animal transport Flashcards

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1
Q

examples what of blood plasma carries?

A

glucose

amino acids

mineral ions

hormones

large blood proteins (albumin)

fibrinogen( blood clotting)

globulins (transport/immue system)

wbcs

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2
Q

what are the functions if the blood?

A
transport of:
• O2 & CO2 to and from respiring cells
•digested food from small intestine
•nitrogenous waste
• hormones
•platelets
•cells/ antibodies
  • help maintain:
    BODY TEMP
    pH —> acts as a buffer
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3
Q

how does TISSUE FLUID form FROM PLASMA

A

• as blood flows from arterioles into capillaries
—> is still under pressure from surge of blood from each time the heart pumps
HYDROSTATIC PRESSURE

• at arterial end
hydrostatic&raquo_space; oncotic pressure
= net flow of fluid out of the capillary

—> this fluid fills spaces between cells (containing oxygen/nutrients)
—> TISSUE FLUID

• at venous end
—> the hydrostatic pressure FALLS
—> the oncotic pressure had remained the same

SO
oncotic pressure > hydrostatic pressure
—> water moves back into capillaries by osmosis

= net flow of fluid (containing carbon dioxide/waste products) back into capillary by oncotic pressure

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4
Q

how is composition of tissue fluid different from plasma

A

Its the same apart from things that cant fit through fenestrations in capillaries

so:
- rbcs
- albumin

both STAY IN BLOOD

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5
Q

what is lymph

A

•some tissue fluid doesnt move hack into the capillaries
—> it drains into a system of blind ended tubes —> lymph capillaries

—> this is called LYMPH

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6
Q

what is lymph composed of?

A

similar to tissue fluid/plasma

  • much less oxygen + nutrients
  • fatty acids from intestine
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7
Q

how is lymph transported?

A

squeezing body muscles

—> lymph vessels have valves which stop the backflow of lymph

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8
Q

what do lymph nodes do

A

•lymphocytes build up in lymp nodes
—>produce antibodies into blood when necessary
• intercept bacteria/ other debris

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9
Q

how is oxygen transported?

A

haemoglobin in rbcs

4 oxygen binds to 1 haemoglobin

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10
Q

how do red blood cells carry oxygen?

A

POSITIVE COOPERATIVITY

•blood entering lungs capillaries have low o2 conc
—> creates a steep concentration gradient
between air in alveoli and blood

•o2 enters rbcs
—> binds to haemoglobin

•when one o2 binds to a haem group
—> molecule changes shape
—> making it easier for another o2 to bond to another haem group

• as the FREE o2 conc in an rbc remains LOW
—> steep conc gradient is maintained
—> until haemoglin in saturated with o2

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11
Q

what happens to oxyhaemoglobin when it reaches cell tissue

A

•conc of o2 is lower in cytoplasm of body cells , than in rbcs
—>o2 moves lit of rbc down conc gradient

• once first o2 is released
—> molecule changes shape
—>now easier to remove the rest of the o2

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12
Q

what does an oxygen dissociation curve show?

A

the affinity of haemoglobin for oxygen

—> a very small change in p(o2) causes sig diff to the saturation of haemoglobin

•this us because:

  • once the first o2 molecule is attached
  • Δshape of Hb causes other o2 to be added very rapidly
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13
Q

what is the shape of an oxygen dissociation curve?

A

it is sigmoidal
—> due to +ve cooperativity

•higher p(o2) in pulmonary capillaries
—> allows more o2 to bind with Hb
—> until the Hb becomes saturated so little addition binding of o2 occurs
= curve flattens out at this point

•with lower p(o2) in body cells
—> results in large amount of o2 being unloaded needed by cells
—> shown by steep curve

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14
Q

what is the Bohr effect?

A

change in oxygen affinity of haemoglobin at different p(CO2)

as p(co2) rises
—> Hb gives up more o2 more easily
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15
Q

why is rhe bohr effect important?

A

•in more active cells
—> are respiring more
—> producing more co2
-these cells will jeed more o2 to maintain activity
—> so the increased co2 will cause more o2 to be unloaded by Hb

•in lungs p(co2) is low
—> allows o2 to bind more readily to Hb

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16
Q

why is the curve for foetal hamoglobin steepee than adult?

A

•fetus gets o2 only from mother
•oxygenated blood from mother
—> runs next to deoxygenated fetal blood

• if fetal Hb had same affinity for o2
—> no o2 would be transferred to fetal Hb

SO
a higher affinity is required
—> so fetal Hb can take o2 from adult Hb

17
Q

3 ways co2 is transported?

A

• 5% dissolved in plasma

•10-20% as carbaminohaemoglobin
—> co2 combines with Hb

• 75-85% converted to HCO3-
—> in cytoplasm of rbcs

18
Q

reversible reaction of co2 forming HCO3-

A
19
Q

what is the chloride shift?

A

movement if bicarbonate ions (HCO3-) into red blood cells as H+ ions move out
—> to maintain electeochemical equilibrium

20
Q

how does the chloride shift work

A

• co2 diffuses into rbcs

• co2 is converted to H2CO3
—>using carbonic anhydrase enzyme

•H₂CO₃ dissociates into HCO₃ - and H+ ions

•-ve hydrogen carbonate ions move out of rbcs by diffusion down conc gradient
—> -ve CHLORIDE ions move in
—> maintains electrochemical balance

21
Q

why is co2 converted into hco3- ?

A

so rbcs can maintain a conc gradient for co2 to be removed from body cells

22
Q

how is co2 released back into the lungs

A

• at lungs there is low conc of co2

• carbonic anhydrase
—> reversed reaction
—> h2co3 is converted back into co2 + h20

—>co2 diffuses back into lungs

23
Q

how long does the cardiac cycle last

A

0.8s

24
Q

what happens in diastole?

A

•the heart RELAXES
—> atria + ventricles fill will blood
—>pressure + volume of blood increases

-pressure in arteries is lower

25
Q

what happens in systole?

A

•heart CONTRACTS

•atria contracts
—> blood forced into ventricle
•ventricles contract
—> blood forced into arteries (HIGH PRESSURE)

•at the end if systole
—> pressure lower in heart
—> higher in arteries

26
Q
function of the heart
(how does deoxygenated blood move through the hear/pressures involved)
A

•Deox blood moved into right atrium through inf/sup vena cava
—> this is at a relatively low pressure

•as more blood flows in:
—> pressure builds in atrium
—> causes right atrioventricular valve (tricuspid valve) to OPEN
—> blood passes into ventricle

•when pressure in ventricle = atrium
—> atrium contracts (sinoatrial node fires)
—> all blood forced into right ventricle
—> simultaneously tricuspid valve closes stopping blood going back into atrium

•AV node receives action potential from SA node (after atria are depolarised —> theres a delay)
—> ventricles contract forcing blood through semilunar valves
—> into pulmonary artery

27
Q

what is tachycardia?

A

when heart beat is too rapid

>100bpm

28
Q

what is bradycardia?

A

heart rate too slow

<60bpm

29
Q

what is an ectopic heartbeat?

A

altered rhythm
—> extra beat
—> followed by longer gap

30
Q

what is atrial fibrilation?

A

example of an arrythmia

—> rapid impulses generated from atria
—> they contract very fast

• they dont contract properly
•not all impulses are passed on
—> blood pumped ineffectively

31
Q

what causes heart sounds?

A

•first sound:
—> blood is forced against atrioventricular valves when ventricles contract

•second sound
—> back flow of blood closes the semilunar valves as ventricles relax

32
Q

what happens in P during PQRST

A

contraction of atria in response to SA node depolarising atria walls

33
Q

what happens in QRS during PQRST

A

depolarisation of ventricles

34
Q

why is there a flat line between P and Q in a ecg trace

A

when the action potential potential from sa node reaches av node
—> the ap then travels down Bundle of His( containing purkyne fibres) to the apex of the heart
—> this causes a delay of ~0.1s between:
- contraction of atria
- contraction of ventricles

•this makes sure atria have stopped contracting before ventricles start contracting

35
Q

why does contraction of ventricles start from the apex of the heart?

A

allows for a more efficient emptying of the ventricles

•as they are contracted from the bottom up
—> this prevents blood being left in the bottom of the ventricle