2.5 Phys 2 Blood Flashcards
heart attack is called?
infarction
*symptoms: chest pain, nausea, vomiting, sweating, weakness, short breath
infarction detection?
- changes in EKG (larger Q than normal, mean axis goes away bc dead area is electrically silent)
- creatine phosphokinase in blood (and other proteins)
atherosclerosis caused by?
damage or insult to vascular endothelium,
hemoretic stroke if capillaries break
*caused by: chronic stress, hyptension, diabetes, fat, smoking
*treat: reduce risk factors
Use of excerise as treatment for atherosclerosis
1) decrese resting HR and BP
2) increase vasodilation of heart vessels
3) minimize severity of hypertension and diabetes
4) decrease total plasma cholesterol
5) increase plasma HDL levels
6) decrease clot formation
7) increase ability to dissolve clots
What is fibrinogen? binds to? inactive form of?
important clottingprotein!
inactive form of fibrin
Binds to platelets
anemia
iron defecency (hemoglobin loses ability to carry RBCs)
sickle cell anemia
irregular shape makes them get caught in vessels, needs both copies to get disease, don’t carry iron
polycythemia
increase in the number of RBCs
5 WBCs and what they do
1) Eosinophils- reduce inflammation
2) Basophiles- release histamine and increase inflammatory response
3) Neutrophils- small phagocytic cells
4) Monocytes- macrophages
5) Lymphocytes- immunity
serum = ____ - _____
plasma - fibrinogen
highest protein and highest ion
protein= albumin ion= Na
three mechanisms to prevent blood loss?
1) vasoconstriction
2) platelet plug formation
3) clot formation
what is thromboxane A2? released by?
local control -vasoconstrictor
sticky
released by platelets
damaged vessels expose? What sticks to them?
collagen in the basement membrane
**platlelets stick to collagen and become activated
activated platelets release? What do they do?
- APD and thromboxane= sticky
- serotonin= vasoconstirct
- vWF= form bridges between collagen and platelets
Non injured endothelium cells have ____ and ____ to inhibits clot formation
- prostacyclin= inhibit platelet aggregation
* nitric oxide= vasodilation
what two things make a clot?
platelets and fibrinogen
- fibrinogen is soluble
- fibrin is insoluble
fibrinogen needs WHAT to be converted to fibrin?
thrombin
what is the mainreaction that leads to true clot formation?
fibrinogen to fibrin (using thrombin)
Vitamin K
essential for clotting (2,7, 9, 10 factors)
fat soluble
calcium is essential for?
for clotting
13a is essential for? catalyzed by?
making a strong stable clot
*catalyzed by thrombin
intrinsic vs extrinsic
- intrinsic= all components for clot formation is in the blood
- extrinsic= involves thromboplastin released from damaged tissue as a SHORTCUT to fibrin formation
two important substances required for proper functioning clot cascade?
1) calcium- required by many rxns
2) vitamin K- required by liver to produce prothrombin
as damaged vessel is repairing, factor 7 activates?
Kallikrein
- converts plasminogen to plasmin
- converts fibrin to fibrinogen
- inhibit thrombin
Kallikrein important for?
platelet plug and clot breakdown and inhibition of new plug/clot formation
Anticoagulant drugs?
1) aspirin= inhibits prostalglandin production, resulting in defective platlet release
2) coumarin= inhibits activation of Vit K
3) Heparin= inhibits activity of thrombin
4) combines WITH Ca and therefore inhibits its activity in clotting
what converts plasminogen to plasmin?
kallikrein
