case 5 resp Flashcards

1
Q

what type of cartilage exists in the trachea?

A

hyaline

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2
Q

which cells in the airway make mucus?

A

goblet cells

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3
Q

in which syndrome does mucociliary escalator not work?

A

kartagener syndrome

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4
Q

parasympathetic innervation of the airways has what 3 main functions?

A
  1. bronchoconstriction
  2. vasodilation
    3 mucus secretion
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5
Q

sympathetic innervation of the airways has what 3 main functions?

A
  1. bronchodilation
  2. vasoconstriction
  3. modulation of cholinergic transmission
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6
Q

what is the relationship between airway resistance and airflow?

A

high resistance = low airflow

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7
Q

structurally how can an airway have increased resistance?

purely structurally

A

long airway + small radius = high resistance

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8
Q

low amount of what protein will cause neonatal respiratory distress syndrome?

function of this thing?

A

surfactant

surfactant stops alveolar collapse

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9
Q

how does compliance change in emphysema?

A

high compliance

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10
Q

how does compliance change in pulmonary fibrosis?

A

low compliance

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11
Q

what happens to airways in asthma (structurally)?

A

constricts

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12
Q

is this condition obstructive or restrictive?

asthma

A

obstructive

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13
Q

is this condition obstructive or restrictive?

pulmonary fibrosis

A

restrictive

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14
Q

is this condition obstructive or restrictive?

emphysema

A

obstructive

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15
Q

is this condition obstructive or restrictive?

motor neurone disease

A

restrictive

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16
Q

Va:Q ratio

what does Va stand for?

what does Q stand for?

A

Va - ventilation

Q - perfusion

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17
Q

what is the anatomical dead space?

what is the value of the Va:Q ratio in the dead space?

A

where there is no capillary perfusion but there is ventilation.

infinity

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18
Q

how can an anatomical dead space be created pathologically?

A

pulmonary embolism

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19
Q

in a right to left shunting of blood what is Va:Q ratio?

how can this shunting occur in the lungs pathologically?
-2

A

0

occluded airway or
fluid filled alveoli (i.e. pulm oedema)

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20
Q

how does perfusion change moving down the lung?

A

increases

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21
Q

how does ventilation change moving down the lung?

A

increases

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22
Q

in a normal alveoli, how much O2 is there in mmHg?

A

100 mmHg

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23
Q

in a normal alveoli, how much CO2 is there in mmHg?

A

40mmHG

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24
Q

in a normal alveoli, how much O2 is there in kPa?

A

13.3kPa

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25
Q

in a normal alveoli, how much CO2 is there in kPa?

A

5.3kPa

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26
Q

if there is low Va (ventilation) in a certain area of the lung how does pulmonary vasculature react to stop V:Q matching?

why does it do this?

A

pulmonary vasculature vasoconstricts

stop Va:Q mismatching

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27
Q

someone is at high altitude and gets global lung hypoxia.

how does pulmonary vasculature react in this situation?

what complication will this lead to?
-2

A

global pulmonary vasculature vasoconstricts

pulmonary HTN –> R.sided heart failure

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28
Q

where is the central control area for breathing in the brain?

what is this centre called?

A

medulla, brain

medullary respiratory centre

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29
Q

what two receptors feed the
medullary respiratory centre
information?

A

central chemoreceptors &

peripheral receptors

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30
Q

of the two receptors feeding the medullary respiratory centre with info:

which is sensitive to CO2 only?

A

central chemoreceptors

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31
Q

of the two receptors feeding the medullary respiratory centre with info:

which is sensitive to O2 and CO2?

A

peripheral receptors

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32
Q

of the two receptors feeding the medullary respiratory centre with info:

which has a fast response time?

A

peripheral receptors

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33
Q

of the two receptors feeding the medullary respiratory centre with info:

which has a slow response time?

A

central chemoreceptors

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34
Q

where are the central chemoreceptors found?

A

ventrolateral surface of medulla

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35
Q

where are the peripheral chemoreceptors found?

A

near carotid and aortic arteries

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36
Q

the medullary respiratory centre is most sensitive to what:

hypoxia
hypercapnia
or both

A

both - synergy of hypoxia & hypercapnia increases minute ventilation the most

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37
Q

what are the functions of the lung?

-6

A

blood reservoir
make ACE
bring blood into contract with alveoli (gas exchange)
source of heparin (blood thinner)
source of thromboplastin (blood clotter)
protects body from emboli vis mechanical filtration

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38
Q

how do pulmonary arterioles differ from systemic arterioles?

-4

A

thinner
less elastin
less smooth muscle
more compliant

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39
Q

what happens to pulmonary arterial pressure moving up the lung?

A

decreases

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40
Q

where is ventilation best in lung, bottom or top?

A

bottom

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41
Q

why does top of lung have worst ventilation?

A

top of lung has more negative pressure - so alveoli keep expanded - thus less ventilation

42
Q

as you move up the lung, blood flow through the pulmonary vasculature only occurs when?

why

A

in systole

because pulmonary arterial pressure decreases moving up the lung

43
Q

in which pathologies will there be no blood flow through pulmonary vasculature?
- 2 main ones

why?
- step by step

A

sepsis, massive haemorrhage

because these pathologies have less blood volume, so less BP, so less pulmonary arterial pressure, so blood not pushed through vasculature/ can not overcome alveoli pressure

44
Q

for blood to move through pulmonary vasculature what must the pulmonary arterial pressure overcome?
-2 things

A

alveoli pressure

pulmonary venous pressure

45
Q

there is an over ventilated area in the lung.

how does lung respond to minimise V/Q mismatch?

A

bronchoconstriction

46
Q

there is local ischaemia in an area of the lung.

how does lung respond to minimise V/Q mismatch?

A

bronchoconstriction

47
Q

there is local hypoxia in an area of the lung.

how does lung respond to minimise V/Q mismatch?

A

vasoconstriction

48
Q

if there is increased perfusion pressure (i.e. more blood flow in the lung) say during exercise.

what adaptations does the lung have to stop pulmonary vascular resistance in response to the increased perfusion pressure?
-2

if the lung did not adapt what complications will develop?
-2 (they are linked to each other)

A

vessels distend
recruits dormant pulmonary capillaries

pulm HTN –> R.sided heart failure

49
Q

vasoconstriction will cause what to happen to lumen size?

what does this increase in the airways?

what complication will now occur?

A

decreases/narrower

resistance

pulm HTN

50
Q

pulmonary HTN will eventually lead to what major complication?

A

R.sided heart failure

cor pulmonale

51
Q

Right ventricular failure due to a lung problem is called what?

how will the RV adapt to increased pulmonary HTN?

A

cor pulmonale

RV muscle becomes thicker

52
Q

what happens to cardiac output in cor pulmonale eventually?

A

↓CO

53
Q

where does the oedema occur in R.sided heart failure?

A

systemic oedema

54
Q

where does the oedema occur in L.sided heart failure?

A

pulmonary oedema

55
Q

features or cor pulmonale (basically R.sided heart failure)

A
cyanosis 
SOB 
ascites
raised JVP 
big neck and veins 
swollen ankles
56
Q

drug group to get rid of fluid in cor pulmonale?

A

diuretics

57
Q

restrictive lung diseases can be divided into what two categories?

A

pulmonary &

extra-pulmonary

58
Q

which lung cell type produces surfactant?

A

type 2 alveolar cells

59
Q

which cells in the lung make collagen?

A

fibroblasts

60
Q

which cells in the lung make elastin?

A

fibroblasts

61
Q

define fibrosis

A

tissue scars and thicken (too much collagen)

62
Q

CT of lung with pulmonary fibrosis shows what hallmark feature?

A

honeycomb appearance

63
Q

symptoms & signs of pulmonary fibrosis?

-5

A
dry cough 
SOB 
finger clubbing 
peripheral cyanosis 
fine end inspiratory crackles
64
Q

with pulmonary fibrosis, what decreases on spriometry?

A

FVC, functional vital capacity

65
Q

extra-pulmonary restrictive lung disease examples?

-5

A

obesity
scoliosis/ kyphosis
motor neuron disease
pleural effusion

66
Q

why does pleural effusion cause restrictive lung disease?

A

extra fluid (between parietal and visceral) compresses on lung

67
Q

define FEV1?

A

air you blow out in 1 second

68
Q

define FVC?

A

total volume of air blown out

69
Q

define respiratory failure?

A

pulmonary gas exchange is insufficient and hypoxaemia occurs (with or without hypercarbia)

70
Q

what are the two types of respiratory failure?

A

type 1: hypoxaemia only

type 2: hypoxaemia and hypercarbia

71
Q

what is the cut off value for hypoxaemia?

  • kPa
  • and mmHg
A

PaO2 <8kpa/ 60mmHg

72
Q

what is the cut off value for hypercarbia?

  • kPa
  • and mmHg
A

PaCO2 >7kPa/55mmHg

73
Q

mainstay (immediate) treatment for hypoxaemia?

A

give O2

74
Q

which respiratory failure occurs when there is ventilatory failure?

define this type of respiratory failure?

A

type 2

type 2: hypoxaemia and hypercarbia

75
Q

mainstay (immediate) treatment for type 2 respiratory failure?

A

ventilation

76
Q

high CO2/ hypercarbia symptoms

A

drowsy
sleep in day
confused
headache

77
Q

high CO2/ hypercarbia sign at the hand?

A

hand flap

78
Q

why should you not over oxygenate a pt with hypercarbia which is ultimately result of ventilatory problem?

A

over oxygenation can reduce their ventilatory drive since low O2 tells medulla to ventilate more.

79
Q

what electrolyte is lacking in cystic fibrosis mucus?

what effect does this have on mucus viscosity?

A

Cl-

mucus thick

80
Q

how does peripheral nervous system affect mucus production?

A

more PNS = more mucus

81
Q

2 types of COPD?

A

emphysema

chronic bronchitis

82
Q

pathophysiology of chronic bronchitis?

A

sub mucosal glands and goblet cells hypertrophy –> excess mucus made –> can not get rid of all mucus –> get infected again –> more inflammation and thus more mucus made again.

83
Q

main way smoking causes chronic bronchitis?

A

paralyses mucociliary escalator

84
Q

emphysema pt use what type of breathing?

why?

A

pursed lip breathing

created negative pressure to stop airways collapsing

85
Q

which protein is destroyed in emphysema?

A

elastin

86
Q

step by step outline how COPD can cause cor pulmonale and systemic oedema?

A

sever COPD –> lung hypoxic –> pulmonary vasculature constrict –> more pulmonary resistance –> pulmonary HTN –> pressure on right ventricle, eventually fails –> cor pulmonale –> back pressure in systemic venous now so fluid pushed out

87
Q

obstructive value on spirometry?

A

<0.7

88
Q

restrictive value on spirometry?

A

> 0.7

89
Q

how does sputum become green in infection?

A

neutrophils go to fight infection –> neutrophil rupture –> ooze out myeloperoxidase –> myeloperoxidase make sputum green

90
Q

what score is used for pneumonia severity?

A

CURB65

91
Q

what does CURB65 stand for?

A
confusion 
urea
rep rate 
BP 
65+ age
92
Q

define pneumonia?

A

lung tissue itself infected

93
Q

hallmark feature of bronchiectasis?

A

dilated airways filled with mucus

94
Q

hallmark feature of bronchiectasis on CXR?

A

signet ring

95
Q

main cause of bronchiectasis>

A

infection

96
Q

what test is used to check for CF?

A

sweat chloride test

97
Q

pt has bronchiectasis.

what is head on ausculation?

A

coarse crackles

98
Q

what test is used to estimate left atrium pressure in LV heart failure?

A

pulmonary capillary wedge pressure

99
Q

why is it risky to give lots of opioids in pt with type 2 resp failure?

A

opioids diminish resp drive

100
Q

pt has hypercapnia.

how will headache severity change during day?

A

headache worst in morning

101
Q

how do you treat infant respiratory distress syndrome?

A

cPAP

102
Q

which pneumonia, hospital or community has higher mortality?

A

hospital