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ANP1115 > Lecture 1 > Flashcards

Lecture 1 Flashcards

1
Q

blood components

A

only fluid tissue in body, made of formed elements suspended in plasma.

erythrocytes - RBC
leucocytes - WBC
plateles

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2
Q

characteristics of blood

A

scarlet if O2 rich, dark red if poor
more dense than water

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3
Q

ph of blood

A

7.35-7.45
if lower = acidic
higher = alkaline

respiratory + renal system will bring back to normal range

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4
Q

blood functions, 3 main categories

A

distribution
regulation
protection

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5
Q

distribution

A

carry and distribute (highway and cars analogy)

O2 and nutrients
metabolic wastee
hormones

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6
Q

regulation

A

body temp (controls where blood goes. cold = to core of body, hot= to surface)

ph in body tissues by controlling ph of blood, if blood is ok, tissue is ok, plasma proteins soak up H+ ions, bicarbonate reserve = eqm rxn)

adequare fluid volume , maintain adequate bp = high enough

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7
Q

protection

A

platelets and plasma proteins = against blood loss

antibodies, complement, WBCs = against infection

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8
Q

blood plasma

A

yellow straw color, mostly water and many solutes

carries many molecs, imp blood buffer

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9
Q

plasma protein

A

functional protein stays in blood
made by liver to circle system
to protect body

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10
Q

albumin

A

60% of plasma proteins

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11
Q

leukocytes is the only complete cell bc

A

it has a neuclus, organelles, and cell mb

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12
Q

RBC structure

A

biconcave discs had a nucleus but was discarded after making ribosomes and Hb, so cell is collapsed

pretty much a bag of Hb

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13
Q

spectrin

A

just inside mb of abc, helps rbc to squeeze through skinny caps and rebound into normal shape

helps w folding and seeing

but becomes worse at its job and RBC can’t recreate it, so cell looses flexibility as it ages, gets stuck in caps and is removed form circular system

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14
Q

specialized characteristics that optimize fn

A
  1. small size and biconcave shape = large SA/V ratio
    = easy to bind to O2
  2. if not water, is Hb, rest is 3%
    = abundance of Hb to transport O2
  3. no mitochondria, aneorobic synth of ATP
    = selfless, “O2 doesn’t belong to it”
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15
Q

relation of rate of blood flow and RBC count

A

inc rbc = more viscous blood = harder to circulate = rate of flow dec

thrfr, inc rbc = dec flow

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16
Q

Hb

A

hemoglobin
protein “globin” bound to red “heme” pigment

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17
Q

Hb structure

A

4 polypeptide chains (global part)
4 Fe containing central heme gaps
(where O2 binds)

each Fe binds to one molec of O2, 4/Hb molec).

oxyHb is a diff shape and color than deoxyHb

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18
Q

why is Hb in erythrocytes rather than being a plasma protein

A

keeps it from getting lost/fragmenting

in RBC has good access to O2

keeps it from contributing dirtily to blood viscosity (would be slush/almost solid, bc of high conc) and osmotic pressure

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19
Q

danger of CO, but overall binding spots of molecules

A

O2 binds w heme grp

CO2 binds w global part = forming carbaminohemoglobin

CO binds w heme, has more affinity w Fe so replaces O2, extremely dangerous

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20
Q

hematopoiesis

A

production of formed elements, in gen occurs in bone marrow

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21
Q

erythropoiesis

A

specifically the production of RBCs
takes about 15 days

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22
Q

steps of erythropoiesis

A

1) there is a stem cell - a hematopoietic stem cell is for al formed elements.
2) immature cells become committed to a particular pathway. for RBC, called pro erythroblast
3) ribosome synthesis => Hb accumulation => ejection of nucleus
product = reticulocyte
then erythrocyte

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23
Q

difference between erythrocytes and reticulocytes

A

reticulocytes are immature RBC, and have residual organelles giving it a meshwork type of appearance.
within a day, it looses the ribosomes, proteins and all organelles it needed to make the cell.

matures than migrates through leaky capillary walls to blood (circa system) to carry O2

24
Q

what does reticulocyte count tell us

A

info about bone marrows ability to produce new RBCs

helps distinguish bn diff types of anemia

helps monitor bone marrow response and return to normal bone marrow fn after
chemotherapy,
bone marrow transplant
follow up for treatment for
iron defficiency anemia
B12 deff anemia
renal failure

25
if number of reticulocytes significantly inc, then
burst of formation of RBCs
26
usual reticulocyte count
usually 1-2% of erythrocyte of total RBC in system so regularly loosing 1-2%, (bc were rennewing that amount), why? missing factors
27
regulation of erythropoiesis, too few, too many?
balance bn RBC production and destruction few = anemia many = polycythemia
28
regular production rate
more than 2M per sec if healthy (meaning having enough iron and B vitamins for production) thrfr, that same number/amount are during
29
homeostasis of normal blood O2 levels
Stim = not enough O2, inadequarte O2 delivery = hypoxia due to = - dec in RBC count -dec in amount of Hb - dec availability of O2 2) kidneys release erythropoietin 3)erythropoietin stimulates red bone marrow 4) enhances erythropoiesis inc RBC count 5) O2 carrying ability of blood inc
30
erythropoietin, EPO
glycoprotein hormone made by kidneys
31
EPO is always in blood, but inc release if
hyperopia due to ____ occurs i. hemorrhage/excess destruction ---sickle cell anemia = shortened lifespan, turnover rate inc ii. high altitude or pneumonia ----O2 is limiting, kidney doesn't know why so makes more RBC ---- O2 is having trouble having access to blood bc of fluid in lungs, so again kidneys do the same
32
erythropoietin
enhances maturation rate of RBC precursors
33
what happens in renal patients, regarding ego
aside from kidney failure, they lack EPO so RBC count is half of what it should be so helped by recombinant EPO
34
what happens in athletes, regarding ego
EPO inc hematocrit from 45 to 65% meaning amount of RBC from 45 to 65 but inc viscosity of blood, along with the expected dehydration in running/excersie can cause clotting (stroke, heart attack/failure)
35
why women have lower hematocrit (% of RBC in blood) than men
testosterone stimulates the kidney to produce EPO, men have more testosterone menstruation, loss of blood on a monthly basis
36
dietary requirements for erythropoiesis (iron and b vitamins)
absorption is regulated by body's storage levels 65% alr in Hb molecs rest stored in spleen, liver, bone marrow (as ferritin, hemosiderin)
37
transport of iron
from spleen to blood transported in blood loosely bound to transferrin
38
loss of iron
via sweat, urine, feces, menstrual blood
39
B12, B9 (folic acid) essential for
DNA synthesis so can maintain stem cells to make new RBC
40
destruction of erythrocytes RBC graveyard
as they mature, they become rigid and fragile w time since Hb begin to degenerate spleen grave, gets stuck anywhere but most likely in spleen + where it gets destroyed
41
what happens to components after RBC is destroyed
Iron is stored and reused/recycled aa of global recycled heme degraded to bilibrubin = becomes bile pigment, eventually to stercobilin or urobilinogen
42
anemia
reduced O2 carrying capacity of blood
43
causes of anemia
not enough RBC being produced significant blood loss episodes RBC too quickly destroyed (sickle cell anemia)
44
polycythemia
too much RBCs
45
3 types
polycythemia vera = true poly = cancerous condition in bone marrow so conc of RBC is HIGHHHH secondary polycythmia = as a result of smth else, ex high altitufe artificial polycythemia = blood doping, in athletes, artificially inc rbc to carry more O2
46
danger of polycythemia
blood becomes to viscous, hard to circulate, thrfr more workload in circ system
47
platelets formation
pretty much just cytoplasmic fragments of megakaryocytic has purple staining granules that have clotting factors and enymes regulated by hormone = thrombopoietin from liver
48
Hemostasis 3 phases
blood clotting vascular spasms formation of platelet plug coagulation
49
vascular spasm
vasoconstricition of vessel when damaged to slow down the rate of blood loss, make it easier for clot to form, slow down blood flow
50
platelet plug formation
usually platelets don't stick to e/o, imp so they don't form when not needed. this is bc of NO and prostacyclin from endothelial cells when collagen is exposed (from beneath endothelial cells of vessel walls) becomes a trigger smth is wrong, platelets swell + become sticky so adhere to collagen.
51
coagulation
platelet plus converted to a sturdier strucutre prothrombin activator formed prothrombin => thrombin fibrinogen molecs => fibrin mesh.
52
platelet products that promote clumping
ADP = inc aggregation and degranulation (stickiness and release) serotonin and thrombin A2 = inc vascular spasm and aggregation.
53
2 pathways to coagulation and PA (prothrombin activator)
Intrinsic = don't need to be injured, only collagen as trigger, takes time (so can be undone if not needed) can be in a test tube or slightly damaged vessel Extrinsic = damage, cut, injury, exposure to TF in epithelial cells tells blood that wall is broken fast but limited capacity, so jumpstarts for intrinsic to keep working.
54
Pathway, how it works.
Intrinsic has many factors being activated, extrinsic adds things here and there, jumpstarts it and all that, main goal is to get to the prothrombin activator which turn prothrombin to thrombin thrombin is an enemy that then catalyzes (fibrinogen => fibrin mesh in this path, Ca+ is an imp cofactor in clotting and XII (factor 13) is a fibrin stabilizing cofactor)
55
Clot retraction and repair
clots occur with 30-60 mins platelets contract ( bc they have actin and myosin) and pull on surrounding fibrin strands serum is squeezed from clot and ruptured edges of vessels are pulled closer PDGF is released during degranulation stimulates the divisision and rebuilding of the wall end cells multiply to fill gap in lining and clot covers the damage while healing begins

ANP1115 (14 decks)

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