusion

clinical symptom; hypotension, tachypnoea, altered mental state

77
Q

airway inflammation presents as:

A

wheeze, breathlessness, chest pain

clinical symptoms: respiratory distress, hypoxia

78
Q

investigations for pneumonia

A
  1. blood tests - WBC and which
  2. blood cultures - which pathogens
  3. urinary antigen testing - which pathogens
  4. viral swabs - flu/rhinovirus
  5. CXR/CT scan - see blocks
79
Q

what is the CURB-65 scoring system used for

A

to see whether to admit to hospital
considers confusion, respiratory rate, BP, age

80
Q

treatment for pneumonia

A
  1. antibiotic therapy
    amoxicillin 500mg
    OR
    amoxicillin 1g + consider doxycycline
    OR
    co-amoxiclav 1.2g IV + clarithromycin 500mg oral

supplemental oxygen
fluids
analgesics
chest physiotherapy

81
Q

What is a pulmonary embolism

A

the obstruction of the pulmonary artery or one of its branches by material – usually a thrombus (blood clot)

82
Q

risk factors for PE

A

previous PE/DVT
malignancy
recent surgery
immobility
pregnancy
age
smoking
obesity
clotting problems
acute infection/inflammation
cardiac/neuro comorbidities
oral contraceptives
HRT

83
Q

how does a thrombus form?

A

virchows triad
vessel wall injury + hypercoagulability + stasis

84
Q

thrombus migration embolisation

A

deep vein → right atrium → right ventricle → pulmonary trunk → branch of pulmonary artery

85
Q

pathophysiology of persistent hypotension

A

thrombus lodged in pulmonary artery
→ inc pulmonary vascular pressure
→ inc in right ventricular pressure
→ right heart failure
→ reduced CO and hypotension
→ stimulation of sympathetic nervous system - tachycardia and vasoconstriction

86
Q

pathophysiology of respiratory failure

A

thrombus lodged in pulmonary artery
→ reduced blood flow to area of lung supplied by artery
→ ventilation-perfusion mismatch and inflammation → impaired gas exchange - LUNG INFARCTION
→ compensatory hyperventilation
→ persistent hypoxia and hypocapnia causing ALVEOLAR COLLAPSE, RESPIRATORY ALKALOSIS

87
Q

hypotension and respiratory failure can cause?

A

respiratory or cardiac arrest

88
Q

clinical manifestation of right ventricular failure and decreased CO

A

Hypotension
syncope
dizziness
breathlessness

89
Q

clinical manifestation of ventilation perfusion mismatch

A

breathlessness - inc RR
palpitations - inc HR
hypoxia, hypocapnia

90
Q

clinical manifestation of lung infarction

A

chest pain
haemoptysis

91
Q

clinical manifestation of bronchostriction

A

chest pain
wheeze
cough

92
Q

clinical manifestation of original thrombus

A

calf pain/swelling
calf redness

93
Q

investigations for suspected PE (wells score dependant )

A

determined by Well’s score:
<4 - d dimer blood test
>4 definitive diagnostic imaging - CT pulmonary angiogram, non conclusive then v/q nuclear medicine scan

94
Q

other investigations for suspected PE

A
  • blood tests - BNP and troponin
  • arterial blood gas
  • ECG
  • CXR
  • bedside echo
95
Q

wells score criteria

A

symptoms of DVT
PE most likely diagnosis
tachycardia more than 100bpm
immobilization or surgery in last month
prior dvt/pe
hemoptysis
active malignancy

96
Q

management of PE for hemodynamically stable

A

anticoagulation treatment + discharged with follow up

Clinical Physiology (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions