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Cardiopulmonary Exam 1 > Karius Hemostasis > Flashcards

Karius Hemostasis Flashcards

1
Q

Hemostasis

A

the steps taken by the body to limit blood loss, but hemostasis is NOT confined only to the blood clot

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2
Q

Hemostasis four steps

A
  1. vascular spasm
  2. formation of platelet plug
  3. formation of a blood clot
  4. repair of damage
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3
Q

TPO

A

thrombopoietin (TPO)
protein hormone with an amine terminal similar to erythropoietin (EPO) but unique carboxyl terminal
TPO stimulates megakaryocytes to produce platelets

made by liver and kidney

in liver, the parachymal sinusoidal cells
in the kidney, the proximal convoluted tubules
stimulus for its release is uncertain

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4
Q

EPO

A

erythropoietin TPO
produced in liver, stimulates red blood cell production in the bone marrow in response to hypoxia

produced by liver and kidney

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5
Q

Platelet production control

A

they bind thrombopoietin to their mpl receo

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6
Q

mpl receptors

A

found in platelets, megakaryocytes, and other hematopoietic cells

utuilized Jak/Stat and phosphorylation, subsequent transcription and translation of various genes

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7
Q

a high number of platelets indicates

A

lots of TPO bound to the mpl receptors. they internalize signal and destroy it.

not much free to act on megakaryocytes

not much free TPO in the body or to act on megakaryocytes

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8
Q

low number of platelets indicates

A

small amount of TPO bound to platelets; TPO is not being destroyed

there’s LOTS of TPO free in the blood

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9
Q

TPO increases

A

increases differentiation of stem cells and maturation rate/

effects on all cell lines

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10
Q

megakaryoblast –> ______ —> ____

A

megakaryocyte, platelet (thrombocytes)

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11
Q

TPO acts on

A

all cell lines in the body

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12
Q

polycythemia vera

A

mutation in TPO receptor

, platelets unable to internalize and destrou TPO so its actions become continuous

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13
Q

platelet internal mechanisms (7 things)

A

actin and myosin for cell contraction and emptying vesicles
mitochondria for ATP and ADP

remnant of the ER (for calcium storage)
COX1 (prostaglandin production
Cox1 produces thromboxane A2

Fibrin Stabilizing Factor (clot stability)
Platelet derived growth factor (repair)
Serotonin

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14
Q

Platelet membrane becomes ____ when activated. It also contains important ________ and receptors for ______

A

sticky, phosholipids, collagen

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15
Q

If platelet levels drop, what happens to TPO

A

their quantity increases, so they can act

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16
Q

If platelet levels increase, what happen to TPO

A

their quantity decrease, and their destruction marks them off from acting

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17
Q

What cell lines does TPO act on?

A

all cell line

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18
Q

Erythropoiesis vs Thrombopoiesis

What is their respective sources?

A

Ery - kidneys and liver

Thrombo - liver

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19
Q

what triggers EPO and TPO release?

A

EPO: low oxygen
TPO: constitutive (constant)

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20
Q

Control of EPO and TPO hormones, respectively

A

EPO: Hypoxia Inducible Factor (HIF) accumulation in renal cells

TPO: internalization/destruction of TPO

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21
Q

Receptors for EPO and HPO release

A

EPoR and MPL

22
Q

Cells that express receptors for EPO vs HPO

A

EPoR expressed by pluripotent stem cell, RBC precursors

MP: pluripotent stem cells, platelets, all hematopoietic cell lines

23
Q

Erythropoietin’s effect

A

causes daughter cells in Erythroid cell line to undergo mitosis

24
Q

Thrombopoietin’s effect

A

increases division and maturation of all blood cell lineages

25
Q

Hemostasis: step 1

A

MYOGENIC spasm induces vascular occlusion.

occurs spontaneously in response to injury, no neurons or reflexes involved

26
Q

Platelet factors include

A

serotonin and thromboxane A2 contribute to spasm

27
Q

“contributing factors” to the vascular spasm (step 1 of hemostasis)

A

neural reflex from nociceptors (mechanical response)

not sufficient or necessary for spasm to occur, minor contribution

28
Q

Hemostasis Step 2: overview of steps

A

formation of the platelet plug followed by binding of platelets to exposed collagen (two step process)

29
Q

Hemostatic plug formation step 2: platelet activity

A

a. binds to exposed collagen at site of injury using VWF

 1. uses Von Willebrand Factor 
 2. plasma protein 
 3. bind between collagen and platelet receptor

b. platelet integrin receptor binding to collagen

30
Q

during the second phase of a hemostatic plug formation, what do platelets do upon activation?

A
  1. swell and extend podocytes
  2. contraction
  3. granules leave platelet
  4. platelets stick to vessel wall and each other
31
Q

What do thromboxane A2 and ADP do

A

they are released during self aggregation of platelets

32
Q

Hemostasis Step 3: role and steps

A

blood coagulation

  1. formation of prothrombin activator
  2. thrombin activation
  3. conversion of fibrinogen to fibrin

leading to CLOT RETRACTION

33
Q

Hemostasis step 3: Clot Retraction

A

This step gets rid of excess fluid in the clot to solidify it.
Platelets are required (to bind fibrin together, as well as their actin/myosin platelet contractions)
also requires calcium

34
Q

Hemostasis step 4

Repair of damage

A

Repair of damage

Platelet secretion of Platelet derived fibroblast growth factor

stimulates fibroblasts to grow into area

fibroblasts grow into smooth muscle etc to close the hole

35
Q

Getting rid of the clot

A

achieved by plasminogen
floating freely in blood

tPA: tissue plasminogen activator, released by damaged tissues.

tPAi: inhibits tPA, in the blood

36
Q

Thrombomodulin is located on the

A

endothelial cell, and bind thrombin

37
Q

Thrombomodulin activates thrombin on the endothelial cell: what does it activate

A

Protein C, which inactivates tPAi, allowing tPA to activate Plasminogen from zymogen form: Plasminogen —> Plasmin

plasmin lysis fibrin

38
Q

Prevention of Clotting: the role of smooth surfaces

A

prevents platelets from rupturing

39
Q

Prevention of clotting: the role of membrane proteins

A

endothelial cell glycocalyx repels platelets

thrombomodulin activates thrombin

40
Q

Chemicals which limit clotting (4)

A
  1. Fibrin: binds thrombin and prevents it working
  2. Prostacyclin (PG12) made by injured cells, limits platelet aggregation
  3. Antithrombin III: binds and prevents thrombin from working
  4. Heparin: made from mast cells, increases efficacy of antithrombin
41
Q

Protein C

A

Inhibits tPAi AND inactivates the VIIIa–Va complex responsible for activating prothrombin

42
Q

what is the outcome of TPO being internalized by platelets?

A

they are destroyed, so they cant stimulate other hematopoietic cell lines

43
Q

mpl biochemical pathway

A

JAK/STAT

JAK2 activated —> STATs 1, 3, 5 activated (Stat 1/3 dimerize, stat 5 homodimerizes

44
Q

TPO actions on megakaryocytes, platelets, and other hormone interactions

A

causes SIZE and NUMBER of megakaryocytes to increase

causes platelet specific markers to develop

stimulates endomitosis and polyploidy of megakaryocytes

works with erythropoietin to stimulate RBC production
works with IL-3, or Steel Factor to upregulate RBC and WBC factors to differentiate

45
Q

Platelets: actin and myosin?

A

just like in skeletal muscle, they have cross bridges that undergo cycling causing contraction of the cell

they help SQUEEZE extra fluid out of clot

help empty vesicles

46
Q

Cyclooxygenase (COX 1)

A

enzyme that catalyzes production of thromboxane A2. prostaglandins

47
Q

Fibrin Stabilizing Factor

A

XIII, causes covalent bonds to form between fibrin monomers

48
Q

platelet derived growth factor

A

aids in repair of damaged tissue

49
Q

what does Thromboxane do exactly?

A

binds to GPCR on smooth muscle and triggering calcium release

causes an increase in IP3

causes release of calcium from intracellular stores of the smooth muscle cell

50
Q

how is the platelet held in place during clot formation?

A

two points of contact: von willebrand factor between collagen and platelet, and integrins on the platelets interacting with the collagen

Cardiopulmonary Exam 1 (21 decks)

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