Respiratory Flashcards

1
Q

what is boyles law

A

pressure is inversely related to volume

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2
Q

functional residual capacity

A

volume of air in lungs after quiet expiration

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3
Q

vital capacity

A

inspiratory capacity plus expiratory reserve volume

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4
Q

total lung capacitt

A

vital capacity plus residual volume

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5
Q

anatomical dead space

A

air inside lung apart from alveoli that doesn’t take part in gas exchange

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6
Q

alveolar dead space

A

alveolar air that doesn’t get perfused

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7
Q

physiological dead space

A

anatomical plus alveolar

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8
Q

alveolar ventilation rate =

A

(tidal volume-dead space) - resp rate

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9
Q

muscles of forced inspiration

A

scalene, serrates anterior, teres m/m

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10
Q

muscles. quiet inspiration

A

diaphragm, external intercostals

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11
Q

muscles forced expiration

A

internal intercostals and abdo wall muscles

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12
Q

7 causes of interstitial lung disease

A

occupational, treatment, connective tissue, immunological, idiopathic

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13
Q

atelectasis definition and 3 causes

A

lobar collapse, compression/absorption

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14
Q

anatomical dead space vs physiological dead space vs alveolar dead space

A
  • Anatomical deadspace is the volume of air which is inhaled that does not take part in the gas exchange because it remains in the conducting airways
  • alveolar deadspace involves air reaching the lungs that is not perfused or poorly perfused due to dead/damaged alveoli (0.12 L)

Physiological dead space = anatomical + alveolar

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15
Q

How can one calculate the dead space ventilation rate?

A

DSVR = Dead space volume x respiration rate

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16
Q

How can one calculate alveolar ventilation rate?

A

AVR = (tidal volume - dead space volume) x respiration rate

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17
Q

How can one calculate lung perfusion?

A
  • Lung perfusion (Q) = RV output
  • It is the same as cardiac output (approx. 5 litres/min)
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18
Q

value of atmospheric pressure and water vapour pressure(SVP)

A

atmospheric- 101 kPa
water vapour- 6.28kPa

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19
Q

how to calculate partial pressure

A

gas % x atmospheric pressure

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20
Q

solubility coefficient for o2

A

0.01mmol/L

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21
Q

give values of alveolar and arterial pCo2 and pO2

A

pCO2- 5.3kPa
pO2- 13.3kPa

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22
Q

concentration of blood on Hb

A

8.935mmol/L

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23
Q

how to calculate partial pressure of oxygen in URT

A

(101-6.28) x 0.209

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24
Q

Henrys law

A

concentration of gas (mmol/L) = Kh x partial pressure of gas above liquid

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25
Q

what causes curve to shift to right and left

A

right-
lowered affinity, more o2 released
-increased temperature
-increased 2,3BPG
-increases H+

left-
increased affinity, less o2 released
-reduced temperature
-lowered 2,3BPG
-lowered H+
-CO

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26
Q

give atmospheric pressures for co2, o2 and n2

A

co2- 101x0.3 = 0.03kPa
o2- 101x0.29 = 21.109kPa
n2- 101x0.78 = 78.7kPa

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27
Q

give venous pressures for co2 and o2

A

both 6kPa

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28
Q

what is the most important stimulus’s in the minute to minute control of ventilation in a healthy person

A

effect of change in arterial pO2 at central chemoreceptors

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29
Q

how to calculate co2 dissolved

A

pco2 x 0.23 = 1.2mmol/L

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30
Q

Henderson hasselbachs equation

A

pH= pk + log (HCO3)/(CO2)

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31
Q

reaction of co2 and red blood cells in tissues and in lungs

A

in tissues:
co2 diffuses into rbc, reacts to form hco3- and h+
rbc in t state so H+ binds to it, shifting reaction to right

in lungs:
hco3- and h+ converted to co2. co2 diffuses out. rbc in r state so H+ cannot bind. increases h+ pushes reaction to left.

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32
Q

describe neuronal control of breathing

A

afferent-
glossopharyngeal from carotid codes, vagus from lung stretch and aortic bodies

receptor- RPG

efferent-
diaphragm phrenic nerve (c3450
internal intercostals intercostal nerve

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33
Q

where are peripheral chemoreceptors located and what are they sensitive to

A

aortic and carotid bodies

changes in pO2 and H+

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34
Q

where are central chemoreceptors located and what are they sensitive to

A

ventral surface of medulla

changes in co2 and h+

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35
Q

2 types imaging PE

A

pulmonar angiography, ventilation perfusion lung scintigraphy

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36
Q

5 causes hypovolaemia

A

low inspired o2, VQ mismatch, diffusion defect intra lung shunt, hypoventillaiton

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37
Q

most common cause of pulmonary embolism in young people w no risk factors, and 2 other causes

A

protein c resistance secondary to factor V Leiden mutation

  • protein c resistance
  • antithrombin III resistance
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38
Q

what medical conditions are hypercoaguable

A

lupus anticoagulant, homocystinuria. occult neoplasm

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39
Q

3 outcomes of PE

A

RV failure, pulmonary infarction due to haemoptysis, pleuritis and pleural effusion, and resp failure

40
Q

main investigations PE

A

blood gas shows hyperaemia and hypocapoa, CXR shows wedge shape, ECG shows RV strain or SI, QIII, TIII, raised D dimers

41
Q

what is SI, QIII, TIII

A

deep S wave lead 1, q wave lead 3, inverted t wave lead 3

42
Q

immediate treatment PE and why used

A

immediate heparisation

  • stops thrombus propogation in pulmonary arteries and embolic source
  • allows fibronolyssis of embolus
43
Q

how to treat high risk PE patient

A

haemodynamic and resp support, exogenous fibrinolytic, percutaneous catheter directed thrombectomy, surgical pulmonary embelectomy

44
Q

2 long term treatments PE

A

oral warfarin, DOAC- direct oral anticoagulant

45
Q

describe immediate and late phase response asthma

A

immediate-
TH2 cell
IgA interacts with allergen. causes mast cell degranulation and bronchocontriction

late phase
inflammatory cells cause airway inflammation

46
Q

5 hallmarks of asthma

A

chronic inflammatory, variable airflow obstruction, susceptibility, reversibility, hyperresponsiveness

47
Q

effects of inflammation asthma

A

Mucosal swelling ,
Thickening of bronchial walls
Mucous over production
Smooth muscle contraction
The epithelium is shed

48
Q

3 effects of airway remodelling asthma

A

hypertrophy of smooth muscle, mucus glands and basememt membrane

49
Q

describe VQ mismatch asthma

A

early- vasconstricton and hyperventilation can account for Co2 but not o2. type 1 resp failure

late- exhaustion and complete airway closure mean co2 rises. type 2

50
Q

signs and symptoms COPD

A

tachypnoea, barrel chest, cough, dyspnoea, hyperressonance wheezing.

cor pulmonale, co2 flap, cyanosis

51
Q

symptoms bronchiectasis

A

fever, fine crackles, sputum, inspiratory squeak

52
Q

draw a flow volume loop marking PEF and FVC

A
53
Q

draw a volume time loop marking FEV1 and FVC

A
54
Q
A
55
Q

how to calculate CURB-65

A

Confusion

  • Urea > 7 mmol/l
  • RR > 30
  • BP <90/60
  • Age > 65 years

Score 2-5 = manage as severe

56
Q

4 drugs to treat TB

A

rifampicin, isoniazid, ethambutol, pyranzinamide

57
Q

signs pneumonia

A

tachypnoea, crackles, wheeze, dull percussion, increases breath sounds

58
Q

causes of CAP

A

common- S. pneumoniae

uncommon- H influenza, mycoplasma pneumoniae

59
Q

cause of HAP

A

pseudomonas aurginosa

60
Q

cause aspiration pneumonia

A

flora and anaerobes

61
Q

casue immunocompromised pneumonia

A

cytomegalovirus

62
Q

what to look for on xray

A

Rotation

  • clavicle equidistant from spinous processes and spinous processes vertical

I- inspiration

5-6 anterior ribs, the lung apices, both costophrenic angles and lateral rib edges should be visible

P- projection

AP vs PA film

E- exposure

vertebra visible through heart

63
Q

what test is positive for latent TB vs active TB

A

latent- quantiferon and mantoux

active- sputum smear (ziehl-nielsen)

64
Q

what is miliary tb

A

secondary TB returns to lungs

65
Q

what is the gohn complex

A

primary focus and draining lymph node

66
Q

4 concequences of post primary TB

A

pleural effusion, cavitation, haemorraage, infection of lung apex

67
Q

symptoms TB

A

fever

night sweats

weightloss

cough

dyspnea

haemoptysis

68
Q

signs TB

A

crackles, consolidation on CXR

69
Q

cause of primary sponteneous pneumothorax and who does it occur in

A

in young, talll, male, smokers

spontaneous- rupture of pleuritic bleb

70
Q

cause secondary spontaneous pneumothorax

A

COPD, asthma, bronchiectasis, marfans

71
Q

where to insert needle for in needle thoracocentesis for tension pneumothorax

A

2 ICS, mid clavicular line. just above 3rd rib

72
Q

signs and symptoms tension pneumothorax

A

symptoms- pleuritic chest pain, SOB, severe respiratory distress, tachypnoea, tracheal shift, elevated JVP, tachycardia and hypotension

signs- reduced vocal resonance and chest movements, hyper ressonance

73
Q

safe triangle

A

L pec major, L latissimus dorsi, 6th rib, axilla

74
Q

how to treat pneumothorax

A

tension-

emergency insert needle into 2nd ICS, midclavicular line

simple-

chest drain into safe triangle, inserted to the pleural space and connected to an underwater seal, allowing the air to be drained out and the lung to expand.

75
Q

triggers for asthma

A

cold, exercise, alllergy, emotional distress, fumes

76
Q

2 types of treatment for asthma

A

B2 agonists eg. salbutamol

muscarinic antagonists- ipratroprium

77
Q

what type of immunity follows post exposure to TB bacillus

A

cell mediated

78
Q

what cell in granuloma

A

langhans giant cell

79
Q

compare latent and active TB

A

in latent TB bacili are not multiplying in active they are

patient is asymptomatic in latent

patient has negative sputum/smear in latent TB and has a normal CXR

80
Q

2 things that increase risk for reactivation latent tb

A

HIV, malignancy, malnutrition, substance abuse, long term steroids

81
Q

3 investigations TB

A

TB bacilli on sputum smear, Tb bacilli on sputum culture, NAAT on sputum sample

82
Q

location of peripheral chemoreceptroa

A

aortic and carotid bodies

83
Q

what causes hypoxaemia in respiratory distresss syndrome newborn

A

VQ mismatch. partially collapsed alveoli are still perfused. Q>V

84
Q

how to calculate pack years

A

number of years x number of packs a day

85
Q

how does bronchial carcinoma cause left vocal cord paralysis

A

left recurrent laryngeal nerve travels down thorax, loops arund arch aorta amd back up larynx. damaged by carcinoma. causes paralysis

86
Q

cough reflex

A

deep inspiration, closure of glottis, contraction expiratory muscles, glottis opens, forceful expulsion of air

87
Q

2 complications from spread of bronchial carcinoma

A

paralysis of left hemidiaphragm causes breathlessness

pericardial effusion causes pleurtic chest pain

88
Q

why does pco2 increase after oxygen therapy is started

A
  • oxygen reduces pulmonary hypoxia induced vasoconstriction in poorly ventillated alveoli. reduces VQ as blood diverted from better ventillated alveoli.

oxygenated Hb cannot carry as much co2 and so less is removed from tissues

89
Q
A
90
Q

Causes interstitial lung disease

A

Idiopathic- pulmonary fibrosis Immunological- sarcoidosis Connective tissue disease- RA Treatment related- radiation/chemotherapy Occupational- asbestosis and coal worker pneumoconiosis

91
Q

How to calculate pack years

A

Years of smoking x (cigarette number/20)

92
Q

Compare SCC and NSCC

A

SCC is aggressive and lots of metastatic growth NSCC is slower growing and treated with surgery

93
Q

Which cancer associated with aspestos

A

Mesothelioma

94
Q

Parameoplastic symptoms cancer

A

SIADH and cushings - SCC Hypercalcaeima- squamous cell carcinoma

95
Q

4 drugs and side effects TB

A

rifampicin- orange secretions

isoniazad- peripheral neuropathy

pyranimide- hepatotoxicity

ethambutol- visual distrubances

96
Q

exudate vs transudate

A

if the patient’s serum total protein is normal and the pleural fluid protein is less than 25g/L the fluid is a transudate. If the pleural fluid protein is greater than 35g/L the fluid is an exudate.

“Transudate” is fluid buildup caused by systemic conditions that alter the pressure in blood vessels, causing fluid to leave the vascular system. “Exudate” is fluid buildup caused by tissue leakage due to inflammation or local cellular damage.18 Jun 2020