Blood Flashcards

1
Q

Components of blood

A
  1. Plasma
    - small solutes
    - larger molecules ( albunin, globulins (fibrinogen + serum), clotting factors)
  2. Cellular component
    - rbc, wbc, paltelets
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2
Q

How many RBC’s per ml

A

5000 million

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3
Q

In anaemia

A

Capacity of blood to carry O2 is reduced

  • no. RC’s reduced
  • Iron folic acid / vit.b12 deficiencies
  • defective hb (sickle cell)
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4
Q

Haematocrit ratio

A

Proportion of blood made of cells

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5
Q

Normal Ht

A

0.42-0.47

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6
Q

Normal Hb

A

13.5 - 15g dl-1 (larger in men)

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7
Q

Normal Ht depends on ____ then ____

A

age, sex

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8
Q

A lower than normal Ht causes

A
  1. loss of blood
  2. nutritional deficiency
  3. bone marrow problems
  4. abnormal haemoglobin
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9
Q

A higher than normal Ht causes

A
  1. high altitudes
  2. chronic smoker
  3. dehydration
  4. erthropoicten use in athletes
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10
Q

Pc

A

Capillary hydrostatic pressure - force fluid out from capillary

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11
Q

Pi

A

Intestital hydrostatic pressure - force fluid from interstital space

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12
Q

Pi c

A

Capillary oncotic pressure - force pushes fluid from I.S. space to capillary ( 25mmHg)

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13
Q

Pi i

A

Intestital oncotic pressure - caplilary to I.S. space

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14
Q

Jv

A

Net fluix flux, = Kf [(Pc-Pi) - ó (pic - pi i )]

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15
Q

Kf

A

Filtration coefficient

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16
Q

ó

A

Reflection coefficient -> different for diff. capillary beds but same proteins from blood able to cross vessel wall into interstitum

17
Q

If Jv = +ve

A

Fluid wants to leave capillary

18
Q

Kf based on

A

how large + leaky capillary wall is

19
Q

Oedema

A

When filtration forces significantly exceed absorption forces, an accumulation of extravascular fluid occurs

20
Q

Consequences of Oedema

A
  1. Primary increase of hydrostatic pressure gradient
  2. Congentive heart failure
    - primary decrease of oncotic pressure gradient
  3. Liver failure, rephotic syndrome, extensive tissue trauma
21
Q

Normally hydrostatic pressure within blood vessels

A

cause water to filter out into tissue + oncotic pressure in plasma -> water back into blood

22
Q

Haemostasis

A

When a blood vessel is damaged

23
Q

Vasoconstriction in response to haemostasis

A

Contraction of smooth muscle around damaged blood vessel due to physical stimulation of muscle

24
Q

Platelet aggregation

A
  • platelet produced by megakaryocytes
  • bind to injury site forming platelet plug
  • > accelerated by platelets releasing ADP, thromboxane A2 which promotes further platelet aggregation (modulated by aspirin)
25
Q

How does ADP promote further platelet aggression?

A

Activate phospholipases in platelet membrane to form archanidenic acid. Cyclo-oxygenase activates endoperoxidases -> platelet + endothelium

26
Q

Coagulation

A

Conversion of plasma protein from fibrinogen to fibrin

27
Q

Coagulation activating factors 10 and 5 pathways

A
  1. Intrinsic pathway - exp. of blood to damaged tissue

2. Extrinsic pathway - substances released from damaged tissue

28
Q

Factors 10 and 5 cause

A

Prothrombin to thrombin which promotes fibrinogen to convert to fibrin which forms a fibrin mesh

29
Q

Functions of blood

A
  1. Maintenance of cellular function
  2. Gaseous exchange
  3. Nutrients
  4. Hormones
  5. Protection against invading organisms
  6. Thermoregulation