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Physiology 1 (WPH) > L11&L12: RBCs and Hemostasis > Flashcards

L11&L12: RBCs and Hemostasis Flashcards

1
Q

what are the 3 layers you get when you centrifuge blood

A 
plasma (55% on average
buffy coat (WBCs, thin)
formed elements (45%avg RBCs,platelets,etc)
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2
Q

hematocrit =

A

RBC vol / total blood vol
or
formed element vol
total vol

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3
Q

T/F men have a slightly higher hematocrit than women on average

A

true

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4
Q

RBC function
platelet function
WBC function

A

gags exchange
hemostasis
defense

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5
Q

what is the composition of plasma:
% H2O
% proteins
% solutes

A

91% H2O
7%prots (55%albumin,42%glob,3%fibrinogen)
2% solutes

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6
Q

what is the most prevalent protein in plasma?

A

albumin (55% of protein content)

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7
Q

do plasma proteins cross endothelial membrane?

A

no, too large

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8
Q

the bulk of the formed elements in blood are

A

RBCs

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9
Q

why is RBC biconcave disk shaped

A
  • decrease O2 diffusion distance to Hb
  • increase surface area/volume for gas exchange
  • flexibility so it has room to bend and stretch through capillaries
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10
Q

what happens if an RBC is depleted of ATP

A 
it crenates
(ATP plays a role in maintenence of shape)
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11
Q

how does RBC make ATP?

A

glycolysis

no mitochondria

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12
Q

what determines RBC type?

A

membrane glycosylations = antigens

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13
Q

what is ATP used for in an RBC?

A

“ATP powers pumps”

  • Ca++ ATPase pump out
  • Na/K pump
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14
Q

what happens if an RBC Ca++ ATPase pump is defective?

A 
get kynocytes (RBCs with spicules)
because high Ca++ triggers protein linkages
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15
Q

what is spectrins role in an RBC?

A

forms a cytoskeletal meshowrk along inner membrane and maintains cell cell shape
-spectrin defects lead to fragile spherocytes

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16
Q

RBC defects in spectrin result in…

A

fragile spherocytes

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17
Q

how does Hb maintain RBC cell shape?

A

it is packed to very high density, defects / mutations, like HbS can lead to aggreagation, sickling, deformation

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18
Q

3 things that maintain RBC cell shape

A
  • ATP (Na/K pump)
  • spectrin (or else spherocytosis)
  • Hb (HbS can sickle)
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19
Q

why is Hb contained within RBCs not just transported in plasma?

A
  • would be oxidized and broken down very quickly in plasma

- would also change oncotic pressure of plasma drastically

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20
Q

how does the RBC prevent Hb oxidation?

A

2 ways:

  • metHb reductase reduces metHb back to Hb using NADPH
  • contains reduced glutathione GSH, which is oxidized to GSSG to spare Hb (NADPH needed to reduce again)
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21
Q

what is the equation for the reaction catalyzed by metHB reductase in the RBC

A

metHb reductase

HbFe3+ + NADH -> HbFe + NAD

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22
Q

what are 2 reactions that spare Hb oxidation in RBCs?

A

metHb reductase
HbFe3+ + NADH -> HbFe + NAD

H2O2 + GSH -> GSSH + H2O
<-
glutathione reductase + NADPH

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23
Q

what are 2 key enzymes that prevent Hb oxidation in RBCs?

A
  • metHb reductase (reduces metHb with NADH)

- glutathione reductase (reduces GSSH to GSH with NADPH so that GSH will be oxidized before Hb is)

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24
Q

how does the RBC generate its NADPH that it uses for glutathione reductase to prevent Hb oxidation?

A

NADH generated by
G6PD
glucose-6-phosphate dehydrogenase
which functions in glycolysis

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25
Q

what happens to an RBC with reduced G6PD glucose6phosphate dehydrogenase activity?

A
  • glycolysis inhibited
  • NADPH generation inhibited
  • glutathione reductase inhibited
  • less GSH
  • more Hb will be oxidized to metHb
  • hemolysis
  • blood in urine
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26
Q

T/F glucose uptake in RBCs is insulin dependent, just like in most other tissues

A

false

not insulin dependent

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27
Q

where does RBC formation occur…

  • in embryo?
  • 3rd trimester and while young?
  • adult?
A
  • yolk sac
  • marrow cavities
  • axial marrow cavities (distal long bones are infiltrated with fat)
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28
Q

2 precursers to mature RBC

A
  • normoblast (differentiates 4 times over the course of 4-5 days before extruding nucleus)
  • reticulocyte (enters circulation, contains residual RNA for 1-2 days then protein machinery is degraded and becomes adult RBC)
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29
Q

how many blood cells in circulation are reticulocytes?

A

1-2%

they stay in circulation with RNA 1-2 days before maturing completely, RBCs live 120 days, 2/120 = 1-2%)

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30
Q

how can RBC production be increased?

A

in response to low pO2, endocrine mostly in the kidney produce erythropoietin, a hormone that stimulates size of erythroid marrow compartment and rate of erythrocyte precursor maturation

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31
Q

what stimulates erythropoietin production?

A

anything that decreases pO2

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32
Q

what does erythropoietin do?

A

hormone that stimulates size of erythroid marrow compartment and rate of erythrocyte precursor maturation (produce more RBCs)

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33
Q

where does Fe++ for heme synthesis come from?

A

mostly recycled from old Hb, small amount obtained through diet, mobilized body stores

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34
Q

how is Fe++ transported into the normoblast?

A

binds to transferrin receptor and endocytosed

transferrin receptor eventually re-incorporated into the membrane

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35
Q

what does a transferrin receptor do?

A

binds to Fe++ and endoycytosis to bring it into RBC

transferrin receptor eventually re-incorporated into the membrane

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36
Q

what is ferritin

A

storage form of Fe++ in RBC

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37
Q

what is the storage form of Fe++ in the RBC

A

bound to ferritin
or
bound to hemosiderin

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38
Q

what indicates aging of RBC?

A

not entirely clear… seems to be membrane changes… spleen tests flexibility

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39
Q

T/F Fe++ is endocytosed with the tranferrin receptor into the mature RBC for heme / Hb snthesis

A

false

normoblast

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40
Q

how long is an RBC in circulation

A

120 days

41
Q

where does RBC breakdown occur?

A

reticular endothelial cells of the spleen

some liver

42
Q

how does the spleen detect RBC aging?

A

RBC must be very flexible to squeeze through reticular endothelial cells of spleen so probably tests membrane flexibility for membrane changes

43
Q

what is the treatment for spherocytosis

A

splenectomy

keep spleen from degrading too many cells, liver will continue to remove RBCs from circulation

44
Q

is the porphyrin ring of heme recycled?

A

no

45
Q

T/F the α-carbon of the porphyrin ring in heme produces carbon monoxide CO upon RBC breakdown

A

true

46
Q

icterus and jaundice are signs of…

A

hyperbilirubinemias

47
Q

what is the fate of Hb in plasma after hemolysis?

A

2 possible paths:

  • broken into dimers, bound by haptoglobin, pulled in by liver & broken down (if haptoglobin capacity is exceeded, Hb appears in urine)
  • oxidized to metHb, broken down by macrophage and aa’s recycled
48
Q

what is the protein that binds to Hb dimers in the blood after hemolysis and facilitates their transport into the liver?

A

haptoglobin

49
Q

what is haptoglobin’s role in hemolysis?

A

binds free floating Hb dimers and brings them into liver for breakdown

50
Q

what happens to Fe after hemolysis?

A

bound to transferrin and brought into marrow for recycling (mostly)

51
Q

hemoglobinuria

A

Hb in the urine

52
Q

what protein levels in plasma can be used to diagnose an intravascular hemolytic event?

A

serum haptoglobin levels
will be decreased for a time following a hemolytic event because will be bound to Hb dimers to bring them to liver for degradation

53
Q

why higher Fe intake for women necessary?

A

menstrual blood loss

54
Q

the majority of anemias are __

A

hypoproliferative

synthesis of Hb or RBCs too slow

55
Q

anemia is defined in 2 ways:

A
  • insufficient RBCs

- insufficient Hb

56
Q

-hypoproliferation
-iron deficiency
-acute bleeding
-bacterial infeciton
-marrow damage
-erythropoietin deficiency
-hemolysis (HbS, spherocytosis, etc)
-thalassemias
-dietary difficiency (B12, folic acid)
are all possible causes of __

A

anemia

57
Q

how can bacterial infection lead to anemia?

A

body will shut down Fe release to keep it from bacteria… with a long-term infection, FE from catalysis will not make it back to marrow for erythropoesis

58
Q

what kind of treatment can lead to anemia from marrow damage?

A

chemotherapy (targets rapidly dividing cells)

-treat with marrow transplant

59
Q

how can you treat an anemia due to marrow damage?

A

marrow transplant

60
Q

HbS and spherocytosis are both forms of…

A

hemolytic anemia

61
Q

maturation abnormalities that can lead to anemias include

A

alpha and beta thalassemias

62
Q

pernicious anemia is caused by

A

deficiency of intrinsic factor (a glycoprotein produced by parietal cells in stomach), which is needed to absorb vitamin B12
-or a deficiency of vitamin B12 itself

63
Q

deficiency of intrinsic factor production by parietal cells in the stomach can cause…

A

pernicious anemia

because intrinsic factor needed to absorb vitamin B12

64
Q

folic acid must be obtained through the diet for….

A

DNA synthesis and erythropoesis

65
Q

what are two forms of dietary anemias

A
  • folic acid needed for DNA synthesis & erythropoesis

- vit B12 and intrinsic factor to absorb it needed for… erythropoesis?

66
Q

Rhogam

A

anti-D (Rh+) antibodies
injected into Rh- mother late in Rh+ pregnancy to bind and hide Rh+ antigens from mother’s immune system and prevent developing innate anti-D antibodies for next Rh+ pregnancy

67
Q

antibodies are like molecular staples and cause __

A

agglutination

68
Q

how are RBC antibodies developed
anti-A
anti-B
anti-D

A

anti-A from bacterial/allergic exposure
anti-B from bacterial/allergic exposure
anti-D usually only from Rh+ pregnancy

69
Q

this blood type is a universal receptor

A

AB+

70
Q

this blood type is a universal donor

A

O-

71
Q

primary hemostasis consists of…

secondary hemostasis consists of…

A

vasoconstriction
platelet plug formation

coagulation

72
Q

thrombosis =

A

clotting where you don’t want it

opposite of hemorrhagic stroke

73
Q

hemorrhagic stroke =

A

inability to clot when you want it

opposite of thrombosis

74
Q

3 pathways of vasoconstriction

which are quick and which are slower onset?

A

myogenic (quick)
neurogenic (quick)
humoral (TA2) (slow)

75
Q

this formed element has no nucleus but many granules

A

platelet

76
Q

pathway of platelet plug formation

A 
collagen contact
platelet adhesion (VWF von wil factor)
release reaction (exocytose granules ADP)
membrane changes
cyclooxygenase (act on mem lips to produce)
TA2 thromboxane A2
positive feeback (TA2 and ADP)
platelet plug
77
Q

how does aspirin affect platelet plug formation

A

blocks cyclooxygenase from reacting with membrane phospholipids to produce TA2 thromboxane A2

78
Q

thrombocytopoenia =

A

not enough platelets, cannot form plugs

79
Q

need secondary hemostasis (coagulation) because…

A

platelet plug not sufficient in long term (when vasoconstriction lessens will be washed away)

80
Q

quick and dirty secondary hemostasis (coagulation)

A 
prothrombin
thrombin
fibrinogen
fibrin
polymerization
fibrin stabilizing factor (cross-links)
81
Q

hemophilia

A

deficit in clotting (thromboplastic) factors

82
Q

2 pathways for secondary hemostasis (coagulation)

A

extrinsic (trigger)

intrinsic (positive feedback)

83
Q

extrinsic hemostasis pathway

A 
tissue trauma, blood extravisation
tissue thromboplastin (factor VII) + Ca++
prothrombin activator
thrombin 
triggers intrinsic pathway
84
Q

intrinsic hemostasis pathway

A 
trauma
protease cascade
prothrombin activator
thrombin
positive feedback
use platelet lipids for reaction surface
85
Q

how is the extrinsic hemostasis pathway shut off?

A

TFPI tissue factor pathway inhibitor

inhibits tissue thromboplastin

86
Q

what are 2 very important proteins in extrinsic hemostasis pathway

A
  • tissue thromboplastin VII (activates prothrombin cleavage)
  • TFPI (inhibits tissue thromboplastin VII and shuts off pathway)

without these, severe pathology

87
Q

how are clotting factors commonly prepared

A

post translational modification using vitamin K to carboxylate glutamic acid residues into γ-carboxy glutamic acid (- charges can bind Ca++ in the process of clotting)

88
Q

T/F About 2% of red cells appearing in the blood still have their nuclei

A

false

still have some RNA (reticulocytes)

89
Q

T/F here is more hemoglobin in whole blood than all of the plasma proteins combined

A

true

90
Q

T/F platelet aggregation is promoted by ADP

A

true

ADP is exocytosed from platelets in the release reaction

91
Q

TFPI

A

in plasma, inhibits extrinsic hemostasis pathway and brings it to and end

92
Q

antithrombin III

A

binds and inhibits clotting factors

activity increased by heparin

93
Q

how does heparin interact with antithrombin III

A

heparin increases antithrombin III activity, inhibiting clotting factors

94
Q

thrombomodulin

A 
binds thrombin
changes specificity of thrombin
throbmin no longer cleaves fibrinogen
cleaves proteins C and protein S instead
shuts down coagulation
95
Q

plasmin

A

breaks down fibrin

96
Q

TPA tissue plasminogen factor

A

activates plasminogen

plasmin breaks down fibrin

97
Q

von willebrant’s factor

A

helps platelet adhesion in primary hemostasis

98
Q

TA2 thromboxane A2

A
  • produced by cyclooxygenase reaction with membrane phospholipids
  • promotes platelet aggregation with ADP
  • also promotes humoral vasoconstriction*
99
Q

what is ADPs role in primary hemostasis

A

exocytosed from platelets during release reaction

-promotes platelet adhesion

Physiology 1 (WPH) (18 decks)

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