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Applied Biochemistry > Blood Coagulation and Wound Healing Part 2 > Flashcards

Blood Coagulation and Wound Healing Part 2 Flashcards

1
Q

wound healing

A

complex process in which skin or other tissue repairs itself after injury

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2
Q

the classic model of wound healing can be divided into four sequential overlapping phases:

A

hemostasis
inflammatory
proliferative
remodeling

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3
Q

hemostasis occurs within

A

minutes after injury

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4
Q

hemostasis

A

platelets aggregate at the injury site to form a fibrin clot, which acts to control bleeding

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5
Q

inflammatory phase

A

bacteria and debris are phagocystosed and removed from the wound site. factors are released that cause migration and division of cells involved in the proliferative phase

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6
Q

proliferative phase

A

angiogenesis, collagen deposition, granulation, tissue formation, epithelialization, and wound contraction

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7
Q

remodeling phase

A

collagen is remodeled and realigned along tension force lines and cells no longer needed are removed by apoptosis

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8
Q

what is present during hemostasis? (4)

A

clot
platelet
RBC
scab

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9
Q

what is present during inflammation? (2)

A

macrophage

neutrophil

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10
Q

what is present during proliferation phase? (3)

A

granulation tissue
fibroblast
myofibroblast

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11
Q

remodeling phase

A

collagen fiber

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12
Q

what are some examples of diseases which interfere with wound healing progression? (4)

A

diabetes
venous or arterial disease
old age
infection

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13
Q

how are growth factors regulated? (2)

A

specially

temporally

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14
Q

ACD

A

acid citrate dextrose solution

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15
Q

what is ACD anticoagulant?

A

a solution of citric acid, sodium citrate, and dextrose in water

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16
Q

how does citrate work as an anticoagulant?

A

citrate and EDTA. citrate, in the form of sodium citrate or acid-citrate-dextrose is used to disrupt the coagulation cascade and prevent clotting. these citrate compounds bind to the calcium in the blood. by reducing the amount of calcium, there will be no regulation of the binding and the cascade cannot begin

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17
Q

prothrombin time (PT)

A

a test used to help detect and diagnose a bleeding disorder or excessive clotting disorder

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18
Q

the international normalized ratio (INR) is calculated from a

A

PT result

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19
Q

what is the INR used for

A

to monitor how well the blood-thinning medication (anticoagulant) warfarin (Coumadin) is working to prevent blood coagulation

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20
Q

prothrombin time is a measure of the integrity of

A

the extrinsic and final common pathways of the coagulation cascade

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21
Q

the extrinsic and final common pathways of the coagulation cascade consists of tissue factor and factors (5)

A 
VII
II (prothrombin)
V
X
fibrinogen
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22
Q

PT is usually measured in

A

seconds

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23
Q

PT is compared to a

A

normal range that reflects PT values in healthy individuals

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24
Q

Because the reagents used to perform the PT test vary from one laboratory to another and even within the same laboratory over time, the normal ranges also

A

will fluctuate

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25
Q

To standardize results across different laboratories in the U.S. and the world, a World Health Organization (WHO) committee developed and recommended the use of the

A

Internationalized Normalized Ratio (INR)

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26
Q

INR ratio allows for

A

easier comparisons of test results from different laboratories

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27
Q

when is INR used?

A

if you take blood-thinning medications

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28
Q

normal INR in healthy people

A

1.1

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29
Q

effective therapeutic INR range for people taking warfarin for disorders such as atrial fibrillation or a blood clot in the leg or lung

A

2-3

30
Q

in certain situations, such as having a mechanical heart valve, you might need a

A

slightly higher INR

31
Q

When the INR is higher than the recommended range, it means that

A

your blood clots more slowly than desired

32
Q

a lower INR means

A

your blood clots more quickly than desired

33
Q

drugs that prevent blood coagulation (blood thinners) (5)

A 
Warfarin 
Pradaxa
Xareltod
Eliquise
Plavix
34
Q

What does warfarin competitively inhibit?

A

the vitamin K epoxide reductase complex 1 (VKORC1)

35
Q

vitamin K epoxide reductase complex 1 (VKORC1) is an essential enzyme for activating the

A

vitamin K available in the body

36
Q

Warfarin can deplete functional vitamin K reserves and therefore reduce

A

the synthesis of active clotting factors

37
Q

The hepatic synthesis of coagulation factors II, VII, IX, and X, as well as coagulation regulatory factors protein C and protein S, require

A

the presence of vitamin K

38
Q

Vitamin K is an essential cofactor for the synthesis of all

A

vitamin K-dependent clotting factors

39
Q

how is warfarin generally administered? (2)

A

by tablet, but injectable formulations are available

40
Q

effects of warfarin can be neutralized by

A

massive dose of Vitamin K

41
Q

different drugs work through

A

different steps in the clotting cascade

42
Q

which transfusions and blood products are used clinically? (4)

A

whole blood
serum
platelets
factors

43
Q

hemophilia types (2)

A

A

B

44
Q

hemophilia A is

A

x linked recessive

45
Q

hemophilia A can be decreased with

A

factor 8

46
Q

hemophilia A can be treated with

A

recombinant factor 8

47
Q

hemophilia B is

A

x linked recessive

48
Q

hemophilia B can be decreased with synthesis of

A

factor 9

49
Q

hemophilia B can be treated with

A

factor 9

50
Q

what is hemophilia B referred to as? why?

A

christmas disease

the first person diagnosed with it was named Christmas

51
Q

which major family line had hemophilia B? why?

A

Queen Victoria’s royal family

they were marrying and having babies with their family members

52
Q

Scott syndrome

A

a bleeding disorder caused by defective scrambling of membrane phospholipids

53
Q

Normal quescent cells maintain membrane lipid asymmetry by ATP-dependent membrane lipid transporters, which

A

shuttle different phospholipids from one leaflet to the other against their respective concentration gradients

54
Q

When cells are challenged, membrane lipid asymmetry can be perturbed resulting in exposure of — at the outer cell surface

A

phosphatidylserine [PS]

55
Q

translocation of PS from the inner to outer membrane leaflet of activated blood platelets and platelet-derived microvesicles provides

A

a catalytic surface for interacting coagulation factors

56
Q

this process is dramatically impaired in Scott syndrome, a rare congenital bleeding disorder, underscoring the indispensible role of

A

PS in hemostasis

57
Q

This also testifies to a defect of a

A

protein-catalyzed scrambling of membrane phospholipids

58
Q

The Scott phenotype is not restricted to platelets, but can be demonstrated in

A

other blood cells as well

59
Q

The functional aberrations observed in Scott syndrome have increased our understanding of transmembrane lipid movements, and may help to identify the molecular elements that promote the collapse of phospholipid asymmetry during (2)

A

cell activation and apoptosis

60
Q

kvllikrein mutations

A

At least nine KLKB1 gene mutations have been identified in people with a blood condition called prekallikrein deficiency, which does not generally cause any health problems. The condition is usually discovered when blood tests are done for other reasons. The KLB1 gene mutations that cause this condition reduce or eliminate functional plasma kallikrein in the blood of affected individuals and likely impair the intrinsic coagulation pathway. Researchers suggest that this lack (deficiency) of functional plasma kallikrein protein does not generally cause any symptoms because another process called the extrinsic coagulation pathway (also known as the tissue factor pathway) can compensate for the impaired intrinsic coagulation pathway. Either pathway can activate proteins that are needed later in the clotting process.

61
Q

Glanzmann’s thrombasthenia

A

(GpIIb-IIIa def.) frequent nosebleeds (epistaxis), and may bleed from the gums. Red or purple spots on the skin caused by bleeding underneath the skin (petechiae) or swelling caused by bleeding within tissues (hematoma). Prolonged bleeding following injury, trauma, or surgery (including dental work). Affected women may have excessive blood loss during pregnancy and childbirth.

62
Q

Von Willebrand disease

A

(VWF def.) easy bruising, long-lasting nosebleeds, and excessive bleeding or oozing following an injury, surgery, or dental work. Mild forms may become apparent only when abnormal bleeding occurs following surgery or serious injury.

63
Q

Bernard Soulier syndrome

A

(GpIb def.) bruise easily and have an increased risk of nosebleeds (epistaxis). Abnormally heavy bleeding following minor injury or surgery or even without trauma (spontaneous bleeding). Tiny red or purple spots on the skin called petechiae. Women with Bernard-Soulier syndrome often have heavy or prolonged menstrual periods (menorrhagia).

64
Q

factor 5 gene mutations

A

At least 100 mutations in the F5 gene have been found to cause a rare bleeding disorder called factor V deficiency. These mutations prevent the production of functional coagulation factor V or significantly reduce the amount of the protein in the bloodstream. People with this condition typically have less than 10 percent of normal levels of coagulation factor V in their blood; the most severely affected individuals have less than 1 percent. A reduced amount of functional factor V prevents blood from clotting normally, causing episodes of abnormal bleeding that can be severe. Factor V deficiency results from mutations in both copies of the F5 gene, although some people with a mutation in a single copy of the gene have mild bleeding problems.

65
Q

factor 2 gene mutations

A

The mutation that causes most cases of prothrombin thrombophilia changes one DNA building block (nucleotide) in the F2 gene. Specifically, it replaces the nucleotide guanine with the nucleotide adenine at position 20210 (written G20210A or 20210G>A). This mutation, which occurs in a region of the gene called the 3’ untranslated region, causes the gene to be overactive and leads to the production of too much prothrombin. An abundance of prothrombin leads to more thrombin, which promotes the formation of blood clots. Also known deficiencies of prothrombin too.

66
Q

factor 7 gene mutations

A

Almost 300 mutations in the F7 gene have been found to cause a rare bleeding disorder called factor VII deficiency. This disorder commonly causes nosebleeds, easy bruising, bleeding of the gums, and prolonged or excessive bleeding following surgery or physical injury. In severe cases, life-threatening episodes of bleeding inside the skull or gastrointestinal tract can occur. Some affected individuals have no bleeding problems. The F7 gene mutations involved in this condition reduce the amount of coagulation factor VII in the bloodstream. A shortage of coagulation factor VII prevents blood from clotting normally, causing episodes of abnormal bleeding that can be severe. What determines the severity of the condition is unclear; it does not appear to be related to the amount of coagulation factor VII in the blood.

67
Q

factor 10 gene mutations

A

At least 130 mutations in the F10 gene have been found to cause a rare bleeding disorder called factor X deficiency. This disorder commonly causes nosebleeds, easy bruising, bleeding under the skin, bleeding of the gums, blood in the urine (hematuria), and prolonged or excessive bleeding following surgery or trauma. Some F10 gene mutations that cause factor X deficiency reduce the amount of coagulation factor X in the bloodstream, resulting in a form of the disorder called type I. Other F10 gene mutations result in the production of a coagulation factor X protein with impaired function, leading to type II factor X deficiency. Reduced quantity or function of coagulation factor X prevents blood from clotting normally, causing episodes of abnormal bleeding that can be severe.

68
Q

factor 8 gene mutations

A

Mutations in the F8 gene cause hemophilia A, the most common form of this bleeding disorder. More than 1,300 alterations in this gene have been identified. Some of these mutations change single DNA building blocks (base pairs) in the gene, while others delete or insert multiple base pairs. The most common mutation in people with severe hemophilia A is a rearrangement of genetic material called an inversion. This inversion involves a large segment of the F8 gene.Mutations in the F8 gene lead to the production of an abnormal version of coagulation factor VIII or reduce the amount of this protein. The altered or missing protein cannot participate effectively in the blood clotting process. As a result, blood clots cannot form properly in response to injury. These problems with blood clotting lead to excessive bleeding that can be difficult to control. Some mutations, such as the large inversion described above, almost completely eliminate the activity of coagulation factor VIII and result in severe hemophilia. Other mutations reduce but do not eliminate the protein’s activity, resulting in mild or moderate hemophilia.

69
Q

the body ability to prevent fatal blood loss involves

A

a complex symphony of many systems

70
Q

understanding how blood clotting occurs and can be manipulated clinically will be important in

A

how you practice dentistry

Applied Biochemistry (52 decks)

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