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Phase 1 > Respiritory > Flashcards

Respiritory Flashcards

1
Q

what do slow adapting stretch receptors do?

A

• Slow adapting strech receptors - in the airways of smooth muscle, inhibit inspiration in response to stretch

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2
Q

what do rapidly adapting stretch receptors do

A

Rapidly adapting stretch receptors – airway epithelial cells, respond to rate of change of volume as well as irritants,
possibly initiating cough as well as asthma exacerbations as can cause bronchoconstriction with high stimulation. Conversely can also stimulate long, deep breathing

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3
Q

what do juxtapulmonary receptros do

A

Juxtapulmonary receptors – respond to irritants, lung volume, interstial fluid volume and noxious agents. Cause bronchoconstriction, rapid & shallow breathing, reduced CO

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4
Q

what is the last ring of cartilage in teh trachea called

A

carina

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5
Q

what is respiritory epithelium

A

pseudostratified cilliated columnar epithelium interspersed with goblet cells

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6
Q

what are teh two centres of breathing?

A

• Apneustic centre - pontine centre that acts on dorsal respiratory groups to increase respiration
Pneumotach centre - stops inhalation to allow for exhalation, increased stimulation leads to shallower ventilation

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7
Q

where are the peripheral chemoreceptors

A

carotid arteries and aortic arch

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8
Q

describe teh embryology of the lungs

A
  • Lungs develop from the lung bud, an outpunch of the foregut called respiratory diverticulum, this happens in weeks 4-5 an is called the embryonic phase
    • Pseudo glandular phase - 5 - 17 weeks - development of conducting airways
    • Canalicular phase - 16-25 weeks, capillaries, vasculature and alveoli form
    • Alveoli - the alveolar continue to develop up to birth (and beyond)
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9
Q

when is lung surfacnctant produced in teh feotus

A

between 24-28 weeks but enugh to breateh from 34 weeks onwards

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10
Q

what is a mysfunction that can happen during teh embryological creation of teh lungs?

A

• Oesophageal atresias - the oesophagus and trache don’t separate properly

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11
Q

what are the circulatory changes that happen at birth?

A
  • At birth, there is a big increase in systemic circlatory pressure when the umbilical chord is clamed as the blood is no lobger trvelling out to the placenta
    • The amniotic flid inside the lungs is then expelled and the pulmonary pressre will decrease to increase flow
    • Reducced pressure also prevent cardai shunting so the ductus arteriosus and foramen ovale close
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12
Q

what are 4 non immune protecors of teh lungs

A

mucocillary esculator, coughing and sneezing, antimicrobial molecules that act as opsions, multipotent basal epitheloum that can specalise to replace damaged epithelium

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13
Q

what is teh innate immune systme of teh lungs?

A

alveolar macrophages

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14
Q

how do neutrophills kill?

A

repiritory burst, using the NADPH oxidase complex

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15
Q

what is immune tolerance

A

the prevention of an immune response against a specific antigen, this is done by T regulator cells

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16
Q

what is teh first hypersensitivity reaction?

A
  1. Allergy, anaphlaxyis and atopy: IgE - release of histamine from mast cells, cuasing vasodilation which alows from inflamation
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17
Q

what is teh second hypersensitivity reaction?

A

Autoimmune - IgM and IgG - cytotoxic (cell killing) attacking own body cells

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18
Q

what is teh third hypersensitivity reaction

A
  1. Immune complex diseases - IgG - there is a lareg gscale immune response leading to clumps og IgG antibodies that cant be cleared by macrophages wihc causes inflimatio to happen and it’s a bit like an allergic reaction to the bodys own immune system
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19
Q

what is teh fourth hypersensitivity reaction

A

Delayed hypersensitivity reaction - t helper cells form granulomas and release loads of cytokines and basically go cray cray ebing little rascals and casuign inflamation and cell death - the psycho girlfrind perhaps? It’s a bit delayed as well.

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20
Q

whihc of the lungs is food more likely to go doen

A

the right one as it is more vertical

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21
Q

what are the 2 pneumocytes?

A
  • Type 1 is for gas exchange

* Type 2 for surfactant production

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22
Q

what in the lungs heps teh macrohages to move though

A

• Adjacent alvioli are connected though the pores of kohn which allows the movement of macrophages though

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23
Q

which nerves inorvate bronchodilation

A

• T2-4 sympathetic ganaglia do bronchodilation

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24
Q

what receptors cause broncho dilation?

A

Beta 2 adrenaline cause vasodilation

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25
Q

what causes bronchoconstriction

A

vagal nerve causes bronchoconstirction, this is the muscarinic receptors and help to protect agist irritant s and such

26
Q

how can knowledge of bronchocnsitrictors help to cure asthma

A

• Treatments for asthma are either beat 2 agonists or antimuscarins

27
Q

whatt are the three types of dead space and their corrosponding figures?

A
  • Anatomical dead space - the conducting airways (150ml)
    • Alveolar dead space - where there is no perfusion inside of the alvioli (25ml)
    • Physiological dead space - 175ml (alveolar and anatomical added together)
28
Q

what is teh parietal pleura of teh lungs inorvated by

A

teh phrenic nerve

29
Q

what are the 7 layers of gas exchange

A

1.Fluid lining alveolus 2. Layer of epithelial cells – type I pneumocytes 3. Basement membrane of type I cells 4. Interstitial space 5. Basement membrane 6. Endothelia 7. Erythrocyte

30
Q

how do te different muscels help inspiration

A

• The diaphragm does 70% of inhalation
• Pectoral major helps to lift ribs 3-5
• Sternocliedo mastoid helps to elevate the sternum
Internal intercostals and the rectus abdominals are the only muscles of active expiration

31
Q

what is hypoxic pulmonary vasoconstriction

A

Hypoxic pulmonary vasoconstriction (HPV) is a reflex contraction of vascular smooth muscle in the pulmonary circulation in response to a low regional partial pressure of oxygen. It is an important mechanism for matching of regional perfusion and ventilation in the lung

32
Q 
what do all of tehse stand for - 
PaCO2
PACO2
PaO2
PAO2
PIO2
VA
VCO2
A

• PaCO2 arterial CO2 • PACO2 Alveolar CO2
• PaO2 arterial O2
• PAO2 Alveolar O2 (~14kPa)
• PIO2 Pressure of inspired O2 • V’A Alveolar ventilation
V’CO2 CO2 production

33
Q

what is boyles law? what does it mean?

A

Boyles law: P1V1=P2V2
• This means that if you increae th evolume of the thorassic cavity air flow to the lungs will increae in order to equalise the pressre

34
Q

defien compliance

A

Compliance - the change in volume in the lungs for a given change in transpulmonary or transmural pressure. This is permissed by elastic fibres and surfactant.

35
Q

what is teh henderson hassleback equation for the lungs?

A

• HH equation - pH=6.1 + log10([HCO3-]/[0.03PCO2])

36
Q

what is tidal volume and its ml?

A

Tidal volume- normal breathing 500ml

37
Q

inspitiroy reserv volume deofrnition and amount?

A

Inspiritory reserve volume - max air that can be inhaled over tidal - 3l

38
Q

• Expiritory reserve volume + amount?

A

• Expiritory reserve volume - max air that can be exhaled minus tidal 1.2l

39
Q

what is residual volume and its amount

A

Residual volume - air remaining in lungs after max expiration - 1.2l

40
Q

what is vital capcity and its amount

A

Vital capacity - max air expired after max inhilation - 4.7l

41
Q

what is insp. capacity, its amount, and its equation

A

• Insp. capacity – max inhalation after normal tidal expiration 3.5L (IRV + TV)

42
Q

wha is functional residual capacity, its amount and its equation?

A

Functional residual capacity – air in lungs after tidal expiration 2.4L (RV + VC)

43
Q

what is teh amount of total lung capacity

A

5.9l

44
Q

what is teh FEV1 and FVC

A
  • FEV1 - maximum amount that can be forced out in the first second of expiration - should be 80% of vital caoacity if healthy
    • FVC - max air expelled under max force
45
Q

what is peak air flow

A

• Peak air flow - highest velocity of air measured during FVC

46
Q

define obstructive and restirictive airway diseases and give and example for each

A

• Airway obsturction - the tubes are smalles (ie in asthma), this leads to a FEV1 below 0.7 but FVC wont change overall
Airway restriction - reduced compliacen of the lunds - reduces both FEV1 and FVC (pulmonary fibrosis

47
Q

what are the three ilnesses that can occur due to high altitudes

A
  • Acute mountain sickness - feels like a hangover but not too dangerous
    • High altitude pulmonary oedema - they have ascended too quickyl for acclimatisation to occur
    • Hight altitude cereberal oedema - water n the brain - bad innit
48
Q

what are the normal readings for blood gasses - PaO2, PaCO2 and pH?

A
  • PaO2 = 10.5 - 13.5KPa
    • PaCO2 = 4.5 - 6KPa
    • pH = 7.36 - 7.44
49
Q

what are the three conditions caused by depth

A
  • Inert gas narcosis - N2 collects in the cells of the brain and can lead to unconsicousness and death
    • Decompression sickeness - N2 forms bubbles in the blood system, cuases rash and join pain then neruological imparmetn
    • Arterial gas embolism - rapid overexplansino of pulmonary veins causes tear sin the walls and so air can get in and causes an embolism
50
Q

what is daltons law

A

Daltons law - sum of the parital pessure of gasses is the same as the total partial pressure

51
Q

what is poisulles law

A

Poisulles law - resistance ina dube is dependant on the radius of te tube and viscocity of the fluid

52
Q

what is laplaces law

A

• Laplaces law- wall tention is proportional to cessle radius, increase surfactent reduces surface tention p= 2T/r

53
Q

what ios henrys law

A

• Henrys law - at high pressure insoluble gasses are more lilely to dissolve

54
Q

what ios henrys law

A

• Henrys law - at high pressure insoluble gasses are more lilely to dissolve

55
Q

what causes the oxygen graph to shift to the right

A

Right shift - there is a reduced affinity for oxygen, this is caused by increased:temp and H+

56
Q

what are the two types of respiritpry faliure

A
  • Type 1 - low O2, normal CO2
    • Can be due to ventilation perfusion mismatch, pneumonia, pulmonary oedema or heart faliure
    • Type 2 - hypoxemia and hypercapnia, low O2, high CO2, COPD, loss of respitory drive (opiods) obesity, motor neuorn disease
57
Q

what are the 4 types of hypoxia

A

• Hypoxic hypoxia - not enough O2 in the blood
• Aneamic hypoxia - not enough Hb to carry the O2
• Stagnent hypoxia - blood flow to tissues uis too slow
Histotoxic hypoxia - toxic agent stops cell from using O2

58
Q

how can obstructive airway disorders such as COPD be diagnosed

A

• COPD can be diagnosed if the FEV1 is low but the FVC is normal - due to the narrowing of the airways

59
Q

what is emphysema

A

• Emphysema is a lung condition that causes shortness of breath. In people with emphysema, the air sacs in the lungs (alveoli) are damaged. Over time, the inner walls of the air sacs weaken and rupture — creating larger air spaces instead of many small ones

60
Q

how thick us teh air blood barrier

A

0.2um- 1um

Phase 1 (11 decks)

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