LO HEMATO WEEK 3

LO: Week 3, Monday

1. Anatomi lutut
- Strukturnya ada apa saja
- vaskularisasinya ada apa saja
- TrA hematoma is a collection of blood and blood products underneath the subcutaneous layer
of skin. It is most commonly associated with a sutured laceration or surgical incision but may also
be seen following trauma, especially when the mechanism involves sheering or blunt forces over
the skin, or in the presence of a muscle, tendon, or ligament tear auma di lutut apakah selalu terjadi
hematoma

- Normal atau engga pada kasus minggu ini

2. Bagaimana hematoma terbentuk (patologis/physiologis)

3. Bagaimana proses physiology dari hemostasis (bagaimana tubuh mencegah perdarahan

4. apakah normal perdarahan di joint cavity & apa penyebab hemarthrosis

The exact prevalence of hemarthrosis in the hemophiliac population is unknown; however, there
have been reports that approximately 50% will develop hemarthrosis at some time during their life.
Joint trauma increases the chance of developing hemarthrosis in this population.

Traumatic hemarthrosis typically occurs in the setting of intra-articular injury with ligamentous,
osseous, and/or cartilage damage leading to a bloody synovial fluid collection. Post-operative
hemarthrosis from total knee arthroplasty has been attributed to the development of intra-capsular
vascular tissue which subsequently causes bleeding into the joint after joint replacement surgery.
The development of a lipohemarthrosis stems from marrowfat leakage into the synovial fluid; this is
usually the result of intra-capsular fractures or extensive intra-articular soft tissue injury.

5. Laboratory results interpretation

6. Cascade pembekuan darah
the factors that keeps the blood from clotting
1. endothelial cells secret NO, and PGI2 (prostacyclin) for inactivating the platelets t not bind to
endothelial

2. heparin sulfate in plasma membrane binds with antithrombin III helps to degrade clotting factors II,
IX, X (inactivated)
3. thrombomodulin in plasma membrane binds to thrombin (factor II) binds to protein C, when it
moves around thrombin it activates protein C
- protein c degrades factor V, VIII (inactivated)

Mechanisms for coagulation cascade

1. vascular spasm
definition; when there is damage to the smooth muscles/ endothelial lining the muscle will constrict to
try to not lose blood

a. endothelin
- endothelial cells will produce endothelin
- binds to calcium receptor outside the plasma membrane and it will cause contraction

b. myogenic mechanism
- when there are direct injury to smooth muscle
- the smooth muscle will always contracts

c. noicoreceptor activation
- when there are lots of inflammation cytokines being released (prostaglandins, dll)
- when they stimulate noicoreceptor, due to local inflammatoon
- initiate reflex that causes contraction

2. platelet plug formation

- when theres injury to the endothelial cells, all of the hemostasis steps are inhibited therefore the
endothelial cells will produce VON WILDEBRAND FACTOR
- the platelet will bind to Gp1b
- This bond will create ADP, Thromboxane A2, and serotonin
- ADP and TxA2 will activate the platelets and platelet aggregation will occur
- the platelets are bonded together by fibrinogen and they are linked towards GpIIb/IIIA
- thromboxane A2 and serotonin loves to bind with the smooth muscle -> contractions ->
vasoconstriction -> enhance vascular spasm

3. coagulation
- Phosphatidylserine around the platelet plugs eill create negative charge
- liver will always create clotting proteins
- factor XII interact with rhe negative charge and become factor XIIa (activated)
- factor XII activates factor XI to factor XIa
- Factor XIa activate factor IX -> IXa
- factor IXa wll activate factor VIII
- IXa (precursor PF3 + Ca++) + VIIIa -> activate factor Xa
- Xa will react with factor V
- Xa (precursor PF3 + Ca++) + V -> prothrombin activators
- factor II (thrombin) will be activated to IIa
- IIa will react with fibrinogen (soluble) will link them together
- create FIBRIN (insoluble)
- thrombin reacts with factor XIII (fibrin stablising factor) to activates it
- Factor II + XIIIa (cofactor Ca++) to crosslink fibrin -> fibrin mesh
- fibrin mesh to hold the platelet plug in place

4. clot retraction & repair

- platelet contraction
- the clot will create platelet derived growth factor (PDGF)
- will trigger the mitosis for sooth muscle
- connective tissue patches to repair collagen
- VEGF (vascular endothelial growth factor) is going to regenerate the endothelial lining

5. fibrinolysis
- the platelet plug could be so big that could cause occlusion therefore fibrinolysis needs to occur
- endothelial has tissue plasminogen activator (tPA), plasminoge is free around the blood and jt reacts
with tPA and resilting in plasmin
- plasmin loves to eat fibrin
- plasmin will release fibrinogen and D-dimer when degrading platelet plug
7. Penyakit dari masing2 interpretasi hasil lab
- etiology
- pathophysiology
- manifestasi klinis
- complication

8. management and treatment

9. all about dic