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Biochem Final > Blood wk 1, co-ag/heme > Flashcards

Blood wk 1, co-ag/heme Flashcards

1
Q

What is the definition of hemostasis?

A

“blood stoppage”
-a physiological and biochemical response to circulatory system injury

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2
Q

what is involved with Physical Aggregation/Clumping of circulating blood cells?

A

Platelets

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3
Q

what is a platelet structure?

A

The platelet mass is held together by blood proteins
-bind to platelet cell surface receptors
-form multiple non-covalent cross-links between platelets.

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4
Q

what mechanism occurs to plug small holes in blood vessels?

A

clumping of platelets

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5
Q

The hemostatic response is governed by two strict
requirements:

A

(1) When blood vessels are broken, and blood begins to
leak out, hemostasis must be fast and effective.
(2) Hemostasis does not occur normally inside intact
blood vessels.

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6
Q

how are large lesions to blood vessels plugged?

A

gel formation or clotting

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7
Q

what does Fibrinogen do for clotting?

A

forms the non-covalent cross links of the platelet clump, and is also the precursor of the protein (fibrin) that polymerizes to form the blood clot.

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8
Q

A slow or ineffective hemostatic response can lead to:

A

-loss of blood components (especially red blood cells)
-loss of volume and blood pressure (->shock)
-hypoxic damage

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9
Q

There isn’t time to synthesize clotting components at the time of injury, so

A

all the cells and proteins that participate in the hemostatic response CIRCULATE IN THE BLOOD AT ALL TIMES, in an INACTIVE FORM, ready to be activated the moment they are needed

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10
Q

Formation of a clot inside a blood vessel is called

A

thrombosis

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11
Q

all the cells and proteins that participate in the hemostatic response __________________, in an ________ FORM

A

CIRCULATE IN THE BLOOD AT ALL TIMES
inactive

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12
Q

The resulting clot is called a

A

thrombus

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13
Q

A thrombus that dislodges and travels through the circulation is called a

A

thromboembolism

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14
Q

what is the danger associated with venous thrombi?

A

tend to dislodge, travel through the right heart, and lodge in the lungs (pulmonary embolism) block pulmonary artery

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15
Q

what is the risk associated with atria thrombi?

A

block circulation localized tissue ischemia.
- a brain embolism causes ischemic stroke.

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16
Q

External trauma to blood vessels damages the surrounding ______________, triggering massive activation of _____ and ______

A

subendothelial tissue
platelets and clotting factors

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17
Q

what are the major players in the balance of procoaguents and anticoaguents?

A

pro: platelets and clotting factors
anti: plasminogen and antithrombotic

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18
Q

what is Platelet aggregation?

A

formation of a “platelet plug”,
a.k.a.”primary hemostatic plug”
NONCOVAENT bond

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19
Q

Internal injury to the endothelial cell layer can be caused by: may expose the subendothelium locally, leading to limited local activation of platelets and clotting factors.

A

(caused by atherosclerosis and inflammation)

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20
Q

Blood coagulation results in the formation of

A

“secondary clot” of polymerized blood protein

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21
Q

Blood coagulation has clots with what type of bond?

A

covalent

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22
Q

Internal injury to the endothelial cell layer may expose the
subendothelium locally, leading to

A

limited local activation

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23
Q

what is vasoconstriction?

A

restricts flow of blood through narrowed blood vessels

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24
Q

what are some key facts about vasoconstriction?

A

-very fast
-directly reduces volume of blood loss
-reduced blood flow promotes platelet aggregation and blood
coagulation

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25
Q

describe the structure of Platelets and how are they formed?

A

–Platelets are very small non nucleated cells that circulate in the blood
–They are formed by budding from the membrane of megakaryocytes

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26
Q

what is different about blood coagulation?

A

-slower (seconds to minutes)
-includes the entire blood volume (including blood
cells)
-blood is transformed from a fluid to a gel

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27
Q

what is the lifetime on platelets?

A

7-9 days

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28
Q

Platelets circulate in an what form?

A

They are metabolically active but hemostatically inactive

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29
Q

Inactive platelets are what shape?

A

disc shaped smooth cells with surface receptors for collagen, thromboxane A2 (TXA2), and ADP

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30
Q

receptors on inactive platelets are couped to what? How relate to activation?

A

membrane-bound
phospholipase C – produces the second messenger IP3,
leading to Ca2+ release and platelet activation

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31
Q

what kind of granules on platelets?

A

dense (ADP and TXA2)
alpha (cytokines/proteins)

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32
Q

Drugs which increase the activity
of the PGI2 pathway and increase
intracellular cyclic AMP levels will
have what effect on rate of platelet aggregation?

A

decrease rate of platelet aggregation

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33
Q

Drugs which block the physiological actions of TXA2 or ADP will have what effect on platelet aggregation?

A

inhibit platelet aggregation

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34
Q

Sequence of events in formation of the platelet plug:

A

endothelial injury,
exposure,
adhesion,
activation,
aggregation

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35
Q

what occurs during the adhesion stage of platelet plug?

A

-Collagen is exposed after injury to vessel
-platelet’s bind via GP VI receptor (immobilizing platelets)
-Damaged endothelial cells release Von Willebrand Factor (VWF
-unrolls adhering to injury site, esposes sites that bind to plateet membraneGP ib receptor

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36
Q

what does Von Williebrand factor do?

A

“unrolls” like a carpet, adheres to the injured site, and
exposes sites that bind the platelet membrane GP Ib receptor

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37
Q

what occurs during activation stage?

A

–Occupation of collagen receptors activates
immobilized platelets
–Fibrinogen receptors and von Willebrand factor receptors
appear on the surface of the activated platelets
–Activated platelets release TXA2 and ADP, which activate
neighboring platelets, creating a cascade effect

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38
Q

what does

A
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39
Q

what do activated platelets release? what does it cause?

A

TXA2 and ADP, which activate
neighboring platelets, creating a cascade effect

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40
Q

what occurs with aggregation of platelets?

A

–Platelet fibrinogen receptors bind to fibrinogen receptor binding domains, one at each end of the molecule
–Fibrinogen (non-covalent) binds platelets together to create the platelet plug

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41
Q

Activation of a platelet is an ____ process, why?

A

irreversible
changes shape

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42
Q

what changes occur that make activation irreversible?

A

–Changes in the cytoskeleton cause activated platelets to become irregular,
elongated, and amoeboid in shape

–New receptors appear on the surface of the cell, most importantly receptors
for fibrinogen and von Willebrand factor

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43
Q

VWF and collagen access platelet receptors, _____ and ____, leading to?

A

GPIb-IX- V and GPVI, leading to adhesion

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44
Q

what is thrombocytopenia?

A

not enough platelets

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45
Q

what is Glanzman’s thrombasthenia?

A

defective fibrinogen receptors

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46
Q

what physical symptom is usually associated with platelet deficiency?

A

petechiae (multiple small reddish
hemorrhages), resulting from
injury to blood capillaries due to
mechanical stress or inflammation

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47
Q

after vascular injury, VWF and collagen access platelet receptors, GPIb-IX- V
and GPVI, leading to ______

A

adhesion

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48
Q

These interactions lead to rapid elevation of cytosolic
Ca2+ , cytoskeletal rearrangements, and _____

A

activation

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49
Q

Activation of GPIIb/IIIa allows binding of fibrinogen to
mediate platelet ______

A

aggregation

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50
Q

Formation of a secondary clot is initiated _______ of
platelet aggregation

A

independently (but it is stimulated and accelerated by
activated platelets and the platelet plug)

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51
Q

what causes clotting?

A

formation of a network of aggregated (covalently) cross-linked fibrin derived from fibrinogen

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52
Q

what are the three stages of blood clotting mechanism?

A

vascular spasm
platelets plug formation
coag. factor activate

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53
Q

what are the stages of bood clotting?

A

formation of prothrombinase
-intrinsic
-extrinsic
prothrombine – thrombine to activate fibrin from fibrinogen

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54
Q

what occurs in the intrinsic pathway?

A

Contact activation of Factor XII by exposure to negatively charged molecules, i.e., collagen

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55
Q

what does the intrinsic pathway depend on?

A

vessel injury
collagen contact
factor VII, XI, VIII, Ca

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56
Q

what triggers the extrinsic pathway?

A

Disruption of the endothelium exposes platelets to extravascular Tissue Factor (a.k.a. Factor III or tissue thromboplastin)

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57
Q

In a myocardial infarction
caused by coronary artery plaque rupture, aggregated platelets are non-covalently cross- linked to one another by:
A. Plasmin
B. Thrombin
C. Fibrinogen
D. Fibrin
E. Collagen

A

C. Fibrinogen

58
Q

what is the common pathway?

A

where the intrinsic and extrinsic pathways meet to continue co-ag

59
Q

what works in the common pathway to convert prothrombin to thrombin?

A

Factor Xa along with its cofactor (factor V), phospholipids, and calcium forms the prothrombinase complex which converts prothrombin to thrombin

60
Q

review image of clotting cascade

A

side 44

61
Q

what is factor I?

A

Fibrinogen (made in Iiver)

62
Q

What is factor II?

A

Prothrombin is produced in the liver, present in the blood
– Prothrombin is a vitamin K-dependent clotting
factor (II, VII, IX, X)

63
Q

what is the most abundant and longest half life clotting factor?

A

factor II, prothrombin

64
Q

prothrombin:

A

Prothrombin is converted to thrombin which in turn cleaves fibrinogen to fibrin

65
Q

what is factor IV?

A

ionized Ca

66
Q

what happens if you do not have Ca?

A

no clotting can occur

67
Q

The clotting factors that bind Ca2+ all have ________ at several positions in their polypeptide chain

A

a modified amino acid, y-carboxyglutamate,

68
Q

y-carboxyglutamate is on;y found:

A

endoplasmic reticulum of the liver cells that synthesize clotting factors

69
Q

If the clotting factors are not gamma carboxylated, they can
undergo proteolytic cleavage, but the cleavage product will not be
active, why?

A

because it cannot bind Ca2+ properly

70
Q

What is the required cofactor for y-glutamyl carboxylase

A

Vit K

71
Q

what is Christmas factor dependent on?

A

kit K

72
Q

what does antithrombin III inhibit?

A

Thrombin (Factor IIa) and Xa

73
Q

what does heparin do?

A

catalyzes the irreversible inactivation of thrombin by the plasma serine protease inhibitor antithrombin III (ATIII) and is used pharmacologically as an anti-coagulant

74
Q

Protein C

A
  • Major inhibitor of Factor Va
  • Vitamin K-dependent
  • APC requires Protein S as a cofactor for its enzymatic action
75
Q

what is warfarin?

A

Warfarin is a vitamin K antagonist

76
Q

what does warfin act against?

A

It acts on the liver cells that synthesize clotting factors

77
Q

what is the effect time of warfarin?

A

Warfarin is slow to take affect as an anticoagulant. It takes several days for existing mature clotting factors to be replaced with new, immature factors in the blood

78
Q

what is the recovery from warfarin?

A

recovery from warfarin is also slow, as immature clotting factors in the blood are replaced with new, mature factors

79
Q

what occurs with a bleeding test?

A

measures the time taken for blood vessel constriction and platelet plug formation to occur. No clot is allowed to form, so that the arrest of bleeding depends exclusively on blood vessel constriction and platelet action

80
Q

Following a scalpel incision, platelet activation is characterized by all of the following except:

A. Occupation of collagen receptors activates the immobilized platelets
B. Fibrinogen receptors appear on the surface of the activated platelets
C. Activated platelets release TXA2 and ADP, which activate neighboring platelets, creating a cascade effect
D. Accompanied by irreversible spheroidal shape change

A

C. Activated platelets release TXA2 and ADP, which activate neighboring platelets, creating a cascade effect

81
Q

WHAT IS prothrombin time?

A
  • Blood is obtained by venipuncture
  • Blood is decalcified by collecting it into a tube with oxalate or citrate ions to prevent the clotting process from starting before the test.
82
Q

when does the prothrombin test start?

A

The test is timed from the addition of the calcium chloride until the plasma clots

83
Q

A prolonged prothrombin time indicates:

A

deficiency in any of factors VII, X, V, prothrombin, or fibrinogen
coud mean vit k def or on warfarin

84
Q

what is international normalized ratio?

A

equ for normal clotting time comparison

85
Q

what is Activated Partial Thromboplastin Time (aPTT) test

A

blood decalcified
centrifuged
Calcium and activating substances kaolin and cephalin are added to the plasma to
start the intrinsic pathway of the coagulation cascade

86
Q

what does PTT measure?

A

integrity of the intrinsic system
(Factors XII, XI, VIII, IX) and common clotting pathways

87
Q

what is heme?

A

dietary constituent and a prosthetic group

88
Q

what is an example of blood electron transport proteins?

A

cytochrome C

89
Q

how is heme different from most prosthetic groups?

A

1- Heme from the diet is degraded to release iron.
2- Heme in cells is synthesized.
3- Heme iron is recycled but the carbon ring of dietary heme is degraded

90
Q

The porphyrin ring is a

A

ring of rings”, consisting of 4 pyrrole rings
-The nitrogen atoms on the inside create a cage for Fe, flat, planar, purple

90
Q

what is the structure of heme?

A

porphyrin ring with an Fe2+ (ferrous ) ion bound in the center

91
Q

The porphyrin ring
structure in heme B is:

A

protophorphyrin IX

92
Q

where is heme synthesized?

A

heme is synthesized in most cells.
The predominant sites of synthesis are bone marrow (the precursor of red blood cells) and
liver

93
Q

what is the first step in syn of heme?

A

Formation of -amino levulinic acid (-ALA) from glycine and succinyl CoA

94
Q

what is the second step of syn of heme?

A

Combination of 2 molecules of d-ALA to form the pyrrole ring molecule, porphobilinogen

95
Q

what is the last step of heme syn?

A

addition of Fe to protoporphyrin IX to make heme

96
Q

where does heme syn occur?

A

-first and last 3 steps in mitochondria
-intermed in cytoplasm

97
Q

what is the most important step of heme biosynthesis?

A

first step, catalyzed by -amino levulinic acid (s-ALA) synthase, which is rate-limiting and regulated by free heme

98
Q

The second step and the last step are also important, because

A

s-amino levulinic acid dehydratase and ferrochelatase are very sensitive to lead poisoning

99
Q

how is heme biosyn regulated in liver?

A

-feed-back inhibited by increased free heme (the end product).
– regulates transcription and translation of d-ALA synthase
- inhibits d-ALA synthase enzymatic activity directly

100
Q

how is heme biosyn regulated in bone marrow?

A

-heme synthesis increased by erythropoietin (in response to low O2 levels) and by iron inducing transcription of the gene for the erythroblast isozyme, -ALA synthase 2

101
Q

Lead (Pb2+) inhibits

A

second and last steps of heme biosynthesis

102
Q

what is lead poisoning?

A

Deficiency of heme synthesis leads to microcytic anemia
over production of s-ALA (neurotoxin)

103
Q

what is porphyria’s?

A

“purple urine” are hereditary
defects in heme biosynthesis.
-symptoms are often episodic
-result in low levels of heme production. d-ALA synthesis is de-repressed

104
Q

Can heme be recycled?

A

yes, When a heme-containing protein breaks down, the heme is
released and can be incorporated into a newly synthesized protein
within the same cell

105
Q

can heme be reused in a cell that did not make it?

A

no, heme can only be reused in cells that it was made in, NO exchange between cells (if gets taken up by different cell it will be broken down

106
Q

where are RBC degraded?

A

liver and spleen

107
Q

what is the life span of a RBC?

A

120 days

108
Q

macrophages that phagocytose aged BC are a part of what system?

A

reticuloendothelial system

109
Q

what is hemoglobin broken down to?

A

-goblin protein
-iron
-porphyrin ring

110
Q

what happens to each of the parts of hemoglobin after it is broken down?

A

Globin protein: degraded to amino acids, which are recycled.
-The iron in heme: recycled back to bone marrow
-Porphyrin ring: part degrade and
excreted

111
Q

Heme degradation and excretion occurs in compartmentalized stages, what are they?

A

I. Conversion of heme to bilirubin in the macrophages of the RES.
II. Conjugation of bilirubin with glucuronic acid in the liver.
III. Reduction to soluble bile pigments in bacteria in the intestine.
IV. Some of the bile pigments produced in the intestine are reabsorbed into the blood and re-excreted through the liver and kidney.

112
Q

what occurs during conversion of heme to bilirubin in macrophages?

A
  1. methylene bridges of heme is
    hydroxylated by heme oxygenase. The porphyrin ring then opens to form biliverdin.
  2. Biliverdin is then reduced to bilirubin.
113
Q

how is the carbon and iron released?

A

The bridge carbon is released as
carbon monoxide, the iron as Fe2+

114
Q

in humans what is the farthest a heme carbon skeleton can be metabolized?

A

billirubin

115
Q

what happens when bilirubin accumulated in the body?

A

jaundice (because the excess B is stored in fatty tissue in the body)

116
Q

what is bilirubin bound to in blood?

A

serum albumin

117
Q

in the liver bilirubin is conjugated with :

A

glucuronic acid to make it water soluble (then secreted into the bile and passed into intestine)

118
Q

what occurs during the Intestinal phase of bilirubin metabolism?

A

Intestinal bacteria reduce bilirubin to the colorless water soluble derivative urobilinogen that can be converted to stercobilinogen (this was in red)

119
Q

in the gut stercobilinogen is oxidized to what? what des this do?

A

stercobilin, a brown pigment, which is excreted in the feces, producing brown color

120
Q

Most urobilinogen passes through the liver back into the
intestine, but some is taken up by the kidney, what happens then?

A

oxidized to urobilin, a yellow pigment, which is excreted in the
urine, and gives it a yellow color.

121
Q

why are bruises blue?

A

heme being released at the site of injury

122
Q

why after a few days might a bruise turn green?

A

heme converted to biliverdin, causing the bruise to change from blue to green

123
Q

after green color what happens to the bruise?

A

turns yellowish as bilirubin is formed from biliverdin

124
Q

what is hemolytic jaundice?

A

hemolytic anemia, which results in abnormally high rates of
hemoglobin synthesis and degradation

125
Q

what else can cause jaundice?

A

–bile duct obstruction (chalk white feces)
–inadequate conjugation of bilirubin in liver

126
Q

what can occur as a result of deficiency of bilirubin?

A

Hepatitis

127
Q

what is hereditary UDP gucuronyl transferase deficiency?

A

cause UDP glucuronyl transferase levels are normally low at birth, so newborn infants often display jaundice, especially premature infants

128
Q

why is bilirubin toxic to infants?

A

they do not have a blood brain barrier so it can accumulate in fat in brain

129
Q

why is there blue ight in nic-U?

A

it reacts with visible ight to alter structure, Soluble bilirubin photoproducts can be excreted in the urine, thereby getting rid of the bilirubin carbon skeleton

130
Q

Hemoglobin and myoglobin account for about _____of the
body’s iron content

A

70%

131
Q

Iron in cytochromes and other enzymes accounts for about ___ of the total.

A

1%

131
Q

how do we excrete iron?

A

There is no known mechanism for active excretion of iron.
Intracellular free iron concentrations are very low

132
Q

how much iron do we absorb from our diet?

A

Absorption of iron in the intestine is very inefficient. Only about 10 -
15% of dietary inorganic (i.e., non-heme) iron is actually absorbed

132
Q

what is the control point for iron absorption?

A

The control point is transfer of iron from intestinal cells into the
blood binding onto transferrin (meat sources abs better than plant)

132
Q

Ferroportin is controlled by the peptide hormone:

A

hepcidin

133
Q

what effect does hepcidin have?

A

down-regulates ferroportin (causes ferroportin to be taken up via endocytosis and degraded in lysosomes)

134
Q

where is hepcidin secreted?

A

liver

135
Q

what is the level of free iron in blood?

A

10^-18M

136
Q

where is iron stored?

A

Ferrin in liver (free iron is toxic so low levels)

Biochem Final (6 decks)

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