Physio Flashcards
(324 cards)
1
Q
Blood is a type of ….. tissue
A
connective
2
Q
Blood anatomy
A
cells suspended in a liquid extracellular matrix (plasma)
3
Q
Blood volume is typically about ..% of body weight
A
8
4
Q
Centrifuges blood sample consists of
A
55% plasma
45% rbc (hematocrits)
Less than 1% buffy coat (platlets and wbc)
5
Q
Volume of blood in body male vs female
A
Female: 4-5 L
Male: 5-6 L
6
Q
Ph of blood
A
7.35-7.45
7
Q
Temp of blood
A
38 C
100.4 F
8
Q
A person who weighs 70 kg has approximately .. L of blood with about .. L of cellular elements and .. L of plasma.
A
5
2
3
9
Q
Plasma consists of
A
92% water
7% Plasma protiens
1% other solutes
10
Q
Plasma proteins
A
60% albumins
35% gloubins
4% fibrogen
Less than 1% regulatory protiens
11
Q
What are the other solues in plasma
A
Organic nutrients
Organic wastes (urea, bilirubin)
Electrolytes (NA+, K+, CL-)
12
Q
How does plasma differ from intercellular proteins
A
Plasma has protiens
13
Q
Hemoglobin range male vs female
A
Female: 12-16 g/dL
Male: 13-18 g/dL
14
Q
Mean RBC count
A
Female: 4.2-5.4 million
Male: 4.6-6.2 million
(per microliter)
15
Q
WBC count
A
5k -10k
16
Q
Platlet count
A
130,000-400,000/L
17
Q
All plasma protiens are made in ….. except immunoglobins are made in …..
A
Liver
Lymphoid tissue
18
Q
Plasma contains
A
.Protien .(Calcium Potassium Sodium Chloride, Bicarbinate) .glucose .urea .arteria ph, PO2, PCO2
19
Q
Blood ratios
A
RBC 95.1%
Platlet 4.8%
Wbc 0.1%
20
Q
Wbc ratios
A
Neutrophil: 54-62% Lymphoctes: 25-33% Monocytes: 3-9% Eosiophils: 1-3% Basophils: less than 1%
21
Q
The formation of blood cells is called…. and occurs in …..
A
hematopoiesis
Bine marrow
22
Q
Active bone marrowin neonates vs adults
A
Neonates: most of the skeleton
Adults: vertebrae, ribs, skull, pelvis, and the proximal femurs.
23
Q
Blood cells are derived from …….
A
stem cells in the bone marrow
24
Q
The production of red blood cells is called
A
Erythropoiesis
25
The production of red blood cells is regulated to provide ...
adequate O2- carrying capacity in blood.
26
primary regulator of erythropoiesis
erythropoletin (EPO)
27
erythropoletin is released from ..... when ...
the kidney when O2 tension in the renal parenchyma is reduced.
28
How do Committed erythroid stem cells in the bone marrow respond to EPO
with increased rates of cell division and differentiation into mature red cells.
29
Mecanism of erythropiosis
Low O2 in Kidney
Kidney secrete EPO
EPO goes to bone marrow & stimulates erythropiosis
More erythrocytes means more oxgen
More O2 relievs the stimulus that triggered erythropoietin secretetion
30
Factors that decrease oxygenation
1. Low blood volume
2. Anemia
3. Low hemoglobin
4. Poor blood flow
5. Pulmonary disease
31
Maturation of RBC requires
1. iron
| 2. essential nutrients folic acid and vitamin B12
32
Why is iron needed for maturation of rbc
for the production of the hemoglobin (O2-carrying pigment)
33
Stem cell differentiation into mature red cells involves
1. decrease in cell size,
2. production of hemoglobin
3. eventual disappearance of cell organelles.
34
In the final stage of differentiation, immature red cells are called
reticulocytes
35
reticulocytes are characterized by
the presence of organelle remnants.
36
There is normally ...% of circulating red blood cells in the immature reticulocyte stage
less than 1
37
Larger numbers of reticulocytes happens when
Theres a rapid decrease in the demand for rbc eg: after acute hemorrhage
38
..... is an index of the rate of red blood cell production.
reticulocyte count
39
small disk-shaped cell fragments without a nucleus
Platelets
40
Why do platlets need an extensive cytoskeleton
Because the shape of a platelet changes upon activation
41
How do platlets help with hemoatasis
Because platlets contain secretory granules containing factors that regulate hemoatasis
42
How does Platelet production occur in the bone marrow
by the cytoplasmic fragmentation of megakaryocytes
43
..... are the largest cells in the bone marrow
Megakaryocytes
44
How are Megakaryocytes formed
They are formed when committed progenitor cells undergo repeated nuclear division without cell division.
45
The rate of platelet formation is regulated by the cytokine.....
thrombopoietin
| TPO
46
TPO is constitutively secreted by
liver and kidneys
47
Plateletes regulate TPO levels by
removing it from the circulation
48
Functions of Blood
Transport
Protection
Regulation
49
Transport
carries oxygen from the lungs to all of the body’s tissues, while it picks up carbon dioxide from those tissues and carries it to the lungs to be removed from the body
picks up nutrients from the digestive tract and distributes them to all tissues
carries metabolic wastes to the kidneys for removal
carries hormones from endocrine cells to their target cells
transports stem cells to their destinations
50
Protection
White blood cells destroy harmful microorganisms and cancer cells
Antibodies and other blood proteins neutralize toxins and help to destroy pathogens
Blood plays several roles in inflammation, a mechanism for limiting the spread of infection and promoting the repair of injured tissue
Platelets and other blood-borne agents initiate blood clotting and other processes for minimizing blood loss
51
Regulation
helps maintain optimal fluid balance and distribution in the body by absorbing or giving off fluid under different conditions
Blood proteins stabilize the pH of extracellular fluids by buffering acids and bases
Shifts in blood flow help to regulate body temperature by routing blood to the skin for heat loss or routing it deeper to retain heat in the body
52
Platelet production is called
Thrombopoiesis
53
WBC ratios
```
Neutrophils: 50-70%
Lymphocytes: 20-40%
Monocytes: 1-5%
Eosiophils: 5%
Basophils: 0.5%
```
54
What type of WBC have B and T cells and generates specific immune resonses
Lymphocytes
55
What type of WBCs specialize in parasitic infestation
Eosiophils
56
What WBC is dominant in early stages and digests microorganism
Neutrophils
57
Is responsible for degranlation and becomes mast cells
Basophils
58
Key part of cell mediated immune response, calls macrophages
Monocytes
59
Mature erythrocytes shape and size
disk-shaped anucleate cells, approximately 7-8 μm in diameter.
60
Why are RBC flexible with an extensive cytoskeleton
so that they can pass through the microcirculation.
61
Rbc are able to withstand large osmotic pressure differences, which are encountered when
they pass through the renal circulation
62
Key cytoplasmic proteins in erythrocytes include:
The O2-carrying pigment hemoglobin
Glycolytic enzymes
Carbonic anhydrase
63
Which enzyme turns H2O + CO2 to H2CO3
Carbonic anhydrase
64
Red Cell Membrane is made up of three major structural elements:
Lipid bilayer,
integral proteins
membrane skeleton
65
Lipid Bilayer is primarily composed of
phospholipid and cholesterol
66
Lipid Bilayer provides an impermeable barrier between
cytoplasm and external
| environment
67
Why does the lipid bilayer maintain a slippery exterior
so that the red cells do not stick to the vascular endothelium.
68
Integral Proteins are embedded in
the lipid bilayer
69
The important membrane proteins are:
band-3 protein (anion exchanger-1),
the glycophorins,
Rh D protein and
Various ion channels .
70
Protiens in cell membrane function
antigenic determination and cellular metabolism.
71
Band-3 functionn
major anion-exchanger (chloride-bicarbonate exchange)
| regulates metabolic pathways
72
How does the protien band 3 regulate metabolic pathways
by sequestering key enzymes like enzymes of glycolytic pathways.
73
What produces glycotic enzymes
Band 3
74
Glycophorins constitute more than....% of negative surface charge of red cells
60
75
There are five different types of glycophorins:
A, B, C, D and E.
76
Which Glycophorin provides stability and shape to the red cell membrane
C
77
Glycophorin-C deficincy causes
elliptocytosis
78
....... is the most abundant skeletal protein in the membrane skeleton
Spectrin
| 75% of membrane skeleton mass
79
Spectrin is composed of
Subunits α and β
80
Subunits α and β structure
Flexible Rod shaped
81
Spectrin function
maintains cellular shape,
provide structural support to membrane lipid bilayer
regulate lateral mobility of integral membrane proteins.
82
defect in association of αβ heterodimers results in
hereditary elliptocytosis and poikilocytosis.
83
Ankyrin
is an asymmetric membrane skeleton polar protein
84
Ankyrin function
provides primary linkage between membrane skeleton and lipid bilayer.
85
most common causes of hereditary spherocytosis
Abnormalities of ankyrin
86
adequate synthesis of proteins and lipids does not occur in red cells, why
Because Red cells have no nuclei, mitochondria and ribosomes.
87
.... is the primary fuel for red cells.
Glucose
88
In RBS enzymes for .... are present but enzymes for ..... are absent
glycolysis
| TCA cycle
89
ATP is formed by ,,,, The HMP shunt provides....
Embden-Mayerhoff pathway (EM pathway)
NADPH
90
Glucose entry into the red cells occurs by
Facilated diffusion
91
Facilitated diffusion of glucose entry is independent of
Insulin action
92
Red cells depend mostly on.... for their energy supply
glucose metabolism
93
90% of glucose is oxidized by ... while 10% is oxidized by
EM pathway
| HMP shunt
94
The tendency of the cells to hemolyze (break down) is called
Fragility
95
On average, a red cell passes about .....times though capillaries during its life span
300,000
96
when red cells become older, the membrane becomes
rigid
97
Lysis of red cells on exposure to different osmotic solutions is called
osmotic fragility
98
ease with which the red cells are ruptured when they are exposed to hypotonic solutions.
Osmotic fragility
99
Hemoglobin is a protein with a molecular weight of
64,450
100
Hemoglobin is a .... protien made up of ... subunits
Globular
| 4
101
Each subunit of hemoglobin contains
a heme moiety conjugated to a polypeptide.
102
porphyrin ring complex that includes one atom of ferrous iron.
Heme
103
the globin portion of the hemoglobin molecule.
polypeptides
104
How many pairs of poly peptides are inneach hemoglobin
2 pairs
105
The synthesis of hemoglobin begins in
polychromatophil erythroblasts
106
normal adult human hemoglobin is called
hemoglobin A
107
The 2 poly peptides in hemoglobin A are called
α chains, and β chains.
108
In hemoglobin A2, β chains are replaced by
δ chains
109
hemoglobin A2 is about .... % of hemoglobin
2.5%
110
The δ chains contain
10 individual amino acid residues that differ from those in β chains.
111
hemoglobin A1c (HbA 1c )
A derivatives closely associated with hemoglobin A that represent glycated hemoglobins.
has a glucose attached to the terminal valine in each β chain.
112
The blood of the human fetus normally contains what type of hemoglobin
Hemoglobin F (fetal hemoglobin)
113
How is hemoglobin f diffrent from hemoglobin a
except that the β chains are replaced by γ chains
114
The γ chains have....
| that differ from those in the β chain.
37 amino acid residues
115
Types of normal Hb (hemoglobin)
```
Hb A (98%) alph & beta
Hb A2 (2%) alpha and delta
Hb F (for baby) alpha and y
```
116
In young embryos there are, in addition ..... chains that form .......
ζ and ε chains
| Gower 1 hemoglobin and Gower 2 hemoglobin.
117
Switching from one form of hemoglobin to another during development seems to be regulated largely by
oxygen availability
118
relative hypoxia (o2 deficincy) favors the production of ..... and how
hemoglobin F
via direct effects on globin gene expression
up-regulated production of erythropoietin.
119
O2 binds to the Fe2+ in the heme moiety of hemoglobin to form
oxyhemoglobin
120
Hemoglobin
Heme: iron ring
Globin: poly peptide like alpha beta
121
The affinity of hemoglobin for O2 is affected by
pH,
temperature,
concentration in the red cells of 2,3-bisphosphoglycerate (2,3-BPG)
quaternary structure of hemoglobin
122
2,3-BPG and H+ compete with O2 for binding to deoxygenated hemoglobin, decreasing
the affinity of hemoglobin for O2
123
Each of the four iron atoms in hemoglobin can reversibly bind
one O2 molecule.
124
The iron stays in the ... state, so that the reaction is oxygenation (not oxidation).
ferrous
125
Oxygenated hemoglobin
Hb4O8
126
Oxygenation of Hb time
less than 0.01 s
127
In deoxyhemoglobin, the globin units are....
tightly bound in a tense (T) configuration,
128
What does the globin units being tightly bound in a tense (T) configuration in deoxyhemoglobin cause
reduces the affinity of the molecule for O2
129
When O2 is first bound to deoxyhemoglobin
the bonds holding the globin units are released, producing a relaxed (R) configuration, which exposes more O2 binding sites.
130
After one oxygen binds to Hb the affininty is increased by
500 fold
131
The transition from one state to another has been calculated to occur .....times in the life of a red blood cell
10^8
132
Binding of CO2 with Hb leads to formation of
carbaminohemoglobin
133
CO2 combines with
Globin
134
When blood is exposed to various drugs and other oxidizing agents in vitro or in vivo, the ferrous iron (Fe2+ ) that is normally present in hemoglobin is converted to ... which forms
Ferric iron
| Methemeoglobin
135
Methemoglobin is dark-colored, and when it is present in large quantities in the circulation, it causes
dusky discoloration of the skin resembling cyanosis.
136
Some oxidation of hemoglobin to methemoglobin occurs normally, but an enzyme system in the red cells, ..... converts methemoglobin back to hemoglobin.
the dihydronicotinamide adenine dinucleotid (NADH)-methemoglobin reductase system
137
Congenital absence of dihydronicotinamide adenine dinucleotid (NADH)-methemoglobin reductase system causes
hereditary methemoglobinemia.
138
Carbon monoxide reacts with hemoglobin to form
carbon
| monoxyhemoglobin (carboxyhemoglobin).
139
The affinity of hemoglobin for O2 is ....than its affinity for carbon monoxide,
much lower
140
formed on exposure to some toxic agents, usually sulfur-containing drugs and chemicals.
Sulfhemoglobin
141
In sulfhemoglobin, the iron is in .. state, but oxygen affinity is about ... than the normal Hb.
ferrous
100 times lower
142
Sulfer attaches to
porphyrin ring.
143
Once sulfhemoglobin is formed, it is
Irreversible
144
The factors controlling erythropoiesis can broadly be divided into three categories:
Hormonal
Dietary
Others
145
Total iron in body
4-5 g
146
Transferrin
Transfers iron
147
Intracellular iron storage protien
Ferritin
148
Ferririn not bound to iron
apoferritin
149
The normal lifespan of a RBC in the circulation is approximately
100-120 days
150
decreased red cell mass
Anemia
151
increased red cell mass
polycythemia
152
After red cells live their normal life, they become less active and more rigid, and get trapped by cells of
reticuloendothelial system, especially by the macrophages in the liver and spleen.
153
macrophages engulf red cells by phagocytosis and release
Hemoglobin
154
In Intravascular Destruction ; Red cells are destroyed in the circulation, when
their cell membrane is breached.
155
Intravascular Destruction of red cells in circulation releases Hb into ... which then binds with ......
Plasma
| Haptoglobin
156
In intravscular destrucction The Hb-haptoglobin complex is transported to ...., where .....
liver
the heme of Hb is converted to iron and biliverdin by heme oxygenase.
157
... is released during cleavage of heme by heme oxygenase.
CO
158
Biliverdin is further degraded to
Bilirubin
159
Heme in the plasma binds with
hemopexin, a plasma glycoprotein.
160
When the capacity of hemopexin to bind with heme is saturated, heme binds with ... to form .....
albumin
methemalbumin
161
Causes of Extravascular Destruction
Decreased Deformability
| Alteration in Surface Properties
162
Decreased Deformability types and examples
change in shape: spherocytosis or elliptocytosis
| increased internal viscosity: sickle cell or Hb-C disease
163
Alteration in Surface Properties
Binding of antibodies or complement components to the surface of red cells, changes the chemical composition of the membrane.
164
binding of IgG or C3 causes
oxidation of membrane components.
165
Causes of intravascular destruction
The membrane of older red cells becomes rigid and becomes susceptible to rupture during circulation inside the blood vessel.
166
In extravascular destruction In the phagocytic cells, red cells are degraded by ... into ....
lysosomes
lipids, protein and heme.
167
In extracellular destruction heme is ...... and protein and lipids are ....
catabolized to bilirubin,
reprocessed in their catabolic pathways.
168
Bilirubin formed from destruction of red cells regardless of their site of destruction is finally excreted through.... into ...
bile into the GI tract.
169
In the intestine, bilirubin is converted to
urobilinogen by bacterial reduction.
170
Urobilinogen is further converted to....&..... that are ...
stercobilinogen and stercobilin
| excreted in stool.
171
A small fraction of urobilinogen is absorbed from intestine and excreted through
urine as urinary urobilinogen.
172
The size of the total red cell mass is described by three variables:
Hemoglobin concentration (Hb)
Hematocrit (Hct) or packed cell volume (PCV)
Red cell count (RBC)
173
Hemoglobin concentration (Hb)
is the amount of hemoglobin in a volume of blood.
174
Hematocrit (Hct) or packed cell volume (PCV)
is the ratio of the volume of red cells to the volume of whole blood.
175
Red cell count (RBC)
the number of red cells per liter of blood.
176
mean cell volüme (MCV)
Describes average size of an rbc
| average volume of a single red cell expressed in femtoliters (fL = 10 ^15 L)
177
MCV is calculated by
dividing the hematocrit by RBC.
178
MCV
80 fL
179
MCV >... indicates that red cells are large (macrocytosis).
100 fL
180
Two derived variables describe the adequacy (capability) of hemoglobin synthesis:
Mean cell hemoglobin (MCH)
| Mean cell hemoglobin concentration (MCHC)
181
MCH
average amount of hemoglobin in the average red cell, expressed in picograms (pg = 10^12 g).
Calculated by dividing hb (hemoglobin concentration) by rbc
182
Mean cell hemoglobin concentration (MCHC)
average concentration of hemoglobin in red cells, calculated by dividing MCH by MCV.
183
Low MHC and MCHC cause
pale hypochromic cells.
184
High MHC and MCHC result in
intensely colored hyperchromic cells.
185
Red cells have the property of rouleaux formation which is
piling one on the other
186
The rate at which the red cells fall (sediment), is known as the
erythrocyte sedimentation rate (ESR).
187
ESR depends on 3 major factors:
the plasma’s protein composition,
the erythrocytes’ size and shape,
the erythrocyte concentration.
188
How does the plasma’s protein composition affect esr
Increasing levels of plasma proteins primarily acute phase reactants result in a decrease of the zeta potential (the overall negative charge of the membrane) surrounding the erythrocytes. (They all negative so they donta attract takes longer to calm them down)
189
Macrocytes settle ... than normal erythrocytes, and microcytes settle ...
faster
| Slower
190
poikilocytes are unable to form rouleaux and settle at a slower rate. Why
Because of their irregular shape,
191
The erythrocyte concentration directly affects the ESR, how?
higher the erythrocyte concentration, the lower the ESR
192
Anemic person has (high/ low) ESR
High
193
Why are antigens called agglutinogens
because they often cause RBC agglutination
194
The A and B antigens are
complex oligosaccharides that differ in their terminal sugar.
195
An H gene
codes for a fucose transferase that adds terminal fucose, forming the H antigen that is usually present in individuals of all blood types.
196
type A
Have a second transferase that catalyzes placement of a terminal N-acetylgalactosamine on the H antigen
197
Type b
express a transferase that places a terminal galactose on the H antigen.
198
type O
Just H antigen
199
Antibodies against red cell
| agglutinogens are called
agglutinins
200
Agglutinins are ...
agglutinogens are ..
Antibodies
| Antigens
201
Antigen vs antibody
Antigen is the bad guy (its antibody generator so it walks into a cell and antobodies are created to kill it)
202
Rh has 6 types of antigens which are ..
| Each person has how many?
C D E c d e
| 3
203
The type.. antigen is widely prevalent in the population and is considerably more antigenic than the other Rh antigens.
D
204
If you have antigen D that mean you are
Rh positive
205
Platelets (also called thrombocytes) are minute discs .... micrometers in diameter.
1 to 4
206
Platelets are formes in ... from ..
Bone marrow
| Megakaryocytes
207
Platelets have the half-life of about
4 days
208
Platlets survive in circulation for about
8-12 days
209
The aged platelets are removed from circulation by
reticuloendothelial systems.
210
.... plays an important role in destruction of platelets.
Spleen
211
Thrombocytopenia
platelet count less than 150.000 /mm3 of blood.
212
significant bleeding occurs when platelet count decreases below
50,000/mm3 of blood.
213
platelet count below 50,000/mm3 of blood is called
critical count.
214
Bleeding that results from defective platelet function typically occura superficially in sites such as
skin (e.g., petechiae and ecchymosis)
| mucous membranes.
215
Deep bleading in muscles cause... and deep bleeding in joints cause...
Hematoma
| Hemarthrosis
216
Platelets contribute to blood coagulation by
releasing platelet factor 4, and synthesizing clotting factors V and XI.
217
Platelets promote vasoconstriction by
producing serotonin that helps in hemostasis.
218
Platelets prevent bleeding by
forming plugs at the
| site of injury (temporary hemostatic plug).
219
Platelets promote clot retraction, which is essential for
stabilization of clot.
220
How do platlets help with thrombolysis (breakdown of blood clots)
Platelet controls fibrinolysis.( breakdown of febrin)
221
Functions of Platelets
```
Temporary hemostasis
vasoconstriction
Blood coagulation
Clot retraction
Thrombolysis
Phagocytosis
Storage and transport
Vascular growth
```
222
Platelets help in growth of vascular endothelium by
secreting platelet-derived growth factor (PDGF).
223
PDGF is also produced by
macrophages and endothelial cells.
224
Platelets
small, anucleate cell fragments adapted to participate in hemostasis that adhere to damaged blood vessels and aggregate with each other.
225
Platlets have ..... systems, when activated, they change their shape due to change in activity of membrane structure and cytoskeleton. This helps in release of .....
canalicular (canals)
| chemicals from its granules.
226
Platlets contain extensive microtubules and microfilaments and numerous granules. Frequently, they change their shape with very long and thin processes extending out from their body called
Filopodia
227
Cell membrane in platlets is covered by
exterior glycocalix coat that consists of:
glycoproteins including glycoprotein receptors, glycolipids,
mucopolysaccharides.
228
Platelets have negative charge on their surface due to presence of
sialic acid residues attached to the exterior coat.
229
Why do platlets have negative charges
To prevent the resting platelets to attach to each other or to the negatively charged endothelial cells.
230
cell membrane of membrans
trilaminar unit consisting of a bilayer of phospholipids in which cholesterol, glycolipids, and glycoproteins are embedded.
231
Glycoproteins function in membrane
to prevent adherence of platelets to the normal vascular endothelium.
232
glycoprotein receptors function
help in adhesion and aggregation of platelets.
233
Platelets have receptors on their cell membrane for
collagen,
ADP,
von Willebrand factor (vWF),
fibrinogen.
234
Important platelet membrane glycoproteins
Gp Ib-IX-V
Gp IIb/III
Gp Ia-IIa
235
Gp Ib-IX-V
active receptor that mediates vWF dependent adhesion of platelets to subendothelial collagen.
236
Gp IIb/IIIa
Binds to fibrinogen and thus mediates aggregation. Also, this is the receptor for vWF, fibronectin, and thrombospondin.
237
Gp Ia-IIa:
active receptor for collagen and mediates platelet adhesion independent of vWF.
238
Activation of platelet leads to
discharge of content of granules that facilitate the process of hemostasis.
239
The granules of platelets are of two types:
the alpha granules and dense granules.
240
About.... alpha granules are present per platelet.
50–80
241
Alpha granules .... nm in diameter
200
242
There are about ...dense granules per platelet.
3–8
243
Dense granules have diameter of about ....nm.
20–30
244
Dense granules contain chemicals like
serotonin, ADP, calcium, ATP, etc.
245
Properties of Platelets
adhesion,
aggregation, and
activation and release.
246
Platelets easily adhere to the damaged vascular endothelium. This is called
platelet adhesion.
247
Platelets have the tendency to stick to .... of the injured vessel wall.
the exposed collagen
248
Adhesion is facilitated by
von Willebrand factor.
249
von Willebrand factor mediates adhesion of platelets to ... via ....
subendothelium
GpIb on the surface of platelets.
250
The property of platelets to stick to each other is called
platelet aggregation.
251
.... mainly promote aggregation of platelet to each other.
Fibrinogen and GpIIb-IIIa
As well as
thrombin, ADP and PAF
252
Platelets are activated when they bind to
collagen or to each other.
253
Activation of platlets is facilitated by
Thrombin and adp
254
Shape change of platlets when activated and why
they become more spherical and form pseudopodia. due to recognition of microtubules and contraction of actomysin of microfilaments.
255
When activated platlets change tgeir shape they
discharge their granular contents.
256
Seretonin is activated by ... and activates ...
Platlet activation
| Platlet aggregation
257
Vwf is activated by
| Functions
Exposure to collagen
Links platlet to collagen
258
Collagen binds... to ...
Platlets
| Begin platlet plug
259
excessive activation of hemostatic mechanisms can cause
thrombosis and embolism (blood vessel occlusion).
260
Three physiologic mechanisms interact to prevent hemorrhage:
1. Vasoconstriction of small vessels reduces blood flow and increases the likelihood of vessel closure.
2. Platelet plug formation occurs at the site of damage in capillaries, arterioles, and venules.
3. Clot formation (coagulation) occurs in which a fibrin mesh forms together with platelets and other trapped blood cells.
261
Vasoconstriction happens because platlets release
vasoconstrictors serotonin and thromboxane A2.
262
The clotting protein thrombin stimulates endothelial cells to secrete the potent vasoconstrictor.... to help with vasoconstriction
endothelin-1.
263
Platelet plug formation occurs at
site of damage in capillaries, arterioles, and venules.
264
primary hemostasis
Plug formation
265
Primaer hemostasis 3 overlapping phases
platelet adhesion, activation, and aggregation.
266
secondary hemostasis
Clot formation
267
Adhesion is mediated by a variety of different platelet receptors, including:
von Willebrand factor
| Receptors of the integrin family
268
vWF is a glycoprotein present in ... and is released by... and by .....
plasma
Endothelial cells
activated platelets.
269
vWF is carrier molecule for
procoagulant factor VIII in plasma
270
Receptors of the integrin family help platlet adhesion by binding
platelets directly to extracellular matrix proteins (e.g., collagen).
271
Other platelet receptors that promote platelet adhesion and activation include ligands associated with
```
platelet activation (e.g. thromboxane)
blood coagulation (e.g., thrombin).
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272
Thromboxane is associated with
| Thrombin is associated with
Platelet activation
| Blood coagulation
273
Platelet activation involves exocytosis of the contents of platelet granules and morphologic changes from a smooth membrane surface to
one with finger-like cytoplasmic projections that increase adhesion and aggregation with other platelets.
274
Activated platelets release many factors that promote hemostasis, including:
```
Adenosine diphosphate (ADP)
Serotonin and thromboxane A2
vWF
Ca+2 and the clotting factors fibrinogen and factor V
Platelet-derived growth factor
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275
Platelet-derived growth factor function
promote wound healing.
276
Ca+2 and the clotting factors fibrinogen and factor V function
facilitate
| coagulation.
277
Serotonin and thromboxane A2- assist in hemostasis as
Vasoconstrictors
278
Adp function
amplify the platelet activation response.
279
The platelet plug is prevented from extending beyond the site of injury by
prostacyclin and nitric oxide
280
prostacyclin and nitric oxide are secreted from .... and inhibit ...
intact endothelial cells
platelet activation.
281
Blood coagulation and blood clot formation
the plasma protein fibrinogen is proteolytically cleaved to produce fibrin, which subsequently becomes cross-linked into a stable mesh.
282
In the classic description of coagulation, clotting may be initiated by one of two pathways:
intrinsic pathway or the extrinsic pathway.
283
cascade of reactions in coagulations
inactive circulating precursor proteins (‘clotting factors') become activated, in most cases by proteolytic cleavage.
284
These chain reactions normally are not activated in the circulation because
clotting factors are present at low concentration in plasma.
285
The intrinsic pathway is triggered when
blood contacts a negatively charged surface (e.g., exposed subendothelial collagen; aggregations of platelets).
286
The extrinsic pathway is activated when
blood contacts cells outside the vascular endothelium:
287
Nonvascular cells express a membrane protein called.... exposure to it activates... which trggers .....
tissue factor .
factor VII
Final fommon pathway
288
The intrinsic and extrinsic pathways converge at the common pathway for
coagulation, which begins with the activation of
factor X.
289
Factor .. is a key cofactor needed for activation of factor X.
V
290
The plasma protein prothrombin (factor II) is cleaved by... to produce ...
activated factor X to produce the protease thrombin.
291
Thrombin is produced when
Factor x cleaves factor ll
292
Thrombin function
cleaves fibrinogen (factor I) and activates factor XIII, which cross-links fibrin into a stable mesh
293
most important pathway for initiating thrombin activation;
The extrinsic pathway
294
.... pathway is more important for maintaining thrombin in generation.
Intenstric
295
Activated factor IX of the intrinsic pathway activates factor ... of the extrinsic pathway.
VII
296
complex formed from tissue factor, activated factor VII, and Ca+2 in the extrinsic pathway activates factors .... ..... of the intrinsic pathway.
IX and XI
297
Thrombin plays a central role in the coordination of the clotting cascades because
stimulates formation of a fibrin clot
| it mediates positive feedback stimulation upstream in the intrinsic and extrinsic pathways.
298
Vwf regulates level of factor
Vlll
299
Several clotting indicate teste are uesd to assess the function of primary and secondary hemostatic mechanisms, including
The bleeding time
The prothrombin time (PT)
The partial thromboplastin time (PTT
300
Diffrence between The prothrombin time (PT)
| The partial thromboplastin time (PTT
PT: extrensic pathway
PPT: intrensic pathway
301
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hemophilia A (classic hemophilia)
hemophilia B (Christmas disease) are ..... linked recessive disorders
```
X-linked
302
hemophilia A (classic hemophilia) results in the deficincy of
clotting factors VIII
303
hemophilia B (Christmas disease) results in the deficincy of
Factor IX
304
An increase in PTT is expected in hemophilia A and B because
Both factors Vlll and lX are a aprt of intistric pathways
305
Clotting factors II, VII, IX and X (and the anticoagulant proteins C and S) are produced in
And rely on
liver
rely upon a vitamin K dependent enzymatic reaction, γ-carboxylation of a glutamyl residue.
306
Liver produces
factors II, VII, IX and X (and the anticoagulant proteins C and S)
307
The .... is the main source of anticoagulant factors.
capillary endothelium
308
Anticoagulation factors
```
Tissue factor pathway inhibitor (TFPI)
Antithrombin III
Heparin
Thrombomodulin
Protein C and S
```
309
Tissue factor pathway inhibitor (TFPI)
anchored to the endothelial cell membrane and blocks the action of activated factor VIl in the extrinsic pathway.
310
Antithrombin III
inhibits coagulation by binding to activated factor X and thrombin
311
Heparin
released endogenously from mast cells and basophils and is widely used as an anticoagulant drug.
functions by increasing the anticoagulant effects of antithrombin III.
312
Thrombomodulin inhibits coagulation by
binding to thrombin.
313
Protein C and S act together to
inactivate activated factors V and VIll.
314
Why does fibrinolysis begins soon after a clot is formed
plasma protein plasminogen is among the serum proteins that are adsorbed into the clot at the time of its formation.
After Plamminogem gets cleaveged it produces protease plasmin witch breaksdown fibrin and fibrinogen
315
The cleavage of plasminogen produces ...
the protease plasmin
316
the protease plasmin function
breaks down fibrin and fibrinogen
317
breakdown products of the fibrin mesh are scavenged by
macrophages
318
The activation of plasminogen is mainly regulated by two factors, which are released from capillary endothelial cells
tissue plasminogen activator (tPA) and urokinase.
319
a fibrin breakdown product not normally present in blood.
D-dimer
320
Levels of D dimer are increased in
thromboembolic diseases such as deep vein thrombosis, pulmonary embolism, and disseminated intravascular coagulation;
321
absence of D-dimer helps to rule out
Thrombosis
322
If plasmin escapes from the clot, it is rapidly bound and inactivated by the
circulating plasma protein α-antiplasmin.
323
fibrinolytic agents (thrombolytics or clot busters) are used in some patients suffering from
acute clotting emergencies such as stroke, coronary thrombosis, pulmonary embolism, or deep vein trombosis
324
Fibrinolytic drugs example
tPA, urokinase, streptokinase
