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