HEMA RODAKS ADD INFO (PRE-MID) Flashcards by Sharmaine Madjid

Q

keeps circulating blood in a fluid state

A

HEMOSTASIS

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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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Q

Dissolves the clot as the wound heals

A

Hemostasis

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Q

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

A

vasoconstriction, platelet adhesion and aggregation; coagulation enzyme

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Q

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

A

(vasoconstriction)

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Q

proteins circulate as inactive zymogens

A

pro-enzymes

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Q

DETERMINE IF PRIMARY OR SECONDARY HEMOSTASIS…

Activated by desquamation and small injuries to blood vessels.

A

PRIMARY HEMOSTASIS

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Q

DETERMINE IF PRIMARY OR SECONDARY HEMOSTASIS…

Involves vascular intima and platelets

A

PRIMARY HEMOSTASIS

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Q

DETERMINE IF PRIMARY OR SECONDARY HEMOSTASIS…

Rapid short lived response.

A

PRIMARY HEMOSTASIS

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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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Q

DETERMINE IF PRIMARY OR SECONDARY HEMOSTASIS…

Activated by large injuries to blood vessels and surrounding tissues.

A

SECONDARY HEMOSTASIS

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Q

DETERMINE IF PRIMARY OR SECONDARY HEMOSTASIS…

Involves platelets and coagulation system.

A

SECONDARY HEMOSTASIS

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Q

DETERMINE IF PRIMARY OR SECONDARY HEMOSTASIS…

Delayed, long term response

A

SECONDARY HEMOSTASIS

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Q

DETERMINE IF PRIMARY OR SECONDARY HEMOSTASIS…

The activator, tissue factor is exposed on cell membranes.

A

SECONDARY HEMOSTASIS

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Q

VASCULAR INTIMA IN HEMOSTASIS

A

Endothelial Cells
Anticoagulant Properties

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Q

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

A

Prostacyclin

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Q

induces smooth muscle relaxation and subsequent vasodilation

A

Nitric oxide

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Q

promotes angiogenesis and healthy arterioles

A

Nitric oxide

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Q

Inhibitors of thrombin formation

A

Thrombomodulin

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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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Q

enhances the activity of antithrombin

A

Heparin sulfate

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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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Q

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

A

factors V and VIII ; thrombin

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Q

necessary for platelets to adhere to exposed subendothelial collagen in arterioles

A

VWF

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Procoagulant Properties of Damaged Vascular Intima

- 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.

PROCOAGULANT PROPERTIES OF DAMAGED VASCULAR INTIMA... induces vasoconstriction in arteries and arterioles

any harmful local stimulus (mechanical or chemical)

PROCOAGULANT PROPERTIES OF DAMAGED VASCULAR INTIMA... a flexible, elastic structural protein that binds and activates platelets

(At subendothelial connective tissues) collagen

PROCOAGULANT PROPERTIES OF DAMAGED VASCULAR INTIMA... ECs secrete _________ when activated by vasoactive agents such as _______

von Willebrand factor (VWF) ; thrombin

PROCOAGULANT PROPERTIES OF DAMAGED VASCULAR INTIMA... on activation, ECs secrete and coat themselves with _______, an adhesion molecule that promotes platelet and leukocyte binding

P-selectin

an adhesion molecule that promotes platelet and leukocyte binding

P-selectin

PROCOAGULANT PROPERTIES OF DAMAGED VASCULAR INTIMA... : further promote platelet and leukocyte binding

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

PROCOAGULANT PROPERTIES OF DAMAGED VASCULAR INTIMA... EC disruption exposes tissue factor in ______ and activates the coagulation system through contact with _________.

subendothelial cells ; plasma factor VII

Fibrinolytic Properties of Vascular Intima

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

In ECs support fibrinolysis with the secretion of tissue plasminogen activator (TPA)... During thrombus formation, both ______ and ______ bind to polymerized fibrin.

TPA ; plasminogen

In ECs support fibrinolysis with the secretion of tissue plasminogen activator (TPA)... TPA activates ______ by converting plasminogen to ______, which gradually digests ______ and restores _____

fibrinolysis ; plasmin ; fibrin ; blood flow

the removal of fibrin to restore vessel patency

Fibrinolysis

storage sites of vwF

Weibel-Palade bodies

IN ECs also regulate fibrinolysis by providing inhibitors to prevent excessive plasmin generation... secrete ____________, a TPA control protein that inhibits plasmin generation and fibrinolysis

plasminogen activator inhibitor 1 (PAI-1)

a TPA control protein that inhibits plasmin generation and fibrinolysis

plasminogen activator inhibitor 1 (PAI-1)

IN ECs also regulate fibrinolysis by providing inhibitors to prevent excessive plasmin generation... __________, is activated by thrombin bound to EC membrane thrombomodulin

thrombin-activatable fibrinolysis inhibitor (TAFI)

- 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

Adhesion

In platelet adhesion, platelets bind _______ (subendothelial collagen)

nonplatelet surfaces

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

collagen

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

veins and capillaries

- 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+)

Aggregation

In platelet aggregation, platelets bind to ________

one another

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

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

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

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

- 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

Secretion

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

platelet activation process

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

ADP and Ca2+ ; phospholipase A2

converts membrane phospholipid to arachidonic acid

phospholipase A2

In platelet secretion, _______ converts arachidonic acid into prostaglandin endoperoxides

cyclooxygenase

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

prostaglandins ; thromboxane A2

platelets roll and cling to nonplatelet surface

Adhesion

platelets adhere to each other

Aggregation

platelets discharge the contents of their granules.

Secretion

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

adhesion ; (Adhesion Characteristics)

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

Aggregation

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

Secretion

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

cyclooxygenase ; thromboxane A2 ; impairment of platelet function

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

Hereditary Hemorrhagic Telangiectasia (Rendu-Osler-Weber Syndrome)

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

Telangiectasias

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

Telangiectasias

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

nosebleeds

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

Oral cavity, gastrointestinal tract, and urogenital tract

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

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

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

Hemangioma-Thrombocytopenia Syndrome (Kasabach-Merritt Syndrome)

acute or chronic disseminated intravascular coagulation & microangiopathic hemolytic anemia

Hemangioma-Thrombocytopenia Syndrome (Kasabach-Merritt Syndrome)

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

diathesis

Autosomal dominant, recessive, or X-linked trait

Ehlers-Danlos syndrome

Ehlers-Danlos syndrome is manifested by

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

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

Ehlers-Danlos syndrome

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

allergic purpura or anaphylactoid purpura

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

Allergic Purpura (Henoch-Schönleain Purpura)

vasculitis is mediated by immune complexes containing IgA antibodies

autoimmune vascular injury (allergic purpura)

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

Allergic Purpura (Henoch-Schönleain Purpura)

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

upper respiratory tract infection (b-hemolytic streptococcus)

allergic purpura, lesions is described as

palpable purpura

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

senile purpura

senile purpura is more commonly in _______ than _____

elderly men than in women

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)

dark blotches in senile purpura

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

Scurvy