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
How does ADP promote further platelet aggression?
Activate phospholipases in platelet membrane to form archanidenic acid. Cyclo-oxygenase activates endoperoxidases -> platelet + endothelium
26
Coagulation
Conversion of plasma protein from fibrinogen to fibrin
27
Coagulation activating factors 10 and 5 pathways
1. Intrinsic pathway - exp. of blood to damaged tissue | 2. Extrinsic pathway - substances released from damaged tissue
28
Factors 10 and 5 cause
Prothrombin to thrombin which promotes fibrinogen to convert to fibrin which forms a fibrin mesh
29
Functions of blood
1. Maintenance of cellular function 2. Gaseous exchange 3. Nutrients 4. Hormones 5. Protection against invading organisms 6. Thermoregulation