Patho17(hemodynamics file16+17)

Question 1

What is hemorrhage?

Answer 1

Extravasation of blood from vessels

Question 2

What are the causes of hemorrhage?

Answer 2

Damage to blood vessels or defective clot formation, trauma, atherosclerosis, inflammatory or neoplastic erosion of a vessel wall, hemorrhagic diatheses

Question 3

Define hemorrhagic diatheses.

Answer 3

Diverse causes, including inherited or acquired defects in vessel walls, platelets, or coagulation factors

Question 4

What can hemorrhage result in? It can be location

Answer 4

External bleeding or accumulation of blood within a tissue as a hematoma

Question 5

The hematoma ranges in importance/significance?

Answer 5

from trivial (e.g., a bruise) to fatal (e.g., a massive retroperitoneal hematoma resulting from rupture of a dissecting aortic aneurysm).

Question 6

Names of large bleeds into body cavities in plural cavity, pericardial cavity, peritoneal cavity, joints

Answer 6

hemothorax, hemopericardium, hemoperitoneum, or hemarthrosis.

Question 7

What can extensive hemorrhages occasionally result in?

Answer 7

Jaundice from massive breakdown of red cells and hemoglobin/mainly in newborns

Question 8

Describe each picture related to hemorrhage

Answer 8

Hematoma strong/large bleed in joint cavity/hematoma fetal in brain / hematoma trivial

Question 9

What is the clinical significance of a hemorrhage depend on with explain ?

Answer 9

the volume of blood lost and the rate of bleeding /site of hemorrhage
* Rapid loss of up to 20% of the blood volume, or slow losses of even larger amounts, may have little impact in healthy adults; greater losses, however, can cause hemorrhagic (hypovolemic) shock.
The site of hemorrhage also is important; bleeding that would be trivial in the subcutaneous tissues can cause death if located in the brain.

Question 10

What is the consequence of chronic or recurrent external blood loss? And in which condition it happens?

Answer 10

iron deficiency anemia as a consequence of a loss of iron in hemoglobin./ due to peptic ulcer, menstrual bleeding

Question 11

What are petechiae?

Answer 11

Minute hemorrhages (1 to 2 mm) into skin, mucous membranes, or serosal surfaces

Question 12

What are some causes of petechiae?

Answer 12

Low platelet counts (thrombocytopenia), defective platelet function, loss of vascular wall support (as in vitamin C deficiency)

Question 13

Define purpura.

Answer 13

Slightly larger (3 to 5 mm) hemorrhages, same disorders that cause petechiae, trauma, vascular inflammation (vasculitis), increased vascular fragility

Question 14

What are ecchymoses?

Answer 14

Larger (1 to 2 cm) subcutaneous hematomas /causes mainly trauma and platelet not involved just coagulation cascade

Question 15

What causes the characteristic color changes of a bruise ( ecchymoses)?

Answer 15

Extravasated red cells are phagocytosed and degraded by macrophages;
Enzymatic conversion of hemoglobin (red-blue color) to bilirubin (blue-green color) and eventually hemosiderin (golden-brown)

Question 16

What is the definition of normal hemostasis?

Answer 16

a series of regulated processes that culminate in the formation of a blood clot that limits bleeding from an injured vessel.

Question 17

What is the pathologic counterpart of hemostasis?

Answer 17

thrombosis, the formation of a blood clot within non-traumatized, intact vessels.

Question 18

What occurs immediately after an injury to reduce blood flow?

Answer 18

Arteriolar vasoconstriction

Question 19

What mediates arteriolar vasoconstriction?

Answer 19

reflex neurogenic mechanisms and augmented by the local secretion of factors such as endothelin.

Question 20

What are the main components of normal hemostasis ?

Answer 20

platelets, clotting factors, and endothelium.

Question 21

What is the transient response in normal hemostasis?

Answer 21

Arteriolar vasoconstriction

Question 22

What is the main mediator cause vasoconstriction?

Answer 22

endothelin (potent endothelium-derived vasoconstrictor)

Question 23

What is primary hemostasis?

Answer 23

Formation of the platelet plug

Question 24

What happenes during the primary hemostasis(steps)?

Answer 24

• Platelet adhesion: interactions with subendotheial VWF, which acts as a bridge between the platelet surface receptor glycoprotein Ib (Gplb) and exposed collagen.
• platelet activation:(Thrombin activates platelets through a special type of G-protein-coupled receptor referred to as a protease-activated receptor (PAR) and by collagen and ADP.Shape change (from small rounded discs to flat plates with spiky protrusions “sea urchins” that markedly increased surface area, and the release of secretory granules.
  *Recruit additional platelets»»(aggregation)to form a primary hemostatic plug.

Question 25

How platelet activation will help in the following steps ( aggregation/secondery Hemostasis)?

Answer 25

In platelet activation step:*the shape change of platelet accomnanied with
1) alterations in glycoprotein (IIb,IIIa)»»that increase its affinity for fibrinogen that important to aggregation
2) translocation of negatively charged phospholipids to the platelet surface»»Phospholipids bind calcium and serve as nucleation sites for the assembly of coagulation factor complexes.
* granules produce the prostaglandin thromboxane A2 (TXA2) and others >potent inducer of platelet aggregation.

Question 26

What are the 3 bleeding disorders related to primary Hemostasis?

Answer 26

1(von Wilbrand disease)= Genetic deficiencies of vWF common in Jordan
2(BernardSoulier syndrome)=GPIb
3*(Glanzmann thrombasthenia)= Inherited deficiency of Gpllb-Illa

Question 27

What is secondary hemostasis?

Answer 27

Deposition of fibrin

Question 28

What happenes during the secondary hemostasis(steps)?

Answer 28

*coagulation cascade:
1)extrinsic and intrinsic pathway >to activate factor 10 (X) > generates thrombin
* Thrombin cleaves circulating fibrinogen into insoluble fibrin, a potent activator of platelets.

Question 29

How coagulation cascade occurs ( steps)?

Answer 29

صورة

Question 30

After secondary hemostasis which step ? And how it’s occer?

Answer 30

Clot stabilization / Polymerized fibrin and platelet aggregates undergo contraction to form a solid, permanent plug that prevents further hemorrhage.

Question 31

After clot stabilization which step+ the aim of it ?

Answer 31

Counterregulatory mechanisms that :
1) inhibit thrombosis by : *inactive the factors in coagulation cascade
* inhibit platelets aggregation
2) activate fibrinolysis
3) clot resorption and tissue repair.
All this happens in normal endothelial cells (platelet inhibitory effects.
/Anticoagulant effects/ Fibrinolytic effects.)

Question 32

Counterregulatory mechanisms In detail?

Answer 32

صورة

Question 33

What is platelets ( shape,origin)?

Answer 33

Disc-shaped/anucleate cell fragments that are shed from megakaryocytes in the bone marrow into the bloodstream.

Question 34

What do platelets depend on for their function?

Answer 34

Glycoprotein receptors, a contractile cytoskeleton, and two types of cytoplasmic granules;
Alfa/ dense gamma granules

Question 35

What are the components involved in each reaction step of the coagulation cascade?

Answer 35

Enzyme (activated coagulation factor), substrate (inactive proenzyme form of a coagulation factor), and cofactor (reaction accelerator).

Question 36

Where are the components assembled in the coagulation cascade?

Answer 36

On a negatively charged phospholipid surface.

Question 37

What does the prothrombin time (PT) assay assess?

Answer 37

The function of the proteins in the extrinsic pathway (factors VII, X, V, II (prothrombin), and fibrinogen).

Question 38

What does the partial thromboplastin time (PTT) assay screen?

Answer 38

The function of the proteins in the intrinsic pathway (factors XII, XI, IX, VIII, X, V, II, and fibrinogen).

Question 39

What are the functions of thrombin?

Answer 39

Conversion of fibrinogen into crosslinked fibrin, platelet activation, proinflammatory effects, and anti-coagulant effects.

Question 40

What is fibrinolysis?

Answer 40

The enzymatic activity of plasmin, which breaks down fibrin and interferes with its polymerization.

Question 41

How is plasmin generated?

Answer 41

inactive circulating precursor plasminogen converted to plasmin by enzymatic catabolism :
1) either by a factor 12(XII)–dependent pathway
2) plasminogen activators (t-PA) that made by endothelial cells/urokinase
**( alpha2 -Anti-plasmin) that regulate fibrinolysis by inhibiting plasmin function

Question 42

What are the elevated levels of breakdown products of fibrinogen called?

Answer 42

Fibrin-derived D-dimers.