week 7 - biol121

blood vessel

blood flows between the heart and peripheral tissues via a network of blood vessel

the thin wall of capillaries allows the exchange of nutrients, dissolved gases, and wastes between blood and interstitial fluid

the walls of larger veins and arteries are too thick for nutrients to diffuse to the cell, therefore they contain small blood vessel within their walls = vasa vasorum to provide them with this exchange

arteries

(efferent vessels) carry the blood AWAY from the heart

veins

(afferent) carry blood TOWARDS the heart

capillaries

(exchange of vessel) connect the smallest arteries (arterioles) and the smallest veins (venules)

tunica intima

this innermost layer is composed of an epithelial (endothelium) and connective tissue layer. The endothelium is continuous throughout the vascular system, including the lining of the chambers of the heart. In arteries, the outer margin of this layer contains a layer of elastic fibers called the internal elastic membrane.

tunica media

this middle layer contains smooth muscle in a framework of loose connective tissue. When the smooth muscle contracts the vessel diameter decreases (vasoconstriction). When the smooth muscle relaxes the vessel diameter increases (vasodilation). In arteries, the outer margin of this later also contains a layer of elastic fibers called the external elastic membrane.

tunica externa 

this outermost layer is a substantial sheath of connective tissue primarily composed of collagenous fibers, that typically bled into those of adjacent tissues, stabilising and anchoring the blood vessel.

arteries cont.

Usually round, with thick walls and small lumens.

Usually rippled because of vessel constriction.  Internal elastic membrane present.

Thick, dominated by smooth muscle cells and elastic fibers. External elastic membrane present in larger vessels.

Collagen and elastic fibers. Thinner then media layer in all but the largest arteries

thick

not present

away from the heart

high

higher in system arteries, lower in pulmonary ateries

veins cont

Usually flattened, with thin walls and large lumens.

Appears smooth. Internal elastic membrane absent.

Thin, dominated by smooth muscle cells and collagen fibers. External elastic membrane absent

Collagen, elastic fibers and smooth muscle cells. Thickest layer in veins.

thin

present

toward the heart

low

lower in system veins, higher in pulmonary veins

blood flow

pressure is need for blood flow, blood will always go from high pressure to low pressure, the source of pressure is the left ventricle (thicker and contracts forcefully, generating pressure) - pushes through to the aorta and then bangs on the wall of the artery, when the ventricle is contracting

mean arterial pressure

the pressure in both systole and diastole pressure

quite high in aorta, when go through the other arteries it drops (pressure drops the further away you go from the heart) - this drives blood flow through the body

• when the ventricle relaxes the arteries slowly recoils = diastolic pressure

cardiac output

heart rate (generated by the SA node) and stroke volume (amount of blood ejected by the ventricle each time the heart contracts), if these increase so does cardiac output

total peripheral resistance

is determined by vessel length, diameter

greater length that blood has to travel, more likely to bang against the wall of blood vessel = friction and resistance and causes a change in mean arterial pressure

vasoconstriction and vasodilation

• decrease diameter - has an influence of mean arterial pressure, blood flow will be slower, pressure upstream will start to rise

• increase diameter, faster flow through vessel and pressure drops

blood viscosity

the more thick the blood is, the slower is able to flow, increase that driving pressure

capillary exchange

capillaries - smallest of blood vessel - makes exchange with the surrounding tissue

blood carrying oxygen and nutrients will exit the left side of the heart - large arteries - small arteries - makes it way to capillaries

• exchanges occur here: arterial end of the capillary fluid carrying oxygen and nutrients

the capillary hydrostatic pressure

the pressure exerted by fluid on the

wall of the capillary. it wants to push fluid (water carrying oxygen and nutrients into the tissues)

capillary colloid osmotic pressure

is generated by the

plasma proteins in the capillary.

• can't leave the capillary.

• they're far too large.

they exert an osmotic pressure - drag fluid towards them, water from low solute concentration to high solute concentration (where the plasma proteins are)

interstitial fluid hydrostatic pressure

pressure exerted by fluid against the

capillary wall, wanting to push fluid into the capillary.

interstitial fluid colloid osmotic pressure

is exerted by the plasma proteins in

the tissues, they are trying to draw fluid towards them

arterial end

positive pressure, the pressure pushing out of the capillaries into the tissue is greater than the pressure which are pulling into the capillary

• oxygen and nutrients are pushed into the tissue via filtration

when all four pressures work together

net filtration pressure

venual end

two pressure which are pushing into the capillary: interstitial fluid & hydrostatic pressure

capillary colloid osmotic pressure - which is quite high at this end, pulling fluid into the capillary

the pressure pulling into the capillary are greater than the pressure pulling out of the capillary: so fluid will move into the capillary carrying waste = reabsorption, thus the net filtration pressure is negative

baroreceptors

short-term maintenance of blood pressure homeostasis

• lying down to sitting, there are receptors that detect changes in our blood pressure (high or low) - baroreceptors

these are found in carotid sinuses, where the common carotid arteries - supply the head, divide into smaller arterial branches & the aortic arch: branches that go to the rest of the body

when baroreceptors detect that there has been change in the blood pressure, they would send messages to the brain - then to the ANS - heart and blood vessel - then changes can be made in order for blood pressure to be restored

baroreceptors cont

decreased blood pressure (going for lying down to standing) - baroreceptors detect change, as there is less stretch in the wall of the arteries due to less blood volume.

• send fewer impulses to the CV system control centre in the brain

• less firing of nerve impulses

• this notifies that the centre that blood pressure has gone down

the brain responds by sending parasympathetic messages to the heart to tell it slow down - HR , SV and Q decrease

• the parasympathetic nervous system doesn't stimulate our blood vessels, but rather - relax that sympathetic control on the blood vessels.

resulting in vasodilation & vasodilation leads to a decrease in total peripheral resistance

components of blood

composition: plasma (55%), buffy coat - white blood cells and platelets, red blood cells (45%)

haemoglobin: main component of blood that carries oxygen

structure = function

RBC production is regulated by the hormone erythropoietin (EPO).

erythrocytes (red blood cells)

• a-nucleated

• biconcave discs

• filled with haemoglobin

• allows us to transport adequete oxygen around the body, without a nucleus it can’t reproduce or repair

haemoglobin

heme group bound to globin protein

• theme contains iron

• iron binds to oxygen

• haemoglobin also binds to carbon dioxide, but its the globin proteins that bind to it

oxyhemoglobin

haemoglobin bound with oxygen

deooxyhaemoglobin

haemoglobin without oxygen after oxygen diffuses into tissues

carbonminohaemoglobin

haemoglobin bound with carbon dioxide

leukocytes (white blood cells)

• only complete cells in the blood, makes up 1% of the total blood volume

• essential to the immune system

• can leave capillaries via diapedesis

• move through tissue spaces

granulocytes

phagocytic (engulf), can contain cytoplasmic vesicles (granules), strain differently, acidic, basic or both, lobed nucleus

neutrophils

most abundant WBC

50-70% of WBC

multi lobed nucleus

granules stain both acidic and acidic - peroxidase and hydrolytic enzymes (break down proteins), defensins (antibiotic like proteins)

main bacteria killers

basophils

releases histamines

0.5% of WBC

bi-nucleated granules stain basic

contains histamines

release causes vasodilation and chemotaxis of other WBC

eosinophils

counter parasitic worms

2-4% of WBC

bi-nucleated

granules stain acidic

digestive enzymes

target parasitic worm

agranulocytes

do not have visible granules

may look similar - but are not

function is different

nucleus shape - spherical (lymphocytes) and kidney-shaped (monocytes)

monocytes

4-8% of WBC

large u-shaped nucleus

monocytes in blood - macrophages in tissue

highly mobile and phagocytic

activate lymphocytes

lymphocytes

< 25% of WBC

large, dark nucleus

two main types: T cells and B cells

natural killer

part of the innate system

2-18% of lymphocytes in peripheral blood

detect MHC class I - deficient cells

presence of MHC-class I on cells inhibits NK function

platelets

megakaryocyte

cytoplasmic fragments of this larger cell

platelet granule contain: serotonin, calcium, enzymes, ADP, platelet-derived growth factor (PDGF)

involved in the clotting mechanism

mast cell

reside in tissue: boundaries between tissues and external environment

important role in inflammation: activation causes release of inflammatory mediators

can be activated by a range of stimuli: allergens, pathogens and physiological mediators

human blood groups

• glycoproteins on the surface of RBC

unique to the individual, recognized as foreign if transfused into another person, promote agglutination - causes severe problems

• antigens used to classify: present or absent

many groups (ABO, Rh, MNS, Dufy, Kell, Lewis)

two main groups (ABO and Rh)

• cause bad reactions in mismatched in the transfusion

• foreign RBC’s destroyed by host immune response

ABO groups

based around tow antigens: A and B

A - A antigens on RBC

B - B antigens on RBC

AB - A and B antigens on RBC

O - neither A nor B on RBC

• our plasma contains pre-formed antibodies recognizing A or B

• no previous contact with antigen required

A blood: anti-B

B blood: anti-A

AB blood: no anti-A or anti-B

O blood: both anti-A and B

rhesus (rh) factor

presence of Rh antigens of RBCs indicated as Rh+

• unlike ABO, Rh antibodies are not pre-formed in plasma

• after first exposure antibodies are formed = no reaction

• second exposure causes typical transfusion reaction = due to immunological memory and that they antibodies are present

but never assume

haemostasis

series of reactions designed stop bleeding

three phases - occur in rapid succession

• positive feedback loop

• short-term, it’s a reflex arch

vascular spasms

immediate vasoconstriction, reduces blood flow to the area, helps the platelets plug the hole

platelet plug formation

collagen fibres - apart of connective tissue in the wall - help the platelets stick them and become activated, change their shape and release substances, and interacts with other platelets

releases contents of the platelets, stimulate further vasoconstriction, reduce blood flow and help activate other platelets nearby and fill the hole

coagulation (blood clotting)

a series of reactions which transforms blood from liquid to gel

• reinforcing the platelet plug

initiated through two ways: intrinsic and extrinsic

both converge to a common pathway

• prothrombin activator: is formed from both pathways

• prothrombin is activated into thrombin

• thrombin catalyses fibrinogen (soluble protein) into fibrin (insoluble protein) mesh, it traps blood cells and seals the hole

clot removal

clot reaction - first step: platelets contract and pulls clot together, brings edges of damage vessels together

repair - second step: platelet derived growth factor (PDGF) stimulates rebuilding of blood vessel walls

• plasmin devolves clots - if there insufficient plasmin, they can occlude blood vessels

fibroblasts form a connective tissue patch

stimulated by vascular endothelial growth factor (VEGF) endothelial cells multiply and restore lining

antibodies and antigens

antigen: present of the surface of the cell, identifies that cell

antibody: immune proteins that elicit an immune response

Rh groups

blood group phenotype	genotype	antigen on blood cell	antibody produced after exposure
rh+	DD, Dd	D	none
rh-	dd	none	anti-D (only after first exposure)

haemostasis pathway

intrinsic: damage to the blood vessel wall (internal trauma), material from the exterior starts to enter and this stimulates clotting

extrinsic: damage to the tissue (external trauma) - rapid response

if you don’t have sufficient calcium = your clotting time slows