respiration Flashcards

1
Q

explain the arrangement of function of the zones of the respiratory system

A

conducting zone = first 16 generations (gen 0 is the trachea as air enters here first), includes the nose, nasopharynx, oropharynx, pharynx, larynx, trachea, bronchial tree
responsible for filtering, warming and humidifying the air

respiratory zone - where gas exchange occurs, gen 17 and onwards, alveoli are present

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2
Q

what is the importance of 1) warming and 2) humidifying the air as it enters the lungs

A

1) gases are more soluble when cold, if the air is cold upon entering the blood and warms up there, decreasing it’s solubility, bubbles may form

2) addition of water vapour helps not to dry out the airways

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3
Q

describe the structure of the bronchi walls

A

Cartlidge rings
smooth muscle to control airway diameter
epithelial cells (ciliated) to remove particles out of the lings
goblet cells in the epithelia to produce mucus (at a closely moderated amount)
elastic tissue

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4
Q

respiratory peithelium - what properties do they have?

A

they are ciliated and are interspersed with goblet cells
there are nerve endings that sense noxious substances

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5
Q

how do bronchioles differ from bronchi?

A

they have no cartilage (but still have the epithelial lining)
they have proportionally more smooth muscle

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6
Q

explain the specialisations of alveoli and their cell types

A

thin walled, very close to surrounding capillaries - short diffusion pathway etc…

gas exchange takes place across epithelium type 1/ type 1 pneumocytes which have a flattened cytoplasm, everything is squished close together to speed up diffusion

type 2 epithelia produce surfactant

they increase SA - 50-100m^2

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7
Q

explain how quiet inspiration works and whose law this follows

A

Atmos. Pressure is greater than alveolar pressure
Diaphragm contracts and flattens,
External intercostal muscles contract lifting rib cage up and out,
Thoracic cavity and lungs inc. in volume, pressure decreases below atmospheric pressure

Boyle’s law

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8
Q

explain how forced inspiration works

A

same as quiet but with some added help -
scalene (neck muscles) and back muscles assist in pulling rib cage up
upper respiratory tract reduces resistance to flow

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9
Q

explain how quiet expiration works

A

passive process
no contraction of muscle contributes, instead elastic recoil is used
the muscles form quiet inspiration (diaphragm, external intercostal), ribcage lowers back, diaphragm domes up thoracic cavity and lung volume decrease, pressure inside exceeds atmospheric, air is forced out

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10
Q

what additional things happen in forced expiration?

A

abdominal muscles contract to push diaphragm up
neck and back muscles do something
internal intercostal muscle pulls ribcage in

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11
Q

explain the structure and function of the pleura

A

there’s one pleural membrane on the outside of the lungs, an interpleural space filled with fluid (allows for movement between lungs and chest as one) and then a membrane on the chest wall

at resting the lungs would collapse inwards due to their elastic nature, while the chest wall would tend to expand

these forces act in opposition on the pleural membranes and find a balance

this creates a sub atmospheric (below atmospheric) pressure between the two membranes

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12
Q

explain what happens in a pneumothorax

A

a collapsed lung
interpleural space is pierced, you lose the outer force of the chest, the inward force of the lungs due to the elastic nature wins, and the lung collapses

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13
Q

define compliance (lungs) and what it means to have high/low compliance

A

the ease with which the lung and thorax expands during a pressure change

low compliance = more effort required to breathe in and get the necessary volume change

high compliance = expiration is difficult, lack of elastic recoil (emphysema)

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14
Q

explain what surface tension is

A

attractive forces occur between water molecules
this means, at the surface, there are sideways and downwards forces toward other water molecules, but no upwards force, resulting in tightly packed water molecules at the surface with a tendency to dive down into the bulk of the solution

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15
Q

explain the forces in a bubble and the equation involved (Lapalace’s equation)

do small or larger bubbles have the greater pressure?

A

the pressure of the gas inside the bubble balances with the surface tension of the surrounding water

P = 2T / r

so the smaller the bubble (smaller radius), the higher the pressure

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16
Q

smaller bubbles have a greater pressure than larger ones
pressure moves from high to low
what problem does this present in the lungs?

how is this problem solved?

A

alveoli are like bubbles, and so gas would move from small alveoli at high pressure to larger ones and the small ones would just deflate which is pointless

surfactant produced by type 2 pneumocytes
it’s made of lipids mostly, plus some proteins, and acts like a detergent to reduce surface tension
hydrophilic head in the water with the hydrophobic tail sticking out provides an upward force to reduce surface tension, making it easier for expansion

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17
Q

surfactant ensures all alveoli inflate, but what else does it do?

A

prevents overexpansion - the surfactant’s density decreases as the alveoli stretches, reducing it’s effects so surface tension increases, assisting alveoli in recoiling/not overexpanding

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18
Q

define anatomical and physiological dead space

A

anatomical = volume of conducting airways

physiological = volume of lungs not participating in gas exchange, so conducting airways + non functioning

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19
Q

there are 8 things to know from a spirometer - what are they?

A

IRV = inspiratory reserve volume (from peak of normal breath to peak of max breath)
FEV = forced expiratory volume (fill lungs AMAP, blow out as hard as possible in 1 sec)
VC = vital capacity - deep breath in then breath out as much as you can
RV = residual volume, volume of air left in lungs you cannot breath out
TLC = total lung capacity RV + VC
TV = tidal volume = volume breathe in after 1 sec
ERV = expiratory reserve volume, how much you can force out after a normal exhale
FRC = functional residual capacity RV + ERV

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20
Q

in exercise tidal volume increases, but our lung’s capacity doesn’t change - how so?

A

residual volume decreases so the sum of TV and RV remains the same

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21
Q

how do you calculate residual volume?

A

put known volume of helium in the air chamber as this isn’t able to cross the alveoli
measure the concentration of helium before and after the experiment, use V1C1 = V2C2

22
Q

what is the relationship between air flow in/otu of the lungs and 1) the pressure gradient
2) the resistance

A

1) proportional
2) inversely proportional

23
Q

what is poiseuille’s law? what does this mean for airflow?

A

resistance is inversely proportional to the fourth power of the radius, meaning it only takes a small change in radius to massively impact resistance (and therefore flow rate)

24
Q

resistance - how is it shared between airways?
smaller radii = greater resistance so why do these proportions not follow that?

A

pharynx to larynx is responsible for 40% of resistance
airways bigger than 2mm are collectively responsible for 40%
airways less than 2mm = 20%

bigger aways are in series - you add resistance

smaller airways are in parallel so total resistance is 1/R + 1/R etc…)

25
Q

things that affect airway diameter increase resistance, so they also…

A

reduce airflow, like mucus or oedema

26
Q

how does smooth muscle control work in the lungs?

A

constriction = parasympathetic system, ACh released from vagus nerve, acts on muscarinic receptors (GPCRs)
dilation = sympathetic, release of noradrenaline = weak agonist of adrenergic receptors leads to dilation

27
Q

humoral factors - two molecules that effect constriction dilation?

A

epinephrine circulating blood = strong agonist causes dilation
histamine - released in inflammatory response = constriction

28
Q

what are the proportions and partial pressures of gas in dry (atmospheric) vs wet (trachea) air?

A

nitrogen - dry = 80% 590 mmHg
wet = 73% 560 mmHg

oxygen - dry = 21% 160
wet = 20% 150

carbon dioxide - dry = 0.03% 0.2
wet = same

Ar - around 1% and 7 in both

water - dry = 0, 0
wet = 6% and 47

29
Q

what is Dalton’s law?

A

total pressure = sum of partial pressures

30
Q

what is Henry’s law?

A

determines the concentration of gas dissolved in a solution
[dissolved oxygen] = S X P
S = solubility coefficient in mM/mmHg
P = partial pressure

31
Q

why do we need RBCs and haemoglobin?

A

plasma cannot deliver enough O2 alone:

where PP of oxygen is around 100 mmHg and its solubility in saline is low, around 0.003ml of O2 per 100ml blood per mmHg

at rest, cardiac output of of 5000ml/min the plasma can provide at most 15ml/min O2 to body, when it needs 250

32
Q

describe the structure of haemoglobin and the role of methaemoglobin reductase

A

tetrameric (four subunits)
each of the four subunits has a haem and a globin chain
in middle there’s a porphyrin ring with a single iron atom that must be 2+

methaemoglobin helps to convert Fe3+ back to Fe2+

33
Q

explain the difference between adult and foetal haemoglobin structure
what are the two states haemoglobin occupies?
what happens when one oxygen binds to a subunit of haemoglobin?

A

adult has two alpha and two beta chains while foetal has two gamma instead of the beta

two states = tensed (low affinity for oxygen)
relaxed = high affinity for oxygen

all the subunits will then change to relax, making it easier for more oxygen o bind (hence the steep rise of the dissociation curve)

34
Q

what proportion of oxygen is actually Hb bound?

A

most of it

in arterial blood 97.5%, in venous blood 75%

35
Q

what are the effects of 1) temperature, 2) pH, 3) 2,3 - diphosphoglycerate
on the Hb dissociation curve?

A

temperature = if high curve shifts right (lower affinity)

pH = if low curve shifts right (Bohr effect)

2,3-DPG = if increases curve shifts right, it indicates metabolic activity

36
Q

how are the sifts in Hb affinity due to temperature/pH/2,3-diphosphogycerate changes useful?

A

in respiring tissue both temperature, CO2 and decreased pH all occur

a shift to the right causes a decrease in affinity making oxygen easier to unload to meet increased demands as respiration rate increases

37
Q

why is foetal haemoglobin not effected by 2,3-DPG and how is this beneficial?

A

2,3-DPG effects haemoglobin by interacting with the beta subunits, of which foetal haemoglobin has none, gamma ones in their place, so has is more leftward in it’s curve compared to adult haemoglobin when 2,3-DPG is high

this means the foetal haemoglobin is better at grabbing O2 at the placenta from the mother

38
Q

what is the total CO2 describing?

A

all forms of CO2 the blood carries:
dissolved CO2
carbonic acid
bicarbonate
carbonate
carbamino compounds

39
Q

how is carbon dioxide transported in the blood?

A

several different ways
majority goes into RBC via aquaporins
4% of that dissolves in plasma
20% binds to haemoglobin (its amino acids) to form those carbamino compounds
the rest will be converted to bicarbonate by carbonic anhydrase, then to be exchanged with chloride via a band three protein, known as hamburger explain

then at the lungs the bicarbonate goes back into the RBC via the chloride exchange to be converted back to CO2 and diffuse back out to be removed

40
Q

obstructive lung disease - what is it and what are some reasons for the narrowing?

A

any narrowing of the airways, resulting in a decrease in diameter and therefore an increase in resistance, meaning reduced air flow
reasons for narrowing -
excess secretions
asthma (bronchoconstriction)
inflammation

41
Q

how odes obstructive lung disease look in spirometry?
- FEV
- volume time curves
- flow-volume loops

A

decreased FEV, less than 80% of VC

volume time curves - vital capacity is the same, takes much longer to get to the vital capacity when exhaling though

flow volume loops - (above axis is exhaling, below is inhaling) concave shape indicates obstructive lung disease, like if it’s just a fatter shape

42
Q

give some examples of obstructive lung diseases

A

asthma
chronic bronchitis (mucus excretion)
chronic obstructive pulmonary disease (structural changes)
emphysema - loss of elastin means airways collapse easier in exhalation

43
Q

what causes asthma - what is it?

A

hyperactive airways in response to atopic triggers - allergies etc..
and non-atopic triggers - infections, cold air, stress, exercise etc…

its an inflammatory cells move into the airways and mediators like histamines cause bronchoconstriction

44
Q

how is asthma treated?

A

salbutamol = a B2 adrenoreceptor agonist, a bronchodilator (blue inhaler)

longer acting treatments = inhaled steroids (glucocorticoids) reduce inflammatory response, or long acting B-adrenoreceptor agonist (brown inhaler)

45
Q

restrictive lung disease - what is it and what are some symptoms?

A

reduced chest expansion

symptoms/causes include -
chest wall abnormalities/muscle contraction deficiencies
loss of compliance
increase in collagen
response to environmental factors

46
Q

what does restrictive lung disease look like in spirometry?
- VC
- volume-time curves
- flow volume loop

A

reduced VC compared to predicted values

volume-time curves - reduced vital capacity and FEV (but FEV as a percentage can still be high)

flow-volume loops - appears normal (rapid increase in flow, then linear decrease)

47
Q

what happens in asbestosis?

A

breathed in asbestos, macrophages identify and attack foreign particles, but the body cannot break down these asbestos particles so there is a build up of fibrous tissue around these particles

the result can be a bit of both obstructive and restrictive lung disease

48
Q

central control of respiration -
what area of the brain
what neurons control quiet inspiration
what is spontaneous activity
what is the ventral respiratory group?

A

medulla - the pre botzinger complex is what controls the automatic but overridable breathing process

dorsal respiratory neurons in the DRG control quiet inspiration

spontaneous activity is the triggering of the phrenic nerve to cause inspiration, shutting it off to allow for expiration, firing it up again for another inspiration etc…

the ventral respiratory group - neurons in the medulla used for forced inspiration/expiration

49
Q

Pons - what two things does it do effecting respiration?

A

it inhibits/stimulates the inspiratory centre in order to modulate basic breathing pattern

the pneumotaxic centre can send signals down to inhibit inspiratory centre to shorten inspiration and increase breathing rate

apneustic centre increases the depth of breathing, slows it down by prolonging inspirations, so stimulates the inspiratory centre

50
Q

what do
1) stretch receptors
2) central chemoreceptors
3) peripheral chemoreceptors

do to effect breathing?

A

1) prevent overinflation using a negative feedback loop

2) monitor cerebral spinal fluid for CO2 and pH, if CO2 too high or pH too low these receptors stimulate inhalation and increase ventilation to remove more CO2

3) in carotid arteries and aorta, respond to increase in CO2, decrease in pH, or decrease in O2