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HL Bio > 6.4 Gas exchange > Flashcards

6.4 Gas exchange Flashcards

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Biology 101 flashcards
1
Q

why can’t multicellular oganisms breathe thru their SKIN ☹️ aka why do multicellular organisms require specialised organs for gas exchange

A
  1. too many cells too far from skin surface
  2. external surface of tough skin unsuitable for gas exchange = require alternate respiratory surface
  3. demand for oxygen is much higher bc of incr metabolic rate
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2
Q

The Lungs are housed in the ____, an airtight chamber formed by the _______ and its _________, with a domed floor, the ______.

A
  1. Thorax
  2. Ribcage
  3. Intercostal muscles
  4. Diaphragm
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3
Q

The right lung has __ (no.) lobes
The left lung has __ (no.) lobes and a ____ _____ (allows space for heart)

A

3

2, cardiac notch

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4
Q

What is ventilation? (short defin)

A

Efficient movement of air in and out of lungs — maintains conc gradient of O2 and CO2 for diffusion

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5
Q

What is gas exchange?

A
  • O2 diffuses into blood, CO2 diffuses out and is expelled
  • lungs have a large, thin surface area: gas exchange in alveoli in the lungs
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6
Q

whats the difference between ventilation and gas exchange

A

ventilation is the lungs and breathing in and out but gas exchange is in the alveoli

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7
Q

2 ways conditions for diffusion at the respiratory surface are improved: ____ ________ system, _______ ________ (rbc)

A

blood circulation system

respiratory pigment (haemoglobin)

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8
Q

how does the blood circulation system improve conditions for diffusion at the respiratory surface

A

rapid movement of O2 to body cells as soon as it crosses respiratory surface = maintained conc. gradient in lungs

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9
Q

how does respiratory pigment (haemoglobin) improve conditions for diffusion at the respiratory surface

A

increases oxygen-carrying ability of the blood

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10
Q

factors affecting rate of diffusion in the exchange of gases (3)

A
  1. size of surface area: incr SA = incr diffusion
  2. diff. in conc.: incr gradient = incr diffusion – rapidly respiring organism has lower O2 conc and higher CO2 conc in cells
  3. length of diffusion path: shorter = greater rate of diffusion
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11
Q

what two concentration gradients does gas exhange depend on

A

oxygen and carbon dioxide

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12
Q

decribe the gas concentration in the alveoli

A
  • O2 higher in alveoli than blood
  • CO2 lower in alveoli than blood
    gradient + thin walls + moisture + short distance = gas exhange (diffusion)
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13
Q

how does ventilation maintain concentration gradients of O2 and CO2 between air in alveoli and blood in adjacent capillaries?

A

longer air remains in alveoli = lower conc of o2 in air = decr conc gradient for o2 into blood
–> ventilation replaces low o2 air with higher o2 air – must ensure o2 continuously diffuses in and co2 out (gas exchange)

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14
Q

how is ventilation rate/ breathing rate defined by

A

number of breaths / minute (including inhaltion and exhalation)

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15
Q

describe alveolar structure (4)

A
  • arranged in clusters (each served by a bronchiole)
  • have elastic connective tissue (integral part of their walls)
  • capillary system wrapped around clusters of alveoli (can be expaneded upon)
  • wall of alveolus is 1 cell thick (formed by pavement epithelium)
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16
Q

describe the structure of the capillary system that wraps around the alveoli clusters 3

A
  • each capillary: conected to branch of pul.artery and drained by pul.vein
  • wall composed of 1 layer of flattened endothelium (type 1 pneumocyte) cells
  • extremely narrow – rbcs squeeze thru = close/in contact with capillary walls
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17
Q

name the 3 types of cells in the alveoli

A
  • type I pneumocytes (thin alveolar cells
  • Macrophages (dust cells)
  • surfactant cells (type II pneumocytes)
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18
Q

how are type I pneumocytes adapted for gas exchange

A
  • extremely thin alveolar cells adapted to carry out gas exchange
  • very flat and thin = incr surface area (for diffusion)
  • decr dist betw inside of alveolus and the capillary (speed up diffusion)
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19
Q

what do macrophages do in the alveolus

A
  • migrate into alveoli from capillaries
  • phagocytic wbcs ingest debris, fine dust particles, bacteria, fungal spores
  • line the surfaces of airways leading to alveoli
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20
Q

what do type II pneumocytes/ surfactant cells do

A
  • prod. a mix of lipoproteins and phospholipid-rich secretion – lines inner surface of alveoli
  • lowers surface tensions = alveoli can flex easily, prevents sides from adhereing to e/o
  • moisture incr speed gases dissolve (helps gas exchange)
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21
Q

path of oxygen and carbon dioxide in alveolus

A

oxygen
- dissolves in alveolar surface film of water
- diffuses into blood plasma and rbcs: combines with haemoglobin to form oxyhaemoglobin

co2
- diffuses from blood into alveoli

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22
Q

describe the structure of the thorax (where the lungs are housed)

A

an airtight chamber formed by ribcage and its (intercostal) muscles + domed floor (diaphragm)
- internal surfaces of thorax are lined by pleural membrane – secretes and maintains pleural fluid

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23
Q

what is the diaphragm

A

sheet of muscle attached to the body wall at the base of the ribcage (seperates thorax from abdomen)

24
Q

what is the pleural membrane + pleural fluid

A

lines the internal surfaces of the thorax
- secretes and maintains pleural fluid: lubricating fluid derived from blood plasma that protects lungs from friction during breathing

25
Q

trace the path from the mouth/nose to the lungs 5

A
  1. air passes larynx: via slit-like opening, glottis + flap, epiglottis
  2. into trachea – runs beside esophagus
  3. trachea divides into 2 bronchi
  4. bronchi divide into bronchioles (within lungs)
  5. bronchioles end in alveoli
26
Q

how does trachea structure prevent wall collapse under pressure from large bolus of food in esophagus

A

(esophagus runs beside trachea)
- incomplete rings of cartilage

27
Q

structure of bronchi and larger bronchioles (that prevent collapse from sudden reduction in pressure)

A
  • walls contain smooth muscle
  • supported by rings/tiny plates of cartilage = prevents collapse
28
Q

the thorax is an _______ chamber = pressure changes in the lungs occur when the _____ of the thorax changes

A

airtight

volume

29
Q

process of inspiration (inhalation) 7

A
  1. external intercostal contract
  2. internal intercostal relax
  3. diaphragm muscles contract, move down
  4. ribs: up and out
  5. volume of thorax incr
  6. thoracic pressure below atmos pressure
  7. air flows in
30
Q

process of expiration (exhalation)

A
  1. external intercostal relax
  2. internal intercostal contract
  3. diaphragm relax, up
  4. ribs down and in
  5. volume decr
  6. thoracic pressure incr above atmos pressure
  7. air flows out
31
Q

external intercostals can only ___ the ribs
internal intercostals can only ___ the ribs___

A

lift
move the ribs down

  • occurs when theyre contracted
32
Q

the interocstal muscles are ____ muscles

A

antagonistic

33
Q

what are antagonistic muscles

A
  • when one contracts, the other relaxes
  • work in pairs to move body parts in opp directions
34
Q

what does a spirometer measure

A

capacity of lungs when breathing at different rates

35
Q

how can a spirometer be altered to measure oxygen consumption by the body

A

a carbon dioxide absorbing chemical eg soda lime added to a compartment on the air return circuit

36
Q

what can be gleaned from the data logged from a recording spirometer

A

the ventilation rate and tidal volume

37
Q

what is tidal volume + average tidal volume

A

the amt of air which enters / leaves lungs in a single breath at rest
avg tidal vol = 500ml

38
Q

ethical concerns about monitoring ventilation of humans – what conditions must be observed when experimenting on humans 5

A
  1. written consent
  2. results must be anonymous
  3. must participate of their own free will
  4. right to withdraw from the investigation at any time
  5. no investigations on body fluids
39
Q

what is residual volume of air

A

air that cannot be expelled (bc air is tidal and enters and leaves by the same route)

40
Q

what is the point of having residual volume of air

A

incoming air mixes and dilutes residual air = air in the alveoli has significantly less o2 than atmosphere

41
Q

structural features of lungs that make gas exchange efficient 4

A
  1. surface area of alveoli: huge surface
  2. wall of alveoli (type I): short diffusion pathway
  3. capillary supply to alveoli: maintains conc gradient
  4. surface film of moisture: o2 dissolves in water, o2 diffuses into blood in solution
42
Q

causes of lung cancer 5

A
  • asbestos dust particles lodged in the lungs (cannot be broken down)
  • smoking (tobacco)
  • passive smoking (Second hand)
  • air pollution (Carcinogens)
  • radon gas (radioactive gas = mutations when inhaled)
43
Q

possible consequences of lung cancer 9

A

○ shortness of breath
○ incessant cough
○ coughing up blood
○ pain (chest etc)
○ accumulation of fluid in the chest
○ spread of cancer to other parts of the body
○ loss of appetite / weight loss
○ Fatigue
○ Repeated problems with pneumonia or bronchitis.

44
Q

state 3 constituents of cigarette smoke that causes lung cancer

A
  1. carcinogens: ‘tar’ component
  2. nicotine: triggers release of dopamine but longterm exposure is the opposite (Addictive)
  3. carbon monoxide: formation of oxyhaemoglobin
45
Q

what is a carcinogen (lung cancer)

A

any agent that may cause cancer by damage to the DNA molecules of chromosomes
- found in the ‘tar’ component of smoke

46
Q

what is nicotine

A
  • stimulating and relaxing drug able to cross blood-brain barrier
  • triggers release of dopamine
  • long term exposure = reverse effect, depressing ability to experience pleasure
    = more required = addiction
47
Q

how does smoking result in lung cancer 2

A
  • damaged epithelium: progressively replaced by an abnormally thickened epithelium
  • carcinogens = permanent mutations in the DNA
48
Q

how does prolonged exposure to carcinogens lead to lung cancer (tumours)

A
  1. mutations in oncogenes/ tumour supressing genes = loss of control over normal cell growth
  2. accumulation of mutations = divide repeatedly = tumour
  3. tumour cells emit signals promoting the devt of new blood vessels (deliver o2 and nutrients at the expense of surrounding cells)
  4. metastasis: tumour cells break away and form a secodary tumour
  5. cancerous cells take over the body = malfunction, death
49
Q

what is metastasis

A

when tumour cells break away and are carried to other parts of the body forming a secondary tumour

50
Q

how was the link between smoking and lung cancer discovered

A

1950 american study of over 600 smokers compared with non-smokers: lung cancer 40 times higher
- incr no. of cigarettes smoked = incr risk of contracting cancer

51
Q

what is emphysema caused by

A

long term exposure to cigarette smoke and other pollutants

52
Q

consequences of emphysema

A
  1. inflammatory response in lungs = narrowing of airways, breakdown of lung tissue
    - alveoli walls lose elasticity = destruction of lung tissue
  2. incr protease activity = breaks down alveolar wall = one large air space
    - enzyme inhibitor reduced activity
53
Q

alveoli walls lose elasticity due to emphysema – how is lung tissue destroyed by this

A

failing elastic fibres = air sacs left over-inflated, air trapped in them
- ventilation becomes difficult

54
Q

emphysema – reduced activity of enzyme inhibitor ______ results in incr protease activity breaking down alveolar wall

A

alpha-1-antitrypsin
- inhibits proteases from breaking down alveolar wall

55
Q

what impacts does the breakdown of the alveolar wall due to increased protease activity have

A
  • reduced surface area of lungs
  • smaller amt of o2 reaching bloodstream
56
Q

symptoms of emphysema 4

A
  • permanent shortness of breath
  • persistent cough
  • fatigue
  • weight loss

HL Bio (52 decks)

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