HEMA RODAKS ADD INFO (PRE-MID) Flashcards

1
Q

keeps circulating blood in a fluid state

A

HEMOSTASIS

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2
Q

In hemostasis, when an injury occur, produces a ___ to stop bleeding; Confines the clot to site of _____

A

clot ; injury

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3
Q

Dissolves the clot as the wound heals

A

Hemostasis

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4
Q

Hemostasis involves the interaction of _______, _________ and ________, and ________ activation to stop bleeding.

A

vasoconstriction, platelet adhesion and aggregation; coagulation enzyme

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5
Q

Blood vessels contract to seal the wound or reduce the blood flow

A

(vasoconstriction)

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6
Q

proteins circulate as inactive zymogens

A

pro-enzymes

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7
Q

DETERMINE IF PRIMARY OR SECONDARY HEMOSTASIS…

Activated by desquamation and small injuries to blood vessels.

A

PRIMARY HEMOSTASIS

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8
Q

DETERMINE IF PRIMARY OR SECONDARY HEMOSTASIS…

Involves vascular intima and platelets

A

PRIMARY HEMOSTASIS

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9
Q

DETERMINE IF PRIMARY OR SECONDARY HEMOSTASIS…

Rapid short lived response.

A

PRIMARY HEMOSTASIS

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10
Q

DETERMINE IF PRIMARY OR SECONDARY HEMOSTASIS…

Procoagulant substances exposed or released by damaged or activated by endothelial cells.

A

PRIMARY HEMOSTASIS

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11
Q

DETERMINE IF PRIMARY OR SECONDARY HEMOSTASIS…

Activated by large injuries to blood vessels and surrounding tissues.

A

SECONDARY HEMOSTASIS

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12
Q

DETERMINE IF PRIMARY OR SECONDARY HEMOSTASIS…

Involves platelets and coagulation system.

A

SECONDARY HEMOSTASIS

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13
Q

DETERMINE IF PRIMARY OR SECONDARY HEMOSTASIS…

Delayed, long term response

A

SECONDARY HEMOSTASIS

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14
Q

DETERMINE IF PRIMARY OR SECONDARY HEMOSTASIS…

The activator, tissue factor is exposed on cell membranes.

A

SECONDARY HEMOSTASIS

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15
Q

VASCULAR INTIMA IN HEMOSTASIS

A

Endothelial Cells
Anticoagulant Properties

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16
Q

platelet inhibitor and a vasodilator, is synthesized through the eicosanoid pathway

A

Prostacyclin

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17
Q

induces smooth muscle relaxation and subsequent vasodilation

A

Nitric oxide

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18
Q

promotes angiogenesis and healthy arterioles

A

Nitric oxide

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19
Q

Inhibitors of thrombin formation

A

Thrombomodulin

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20
Q

binds protein C, and thrombomodulin catalyzes the activation of the protein C pathway

A

Facilitated by EPCR (endothelial protein C receptor)

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21
Q

enhances the activity of antithrombin

A

Heparin sulfate

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22
Q

Heparin is used extensively as a ______ to prevent the ______ of the thrombi manufactured from ________

A

therapeutic agent ; propagation ; porcine gut tissues

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23
Q

protein C pathway down regulates coagulation by digesting activated _________, thereby inhibiting ______ formation

A

factors V and VIII ; thrombin

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24
Q

necessary for platelets to adhere to exposed subendothelial collagen in arterioles

A

VWF

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25
Q

Procoagulant Properties of Damaged Vascular Intima

A
  • any harmful local stimulus (mechanical or chemical): induces vasoconstriction in arteries and arterioles
  • (At subendothelial connective tissues) collagen: a flexible, elastic structural protein that binds and activates platelets
  • ECs secrete von Willebrand factor (VWF) when activated by vasoactive agents such as thrombin
  • on activation, ECs secrete and coat themselves with P-selectin, an adhesion molecule that promotes platelet and leukocyte binding
  • intercellular adhesion molecules (ICAMs) and platelet endothelial cell adhesion molecules (PECAMs): further promote platelet and leukocyte binding
  • EC disruption exposes tissue factor in subendothelial cells and activates the coagulation system through contact with plasma factor VII.
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26
Q

PROCOAGULANT PROPERTIES OF DAMAGED VASCULAR INTIMA…

induces vasoconstriction in arteries and arterioles

A

any harmful local stimulus (mechanical or chemical)

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27
Q

PROCOAGULANT PROPERTIES OF DAMAGED VASCULAR INTIMA…

a flexible, elastic structural protein that binds and activates platelets

A

(At subendothelial connective tissues) collagen

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28
Q

PROCOAGULANT PROPERTIES OF DAMAGED VASCULAR INTIMA…

ECs secrete _________ when activated by vasoactive agents such as _______

A

von Willebrand factor (VWF) ; thrombin

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29
Q

PROCOAGULANT PROPERTIES OF DAMAGED VASCULAR INTIMA…

on activation, ECs secrete and coat themselves with _______, an adhesion molecule that promotes platelet and leukocyte binding

A

P-selectin

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30
Q

an adhesion molecule that promotes platelet and leukocyte binding

A

P-selectin

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31
Q

PROCOAGULANT PROPERTIES OF DAMAGED VASCULAR INTIMA…

: further promote platelet and leukocyte binding

A

intercellular adhesion molecules (ICAMs) and platelet endothelial cell adhesion molecules (PECAMs)

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32
Q

PROCOAGULANT PROPERTIES OF DAMAGED VASCULAR INTIMA…

EC disruption exposes tissue factor in ______ and activates the coagulation system through contact with _________.

A

subendothelial cells ; plasma factor VII

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33
Q

Fibrinolytic Properties of Vascular Intima

A
  • ECs support fibrinolysis with the secretion of tissue plasminogen activator (TPA)
  • ECs also regulate fibrinolysis by providing inhibitors to prevent excessive plasmin generation.
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34
Q

In ECs support fibrinolysis with the secretion of tissue plasminogen activator (TPA)…

During thrombus formation, both ______ and ______ bind to polymerized fibrin.

A

TPA ; plasminogen

35
Q

In ECs support fibrinolysis with the secretion of tissue plasminogen activator (TPA)…

TPA activates ______ by converting plasminogen to ______, which gradually digests ______ and restores _____

A

fibrinolysis ; plasmin ; fibrin ; blood flow

36
Q

the removal of fibrin to restore vessel patency

A

Fibrinolysis

37
Q

storage sites of vwF

A

Weibel-Palade bodies

38
Q

IN ECs also regulate fibrinolysis by providing inhibitors to prevent excessive plasmin generation…

secrete ____________, a TPA control protein that inhibits plasmin generation and fibrinolysis

A

plasminogen activator inhibitor 1 (PAI-1)

39
Q

a TPA control protein that inhibits plasmin generation and fibrinolysis

A

plasminogen activator inhibitor 1 (PAI-1)

40
Q

IN ECs also regulate fibrinolysis by providing inhibitors to prevent excessive plasmin generation…

__________, is activated by thrombin bound to EC membrane thrombomodulin

A

thrombin-activatable fibrinolysis inhibitor (TAFI)

41
Q
  • platelets bind nonplatelet surfaces (subendothelial collagen)
  • VWF links platelets to collagen (glycoprotein GP Ib/IX/V membrane receptor)
  • platelets may bind directly to collagen in damaged veins and capillaries
A

Adhesion

42
Q

In platelet adhesion, platelets bind _______ (subendothelial collagen)

A

nonplatelet surfaces

43
Q

In platelet adhesion, VWF links platelets to
_______ (glycoprotein GP Ib/IX/V membrane receptor)

A

collagen

44
Q

In platelet adhesion, platelets may bind directly to collagen in damaged ______ and _____

A

veins and capillaries

45
Q
  • platelets bind to one another
  • Activated platelets css a change in GP IIb/IIIa receptor allows binding of fibrinogen, VWF and fibronectin.
  • Fibrinogen binds to GP IIb/IIIa receptors on adjacent platelets and joins them together in the presence of ionized calcium (Ca2+)
A

Aggregation

46
Q

In platelet aggregation, platelets bind to ________

A

one another

47
Q

In platelet aggregation, activated platelets causes a change in ________ allows binding of ______, ______ and ______

A

GP IIb/IIIa receptor ; fibrinogen, VWF and fibronectin.

48
Q

In platelet aggregation, Fibrinogen binds to _______ on adjacent platelets and joins them together in the presence of _________

A

GP IIb/IIIa receptors ; ionized calcium (Ca2+)

49
Q
  • secrete the contents of their granules during adhesion and aggregation, with most secretion occurring late in the platelet activation process
  • During activation, ADP and Ca2+ activate phospholipase A2, which converts membrane phospholipid to arachidonic acid
  • Cyclooxygenase converts arachidonic acid into prostaglandin endoperoxides
  • thromboxane synthetase converts prostaglandins into thromboxane A2, which causes Ca2+ to be released and promotes platelet aggregation and vasoconstriction
A

Secretion

50
Q

In platelet secretion, secrete the contents of their granules during adhesion and aggregation, with most secretion occurring late in the __________

A

platelet activation process

51
Q

In platelet secretion, during activation, _____ and _____ activate ________, which converts membrane phospholipid to arachidonic acid

A

ADP and Ca2+ ; phospholipase A2

52
Q

converts membrane phospholipid to arachidonic acid

A

phospholipase A2

53
Q

In platelet secretion, _______ converts arachidonic acid into prostaglandin endoperoxides

A

cyclooxygenase

54
Q

In platelet secretion, thromboxane synthetase converts _________ into ________, which causes Ca2+ to be released and promotes platelet aggregation and vasoconstriction

A

prostaglandins ; thromboxane A2

55
Q

platelets roll and cling to nonplatelet surface

A

Adhesion

56
Q

platelets adhere to each other

A

Aggregation

57
Q

platelets discharge the contents of their granules.

A

Secretion

58
Q

Reversible, seals endothelial gaps, some secretion of growth factors, in arterioles VWF is necessary for _______

A

adhesion ; (Adhesion Characteristics)

59
Q

Irreversible, platelet plugs form, platelet contents are secreted, requires fibrinogen

A

Aggregation

60
Q

Irreversible, occurs during aggregation, platelet contents are secreted, essential to coagulation.

A

Secretion

61
Q

Aspirin acetylation permanently inactivates ______, blocking ______ production and causing ______ (aspirin effect)

A

cyclooxygenase ; thromboxane A2 ; impairment of platelet function

62
Q

autosomal dominant; characterized by thin-walled blood vessels with a discontinuous endothelium, inadequate smooth muscle, and inadequate or missing elastin in the surrounding stroma.

A

Hereditary Hemorrhagic Telangiectasia (Rendu-Osler-Weber Syndrome)

63
Q

dilated superficial blood vessels that create small, focal red lesions; fragile and prone to rupture

A

Telangiectasias

64
Q

most obvious on the face, lips, tongue, conjunctiva, nasal mucosa, fingers, toes, and trunk and under the tongue

A

Telangiectasias

65
Q

In Telangiectasias, The age at which _______ begin is a good gauge of the severity of the disorder.

A

nosebleeds

66
Q

common sites of bleeding in telangiectasias/Hereditary Hemorrhagic Telangiectasia (Rendu-Osler-Weber Syndrome)

A

Oral cavity, gastrointestinal tract, and urogenital tract

67
Q

Hereditary Hemorrhagic Telangiectasia (Rendu-Osler-Weber Syndrome) Diagnosis

A

based on the:
- characteristic skin or mucous membrane lesions
- a history of repeated hemorrhage, and
- a family history of a similar disorder.

68
Q

association of a giant cavernous hemangioma (vascular tumor), thrombocytopenia and a bleeding diathesis (visceral or subcutaneous, but rarely both)

A

Hemangioma-Thrombocytopenia Syndrome
(Kasabach-Merritt Syndrome)

69
Q

acute or chronic disseminated intravascular coagulation & microangiopathic hemolytic anemia

A

Hemangioma-Thrombocytopenia Syndrome
(Kasabach-Merritt Syndrome)

70
Q

a constitutional predisposition toward a particular state or condition and especially one that is abnormal or diseased

A

diathesis

71
Q

Autosomal dominant, recessive, or X-linked trait

A

Ehlers-Danlos syndrome

72
Q

Ehlers-Danlos syndrome is manifested by

A

hyperextensible skin,
hypermobile joints,
joint laxity,
fragile tissues,
and a bleeding tendency, primarily subcutaneous hematoma formation

73
Q

defects in collagen production, structure, or crosslinking, with resulting inadequacy of the connective tissues

A

Ehlers-Danlos syndrome

74
Q

generally is applied to a group of nonthrombocytopenic purpuras characterized by apparently allergic manifestations, including skin rash and edema

A

allergic purpura or anaphylactoid purpura

75
Q

condition is accompanied by transient arthralgia, nephritis, abdominal pain, and purpuric skin lesion

A

Allergic Purpura (Henoch-Schönleain Purpura)

76
Q

vasculitis is mediated by immune complexes containing IgA antibodies

A

autoimmune vascular injury (allergic purpura)

77
Q

primarily a disease of children, occurring most commonly in children 3 to 7 years of age.

A

Allergic Purpura (Henoch-Schönleain Purpura)

78
Q

in Allergic Purpura (Henoch-Schönleain Purpura), onset of the disease is sudden, often following an ____________

A

upper respiratory tract infection (b-hemolytic streptococcus)

79
Q

allergic purpura, lesions is described as

A

palpable purpura

80
Q

due to a lack of collagen support for small blood vessels and loss of subcutaneous fat and elastic fibers

A

senile purpura

81
Q

senile purpura is more commonly in _______ than _____

A

elderly men than in women

82
Q

flattened, about 1 to 10 mm in diameter, do not blanch with pressure, and resolve slowly, often leaving a brown stain in the skin (age spots)

A

dark blotches in senile purpura

83
Q

Results in decreased synthesis of collagen, with weakening of capillary walls and the appearance of purpuric lesions

A

Scurvy