Blood Flashcards
Components of blood
- Plasma
- small solutes
- larger molecules ( albunin, globulins (fibrinogen + serum), clotting factors) - Cellular component
- rbc, wbc, paltelets
How many RBC’s per ml
5000 million
In anaemia
Capacity of blood to carry O2 is reduced
- no. RC’s reduced
- Iron folic acid / vit.b12 deficiencies
- defective hb (sickle cell)
Haematocrit ratio
Proportion of blood made of cells
Normal Ht
0.42-0.47
Normal Hb
13.5 - 15g dl-1 (larger in men)
Normal Ht depends on ____ then ____
age, sex
A lower than normal Ht causes
- loss of blood
- nutritional deficiency
- bone marrow problems
- abnormal haemoglobin
A higher than normal Ht causes
- high altitudes
- chronic smoker
- dehydration
- erthropoicten use in athletes
Pc
Capillary hydrostatic pressure - force fluid out from capillary
Pi
Intestital hydrostatic pressure - force fluid from interstital space
Pi c
Capillary oncotic pressure - force pushes fluid from I.S. space to capillary ( 25mmHg)
Pi i
Intestital oncotic pressure - caplilary to I.S. space
Jv
Net fluix flux, = Kf [(Pc-Pi) - ó (pic - pi i )]
Kf
Filtration coefficient
ó
Reflection coefficient -> different for diff. capillary beds but same proteins from blood able to cross vessel wall into interstitum
If Jv = +ve
Fluid wants to leave capillary
Kf based on
how large + leaky capillary wall is
Oedema
When filtration forces significantly exceed absorption forces, an accumulation of extravascular fluid occurs
Consequences of Oedema
- Primary increase of hydrostatic pressure gradient
- Congentive heart failure
- primary decrease of oncotic pressure gradient - Liver failure, rephotic syndrome, extensive tissue trauma
Normally hydrostatic pressure within blood vessels
cause water to filter out into tissue + oncotic pressure in plasma -> water back into blood
Haemostasis
When a blood vessel is damaged
Vasoconstriction in response to haemostasis
Contraction of smooth muscle around damaged blood vessel due to physical stimulation of muscle
Platelet aggregation
- 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)