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Pathology > Hemostasis > Flashcards

Hemostasis Flashcards

1
Q

What is hemostasis?

A

The process to stop bleeding. It is the 1st stage of wound healing.
-Primary, Secondary and Tertiary

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2
Q

What are the processes involved in hemostasis?

A
  • vasoconstriction
  • platelet activation
  • coagulation
  • fibrinolysis
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3
Q

What is primary hemostasis?

A

Form weak plug.

- mediated by interaction between wall and platelets

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4
Q

What is secondary hemostasis?

A

Formation of stabilized platelet plug.

-mediated by coagulation cascade

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5
Q

Steps of primary hemostasis

A

1) Vasoconstriction
- neural stim’n and endothelin released from endothelial cells
2) Platelet adhesion
3) Platelet degranulation
4) Platelet aggregation

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6
Q

Steps of primary hemostasis

A

1) Vasoconstriction
- neural stim’n and endothelin released from endothelial cells

2) Platelet adhesion
- vWF binds to exposed collagen, platelets adhere to vWF via GP1b Rc

3) Platelet degranulation
- adhesion induces change in shape of platelets causing release: ADP, TXA and Ca++

4) Platelet aggregation
- platelets aggregate @ injured site via GPIIb/IIIa using fibrinogen to link molecules
- TXA promotes aggregation

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7
Q

Where does the vWF derive from?

A
  • Endothelial cells (Weibel Palade bodies)

- alpha granules of platelets

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8
Q

What is thrombophilia?

A

Increased risk of thrombosis.

State of hypercoagulability/prothrombic state

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9
Q

What are the risks associated to having thrombophilia?

A

HEREDITARY:

  • factor V (Leyden) mutation
  • anti-thrombin III deficiency

ACQUIRED:

  • lung immobilization
  • contraceptives (estrogen increases coagulation factors in liver)
  • atrial fibrillation
  • smoking
  • obesity
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10
Q

A disorder in primary hemostasis is typically due to what?

A

Platelet abnormalities

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11
Q

What’s the difference between: petechia, ecchymoses and purpura?

A

They are all signs of bleeding in the skin, but differ in size.
Petechia: 1-2 mm
Ecchymoses: >3 mm
Purpura: > 1 cm

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12
Q

What complication can occur with severe thrombocytopenia?

A

Intracranial bleeding

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13
Q

If bleeding time is prolonged, what problem does this indicate….?

A

Primary hemostasis problem i.e. with platelet disorders

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14
Q

What would be assessed in a bone marrow biopsy for primary hemostasis abnormality?

A

Assess megakaryoctes, because they produce thrombocytes (platelets), which is the underlying cause of 1’ hemostasis abnormalities

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15
Q

What is immune thrombocytopenia (aka immune thrombocytopenic purpura ITP)

A

An autoimmune disease where auto-antibodies produced in the spleen bind platelets, which are consumed by splenic macrophages causing thrombocytopenia.

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16
Q

Describe microangiopathic hemolytic anemia?

A

Pathologic formation of micro thrombi in vessels causing platelet consumption because platelets keep going to site of thrombi and are being used up at a higher rate than normal. Results in hemolytic anemia.
The thrombi that form cause RBCs passing by to be sheared, creating a “schistocyte” RBC (helmet-like appearance of cell)

17
Q

In what conditions is microangiopathic hemolytic anemia typically seen in?

A
  • HUS (hemolytic uremic syndrome)
  • thrombotic thrombocytopenic purpura
  • HELLP syndrome
  • malignant hypertension
18
Q

What is HUS ? What is it characterized by?

A 
Hemolytic uremic syndrome is due to endothelial damage due to drugs or infection. 
Characterized by: 
1) thrombocytopenia
2) microangiopathic hemolytic anemia
3) and acute renal failure
19
Q

What is Bernard-Soulier syndrome?

A

Defect in platelet plug formation due to GpIb deficiency. This causes a problem with platelets adhering to vWF.

20
Q

What is Glanzmann thrombasthenia?

A

GpIIb/IIIa deficiency. Platelet to platelet aggregation is impaired. Thus, no platelet plug can form.

21
Q

What cascade do we measure with aPTT?

A

-Intrinsic + common cascade

22
Q

What cascade do we measure with PTT?

A

Extrinsic + common cascade

23
Q

What cascade do we measure with thrombin time?

A

Common

24
Q

What is tertiary hemostasis?

A

Dissolution of the fibrin clot (fibrinolysis)

25
Q

Which blood cells are nucleus free?

A
  • RBCs

- Platelets

26
Q

What does D-dimer measure? What is it the best screening test for?

A

It is released when when cross-linked fibrin is split! (NOT splitting of fibrinogen)
Best used for screening for:
-DIC
- to rule out DVT

27
Q

What does alpha-2-antiplasmin do? What disease state is this reduced in?

A

Inhibits plasmin breaking down fibrin, thus no fibrinolysis.
Cirrhosis of liver –> reduced a2-antiplasmin

28
Q

What can cause DIC?

A 
"STOP Making New Thrombi"
S-epsis  (-ve gram bacteria) 
T-rauma
O-bstetrics
P-ancreatitis (Acute)

M-alignancy
N-ephrotic syndrome
T-ransfusions

  • adenocarcinoma; ,mucin activates aggregation
  • snake bite; venom can also induce aggregation
29
Q

What is Virchow’s triad?

A

The 3 main categories thought to contribute to thrombosis:

1) Blood flow disruption
- stasis
- turbulence
2) Endothelial injury
3) Hypercoagulability

30
Q

What are lines of zahn?

A

Characteristic appearance of a thrombus where there is an alternating layer between platelets/fibrin (light) and RBCs (dark)

31
Q

How can you distinguish a thrombus from postmortem clot?

A
  • look for lines of Zahn on thrombus (alternating bw light and dark, i.e. platelets/fibrin and RBCs)
  • attachment to vessel wall (thrombus)
32
Q

How do endothelial cells prevent thrombosis?

A
  • block exposure to sub endothelial collagen and underlying tissue factor
  • release prostacyclin and NO (blocks platelet aggregation and vasodilator)
  • secrete heparin-like molecules which helps augment antithrombin (III) which inactivates thrombin and coagulation factors
  • secrete tPA (tissue plasminogen activator)
  • secrete thrombomodulin
33
Q

What are the main causes of endothelial damage?

A
  • vasculitis
  • atherosclerosis
  • high homocysteine ( Vit B12 and folate deficiency)
34
Q

What happens in vit B12 and folate deficiency?

A

There is no conversion from homocysteine to methionine, thus there is a build-up of homocysteine causing damage to endothelial cells.
Since folate contributes to synthesis of DNA precursors, this may also be affected.

Pathology (13 decks)

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