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Patho Phys Exam 1 > Thrombosis, embolism, infarction > Flashcards

Thrombosis, embolism, infarction Flashcards

1
Q

Hemostasis:

A

how blood clots form at an injury site

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2
Q

Petechiae

A

Low number of blood platelets or they are not working well-important in clot formation

A petechia, plural petechiae, is a small (1–2 mm) red or purple spot on the skin, caused by a minor bleed from broken capillary blood vessels.

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3
Q

Purpura

A

Red areas-larger bleeding areas also caused by low platelet counts and or trauma

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4
Q

A 47-year-old male falls and strikes the back of his head. Over the next 24 hours, he becomes increasingly somnolent. A head CT shows an accumulation of fluid beneath the dura. Which of the following terms best describes this collection of fluid.

A. Ecchymoses 
B. Hematoma 
C. Petechiae 
D. Purpura 
E. Thrombosis
A

B. Hematoma

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5
Q

Identify the 3 elements involved with normal hemostasis.

A

Platelets, Coagulation cascade, and blood vessel wall (endothelium)

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6
Q

What affect does the release of endothelin from the endothelium following vascular injury have on blood vessels?

How does this affect hemostasis?

A

Endothelin causes vasoconstriction, this does not work all that long so a clot will have to form.

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7
Q

Describe primary hemostasis or the development of a platelet plug
-Explain how an intact endothelium prevents platelet adhesion and activation? (3)

A

Normally the (1) endothelium prevents blood cells from adhering to the ECM which

(2) contains collagen and vWF which are highly thrombogenic (clot causing)
(3) the endothelium also releases nitric oxide and prostacyclin (PG12) which cause vasodilation and inhibit aggregation and activation

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8
Q

What role does nitric oxide and prostacyclin from the endothelium play in hemostasis?

A

Endothelial cell releases nitric oxide and prostacyclin (PGI2) –> These cause vasodilation and inhibit platelet activation
and aggregation

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9
Q

Platelet Adhesion (2)

-how does endothelial cell loss initiate this

A
  1. Collagen and vWF in ECM is exposed

2. Platelet with a GP1b receptor binds to vWF and activates

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10
Q

Platelet Activation

A

Adhesion –> Activation

Activated platelet from vWF releases ADP and Thromboxane
A2 to activate other platelets

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11
Q

Identify the 3 elements involved with normal hemostasis.

A

Platelets, Coagulation cascade, and Endothelin/Endothelium

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12
Q

A 16-year-old boy experienced prolonged bleeding after a tooth extraction. His mother related that her son tended to bleed for a long time after his immunization shots. Which of the following does this boy most likely have?

A. Abnormally high levels of fibrinogen
B. Abnormally high levels of thromboxane A2
C. Deficiency in prostacyclin
D. Deficiency in von Willebrand factor

A

D. Deficiency in von Willebrand factor

  • Cannot activate platelets b/c they have nothing to adhere to…

Note: the rest would cause the reverse

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13
Q

Aspirin irreversibly inhibits cyclooxygenase 1 (COX 1), which is the enzyme responsible for the formation of thromboxane A2 in platelets. What affect will aspirin most likely have in a person who has a cut?
A. Prolong bleeding time by inhibiting platelet
adhesion to the blood vessel wall
B. Prolong bleeding time by inhibiting platelet
activation
C. Shorten bleeding time by inhibiting platelet
adhesion to the blood vessel wall
D. Shorten bleeding time by inhibiting platelet
activation

A

B. Prolong bleeding time by inhibiting platelet

activation

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14
Q

Aspirin irreversibly inhibits cyclooxygenase 1 (COX 1), which is the enzyme responsible for the formation of thromboxane A2 in platelets. What affect will aspirin most likely have in a person who has a cut?
A. Prolong bleeding time by inhibiting platelet
adhesion to the blood vessel wall
B. Prolong bleeding time by inhibiting platelet
activation
C. Shorten bleeding time by inhibiting platelet
adhesion to the blood vessel wall
D. Shorten bleeding time by inhibiting platelet
activation

A

B. Prolong bleeding time by inhibiting platelet

activation

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15
Q

______ is needed for clotting factors II (prothrombin), VII, IX and X
-it is produced by the liver, is endogenous anticoagulant, and protein C

A

Vitamin K

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16
Q

Explain Activation of Coagulation Cascade involving secondary hemostasis

A

Tissue factor activates VII –> activated VII activates IX with cofactor
VIII –> activated IX- with cofactor V
-> –>
activates II (aka prothrombin) which are clotting factors

Numbers are
7-9-10-2

cofactors include: 5a and 8a

17
Q

thrombin Function

A

Cleaves fibrinogen –> fibrin –> clots

18
Q

Explain the effect of a deficiency in factor VIII or IX,

liver disease,

and heparin (it works similar to heparin-like molecules)

on the coagulation cascade and hemostasis?

A

liver Disease: decrease synthesis of clotting factors

Deficiency in factor VIII or IX: hemophilia (no clotting protein)

Heparin, Xa inhibitors or thrombin inhibitors: directly or indirectly
inhibit thrombin/Xa –> no clots

19
Q

Thrombin bound tothrombomodulin

A

anticoagulant-thrombin cleaves Prot C –> activates Prot S –>

Protein C (endogenous anti-coagulant) binds to protein C
receptor on endothelial surface
a. Thrombomodulin on surface binds to thrombin
b. Thrombin + thrombomodulin binds to protein C to
activate it
c. Active protein C binds to protein S and inactivates
cofactors Va and VIIIa

20
Q

Explain the role of endothelial cells in preventing the coagulation cascade or clot development and expansion.

(4)-hint: one involves a secretion, the others are more common sense

A

Clot prevented from expanding and growing outside site of injury via

**Endothelial cells secrete plasminogen activator t-PA which activates plasminogen to plasmin, plasmin degrades fibrin to dissolve the clot

  1. Flowing blood washing away activated clotting factors
  2. Intact endothelium adjacent to injury site

vi. After stable blood clot formed: clot retraction (push fluid out,
promoted by thrombin) and clot dissolves

21
Q

Describe the role of tissue factor pathway inhibitor

thrombomodulin and protein C in preventing the coagulation cascade or clot development and expansion.

(4 big steps)

A 
Protein C (endogenous anti-coagulant) binds to protein C
receptor on endothelial surface

–> Thrombomodulin on surface then binds to thrombin

–> Thrombin + thrombomodulin binds to protein C to activate it

–> Active protein C binds to protein S and inactivates
cofactors Va and VIIIa (this is the key)

22
Q

Explain how plasmin is activated, how it dissolves a clot and produces D-dimers.

3 steps

A

Endothelial cells secrete tissue plasminogen activator (t-PA)

–> t-PA activates plasminogen to plasmin

–>plasmin degrades fibrin to dissolve the clot

**D-dimers can be measured in blood as a marker of thrombosis

23
Q

What breaks down fibrin to dissolve a clot?

A

Plasmin-which is activated plasminogen

24
Q

Elevated D-dimers means?

A 
Had thrombosis (blood clots) b/c these are a result of 
plasmin degrading fibrin to dissolve the clot

**D-dimers can be measured in blood as a marker of thrombosis

25
Q

Warfarin and Vitamin K diet

A

inhibits production of vitamin K-dependent clotting factors-has a narrow therapeutic index (exact dosage required)

26
Q

Warfarin and Vitamin K diet

A

Warfarin inhibits production of vitamin K-dependent clotting factors-has a narrow therapeutic index (exact dosage required)

**this is not that important

27
Q

What is thrombosis?
A. The formation or presence of a blood
clot in a broken blood vessel B. The formation or presence of a blood
clot in an intact blood vessel C. Either A or B

A

B. The formation or presence of a blood

clot in an intact

28
Q

hemorragic disorder

A

a problem with hemostasis, in which clots do not form and there is excessive bleeding

29
Q

thrombotic disorder

A

a problem with hemostasis, in which there is too much clotting

30
Q

Embolism

A

Intravascular solid, liquid, or gaseous mass that is carried by the blood to a site distant from its point of origin

31
Q

Thromboembolism

A

Here just know this definition-

a thrombosis (blood clot) which flows through the blood and may clot elsewhere

EXTRA:
Vein –> deep vein thrombosis –> pulmonary embolus
(b/c hits capillary bed)

Artery or left heart chamber: can be systemic and go
anywhere –> lodge in artery –> cause infarction

–> Infarction causes coagulative necrosis (but
liquefactive in brain)

32
Q

Ecchymoses clinically

A

a discoloration of the skin from bleeding underneath such as from bruising

33
Q

Hematoma clinically

A

a solid swelling from tissue within

34
Q

Compare a hemorrhage - Hematoma, Petechiae, Purpura, Ecchymoses.

Which will most likely be caused by a defect in platelets (either low platelet count or defect in their function) vs trauma?

A

Hematoma-solid swelling: trauma

Hemorrhage-platelets

A petechia, plural petechiae, is a small (1–2 mm) red or purple spot on the skin, caused by a minor bleed from broken capillary blood vessels.

Purpura: Red areas-larger bleeding areas also caused by low platelet counts and or trauma-DO NOT BLANCH

Ecchymoses: a discoloration of the skin resulting from bleeding underneath, typically caused by bruising.

35
Q

Describe the role of tissue factor pathway inhibitor
(TFPI);

where is it and what does it do

A

On the surface of the endothelium-it inactivates tissue factor VIIa complex

36
Q

Describe the role of heparin-like molecules and antithrombin

A

Heparin like molecules are antithrombin activators on the surface of endothelial cells=heparin type molecule

37
Q

Thromboembolism in vein

A

Vein –> deep vein thrombosis –> pulmonary embolus

b/c hits capillary bed

38
Q

Thromboembolism in artery

A

Artery or left heart chamber: can be systemic and go
anywhere –> lodge in artery –> cause infarction

–> Infarction causes coagulative necrosis (but
liquefactive in brain)

39
Q

List and explain the main causes of fat embolism, amniotic fluid embolism, or air embolism?

A

Fat embolism: crushing injury to soft tissue or bone

Amniotic fluid embolism: during labor, there is a tear in the placental or a
uterine vein ruptures

Air embolism: improper IV injection, surgery

Patho Phys Exam 1 (14 decks)

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