CVS Flashcards
Internal Factors affecting BP
Blood volume –> more blood = increased pressure
CO –> increased output = increased pressure
Peripheral Resistance –> Viscosity, vessel length
Vessel elasticity
Definition: cardiac output
Volume of blood pumped from the ventricles per minute (HR x stroke volume)
Definition: Blood pressure
Pressure of the blood in the circulatory system (CO x peripheral resistance)
Arteries structure
lumen
intima: endothelium + basmement membrane +collagen
internal elastic lamina
media (concentric elastin + smooth muscle)
external elastic lamina
adventitia = collagenous connective tissue
Veins structure
lumen
intima: endothelium + basmement membrane +collagen
internal elastic lamina
media (concentric elastin + smooth muscle)
adventitia = collagenous connective tissue
Same as arteries without external elastic lamina, has valves, less muscle and elastin
Basophils
phagocyte have dark blue staining granules Bi-lobed nucleus Migrate to tissues to become mast cells important role in immunity and allergic response as they secrete histamine
eosinophils
Phagocytes
Pink staining granules
Bi-lobed nucleus
Important role in immunity and allergic response, neutralise histamine to restrict inflammatory response
specialist role in protection against parasites
IgE receptors on surface
Neutrophils
Phagocytose and kill bacteria
Rlease chemotaxins and cytokines
numbers increase during inflammation and infection
most numerous WBC
Multi-lobed nucleus, faintly granular cytoplasm
Monocytes
pre-curser to macrophages
like neutrophils but travel in tissue and lymph
Pagocytose bacteria and other foreign material
Phagocyte
Kidney bean shaped nucleus
B lymphocyte
Made and matured in bone marrow
stored in secondary lymphoid organs
differentiate into plasma cells
produce + secrete immunoglobins (antibodies) when expose to corresponding antigen
All lymphocytes look the same histologically
T lymphocyte
Made in bone marrow
Matured in thymus
Helper T-cells = CD4+ –> supress/regulate immune response + help B cells in antibody production
Cytoxic T cells = CD8+ –> target damaged/ infected cells for death
Haemostasis overview
Blood in the vessel = fluid, outside = clot
Platelets circulate in an inactive form
Vascular spasm
Aim = decrease the volume of blood lost
Damage to endothelium causes endothelium to bind to the smooth muscle = contraction
contraction will also occur if there is nerve and muscle damage
Platelet plug formation
VWF produced by endothelial cells
Platelets activated: change their shape (become spiculated, pseudopodia) due to loss in NO
Platelets attracted to exposed collagen + bind to VWF
Platelets secrete their granules: ADP, thromboxane A2 and serotonin
Attracts more platelets = aggregation, and amplification of the granule release
Platelets linked together by glycoprotein IIb/IIIa and fibrinogen
Activation increases the expression of glycoprotein IIb/IIIa
Coagulation
Clotting factors activated –> cascade
prothrombin –> thrombin which converts fibrinogen to fibrin
fibrin causes the blood to thicken and forms a mesh network over the clot
Calcium is needed for the activation of some factors
Clot retraction and repair
Platelets contain actin and myosin to pull the edges of the damage together
Growth factor from platelets trigger mitosis in smooth muscle
Fibrinolysis
Breakdown of clot to prevent blockage
vessel has tissue plasminogen activator which combines with plasminogen = plasmin formation
Plasmin breaks down fibrin mesh
Endothelin 1
Released by endothelial cells = constriction of blood vessels
VWF
temporary adherance to platelets
Glycoprotein 1b
receptors on platelet membrane, bins VWF to collagen
ADP
dense granule –> acts on P2Y1 and P2Y12 causing platelet amplification
Thrombin
binds PAR1 and PAR4 receptors = inducing platelet activation
Glycoprotein IIb/IIIa
expressed on platelets, binds platelets together and to the fibrinogen
Thromboxane A2
dense granule –> vasoconstriction and platelet activation
extrinsic pathway
begins with tissue factor
located on the outer plasma membrane of various tissue cells outside the endothelium
can occur outside the blood system
intrinsic pathway
begins due to exposed collagen fibres
beings with factor XIIa
Pacemaker action potential
Action potential of the AV/SA node. not regulated by other cells
no steady resting potential = has slow depolarization
1. polarization reaches -60mv opens HCN channel, Na enters
2. polarization = -40mv = threshold, voltage gated calcium channels open = depolarization (+ve)
3. at 20mv the potassium channels open, potassium leaves and calcium channels shut
Myocardial action potential
- Action potential arrives, sodium channels open (rapid depolarization)
- +52mv sodium channels close and potassium open
- calcium channels open slowly = partial repolarization (plateau)
- repolarization, calcium closes and potassium leaves (-ve)
- resting potential is reached
preload
volume of blood in the left ventricle before contraction (end diastolic volume)
afterload
pressure the LV must overcome to eject blood during the contraction
Contractility
Force of contraction and change in fibre lengths, how hard the heart pumps
Compliance
How easily the heart chambers expand when filled with blood
External factors affecting BP
Smoking, obesity, lack activity, stress, age, genetics
Order of Heamostasis
- vascular spasm
- Platelet plug formation
- Coagulation
- Retraction and repair
- Fibrinolysis
