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402 Exam 3 > Platelet > Flashcards

Platelet Flashcards

1
Q

What is hemostasis? What mediates it?

A
  • Physiologic process by which bleeding is stopped.
  • Mediated by blood vessels (endothelium), platelets, plasma (coag) factors.
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2
Q

What are the consequences of disruption of hemostasis systems?

A
  • Bleeding disorder (aka hemorrhage)
  • Thrombotic disorder (aberrent clotting events) causes thromboembolic event (aka clot).
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3
Q

True or False:
Hemostasis is a highly regulated and complex process that leads to systemic response and repair of damaged vasculature.

A

False.
Not systemic, only localized.

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4
Q

How many phases of hemostasis? What happened in each stage? What are the factors that involved in each stage?

A
  • 3 stages:

1) Primary hemostasis: Start with vascular damage event, end with formation of platelet plus. Involves endothelium, sub-endothelial connective tissue, and platelets.

2) Secondary hemostasis: Start with formation of platelet plug, end with formation of fibrin clot. Involves platelets and coag factors.

3) Tertiary hemostasis: Start with clot remodeling, end with dissolution of fibrin clot + vascular repair. Involves endothelium, anti-thrombotic factors, and fibrin clot.

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5
Q

What does the term “coagulation cascade” refer to?

A

Secondary hemostasis (phase 2 of hemostasis)

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6
Q

True or False: Hemostasis phases work independently and go step by step.

A

False. All phase overlap and are mutually integrated. They facilitate each other!!

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7
Q

Define platelets and its function.

A
  • Platelet is anucleate cell with 2 main functions: principal facilitators of primary hemostasis; set the stage for coagulation cascade.
  • Other function: immune cells (innate/adaptive), immunothrombosis (lock down foreign invaders by throw a clot), platelet derived growth factor.
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8
Q

Compare platelet with thrombocytes

A
  • Platelets: in mammals, discoid shape 2-5 um, anucleated.
  • Thrombocyte: in birds, reptiles, fish; round to oval shape 5-10 um, nucleated.
  • Functions are IDENTICALLLL!!
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9
Q

Where does thromobopoiesis take place?

A

Mainly in bone marrow; 2nd site is spleen, lungs, liver.

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10
Q

Maturation sequence of platelet? Start from HSC. What cell is the precursor of platelet?

A

HSC > CMP (common myeloid progenitor) > Megakaryoblast > Promegakaryocyte > Megakaryocyte.

  • Megakaryoblast is the earliest identiable stage of platelet.
  • Precursor of PLT = megakaryocyte.
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11
Q

Characters of megakaryocyte?

A
  • Large with multi-nucleation and granular cytoplasm.
  • Endomitosis to produce up to 16 nuclei to support high volume synthesis of platelet.
  • Produce up to 1000 platelets in a lifespan.
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12
Q

How does platelet get into vascular lumen?

A

Megakaryocyte extend PROTOPLATELET cytoplasmic extensions into vascular lumen. Platelet beads bud off into vasculature to become platelets.

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13
Q

What regulates thrombopoiesis?

A
  • TPO (thrombopoietin): primary regulatory hormone that stimulates platelet production.
  • Inflammatory cytokines: IL-6, GM-CSF, IL-11, IL-3.
  • EPO (erythropoietin)
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14
Q

Where is TPO come from?

A

Primarily produced in LIVER by hepatocytes.
Secondary at kidney and bone marrow stromal elements (serve as back-up site).

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15
Q

Explain mechanism of TPO in terms of how it induces platelet production.

A
  • TPO is regulated by total platelet mass.
  • Platelets hold TPO on their surface, internalize and destroy to limit the amount of free TPO in plasma.
  • Low platelet mass leads to less platelets available to hold TPO. Thus increase in free TPO in plasma.
  • These free TPO binds to TPO receptors on megakaryocytes to induce platelet production.
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16
Q

Relationship between TPO and platelet count.

A

Higher platelet count = LOWER TPO.

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17
Q

What is the effect of TPO on megakaryocytes?

A
  • Cut maturation time to accelerate maturation process.
  • Increase megakaryocyte size and numbers.
  • Increase multinucleation.
  • Result in increase platelet production
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18
Q

What is the lifespan of platelet?

A

4-6 days (either in circulation or splenic reservoir).

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19
Q

What organ is platelet reservoir? What do they do?

A

Spleen. They release platelets immediately into circulation if immediate hemostasis need.

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20
Q

How can platelet be removed from circulation?

A

Desialylation = decrease sialic acid on platelet surface. Platelet is internalized by hepatocytes (mostly) or splenic macrophages.

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21
Q

What are the 2 important features for membrane components?

A
  • Phospholipids
  • [Binding] integrins
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22
Q

Describe what happened to phospholipids during resting stage and activation stage. Name the one phospholipid that is a strong procoagulant.

A
  • At rest: neutral phospholipids externally = hemostatic-quiet surface.
  • In activation: procoagulant activity (negative charged phospholipids flip to the surface). PHOSPHATIDYLSERINE is a strongly procoagulant to recruit coag factors to surface of platelet.
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23
Q

What are the important integrins in the membrane components?

A
  • GP1b: bind vWF; helps tether platelets to damage site.
  • GPVI (GP6): binds collagen; helps tether platelets to damage site.
  • GPIIb/IIIa (2b/3a): binds fibrinogen; helps crosslink platelets (aggregation).
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24
Q

What feature in the cytoskeleton does platelet have to follow significant shape change?

A
  • They have circumferential coils of microtubules and microfilaments that allow shape change, release granular constituent into canalicular system to go out in the extracellular space, facilitates clot retraction.
  • At rest: smooth and discoid
  • Activated stage: spherical and spiny
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25
What are the two tubular systems and their function?
- Open canalicular system: facilitate release of granule products to external surface. - Dense tubular system: modify smooth ER and sequester (hide) Ca2+. Calcium got released with platelet activation. Facilitate Thromboxane A2 synthesis.
26
What are the two types of granules? What each of them composed of?
- Alpha granules: receptors + integrins; adhesion molecules; secondary hemostasis factors. - Dense (delta) granules: platelet activation factors; endothelial activity.
27
What are the common thing between alpha and dense granules?
They both contain GP1b and GP2b2a.
28
What are the roles of platelets in hemostasis?
- Primary hemostasis: form platelet plug upon injury. - Secondary hemostasis: facilitate fibrin formation. - Strengthen clot formation.
29
Describe the process of platelet adhesion?
When blood vessel is damaged: - Reflex vasoconstriction to slow platelets down to interact with sub endothelial connective tissues. - Exposed subendothelial connective tissue contained multimer stacks of vWF tethers down and activate platelets. - Platelets bind vWF by GP2b integrin to tether platelets to vascular defect. - Tethering change GP6 integrin to more functional state which further anchor platelets and form initial platelet monolayer.
30
What are the factors/molecules that keep platelet quiet in its resting state?
- Prostaglandin i2 (PGI2) - suppress PLT functions/activities - ADPase - degrade ADP (platelet activator) - Nitric Oxide (NO) - suppress PLT adhesion, activation, aggregation
31
Name all the factors that can activate platelet.
- Binding interactions: GP1b-vWF; GP6-collagen. - Soluble mediators: TXA2 (thromboxane A2); ADP; thrombin
32
What is the result of platelet activation?
- Shape change - Granule content secretion - TXA2 synthesis + release - Recruit other platelets - Aggregation
33
How does given aspirin helps with a heart attack?
Aspirin inhibits COX-1 which is involved in synthesis of TXA2 - a potent recruiter and activator of platelets. Given Aspirin can knock out / attenuate platelet functionality.
34
Describe a platelet shape change once activated?
Shift from discoid, smooth surface to spheroid with cytoplasmic projections. Later, they shift to flat form to cover vascular defect.
35
Describe what happens during platelet aggregation event?
- Conformational change in GP2b3a to make it high affinity binding state to bind fibrinogen. - Fibrinogen cross link many platelets to form aggregation.
36
What is the end product of aggregation?
The platelet plug = the end of primary hemostasis.
37
What molecules help to dock critical coagulation factors to platelet plug surface?
Phosphatidylserine and locally released Calcium. This is the beginning of the coagulation cascade.
38
What are the 2 hemostatic defect? What issues are each dealing with?
- Primary hemostatic defect = issue with platelet numbers, platelet function, vWF, or endothelium. - Secondary hemostatic defect = issue with coagulation factors.
39
What hemostatic disorder do petechia and ecchymosis considered as?
Primary (aka low volume hemorrhage)
40
What is the marker for secondary hemostatic disorder (hint: volume)?
High volume bleeding into cavities. Hemothorax, hemoabdomen, etc.
41
Patient presented with hematuria, epistaxis, hematochezia, and hematemesis. What is your Ddx and issues are you looking at?
- Primary hemostatic defects - Issues to test: thrombocytopenia, thrombopathia (abnormal PLT function), vW disease, vasculopathy (endothelium disfunction).
42
Patients present with hemoabdomen, hemothorax, or hemathrosis. What is your Ddx and what issues are you looking at?
- Secondary hemostatic defects - Coagulation cascade disorders
43
What blood tube do you use to get platelet count from a CBC?
EDTA anticogulated blood on LTT.
44
If you don't have LTT for CBC, can you use blue top for platelet count? Is there add'l step you do to get an accurate count?
Yes, blue top okay. Add 10% to platelet count.
45
What is the main platelet metric we consider for increase or decrease PLT numbers?
Platelet count
46
What are the consequences of platelet clumping?
- Decrease platelet count - Increase mean platelet volume (MPV) - Pseudothrombocytopenia = occurs commonly with cats and horses.
47
What do you do when your CBC machine tells you that your patient is thromobocytopenic?
Manual platelet count
48
What does platelet size tell us?
Younger platelets are bigger. If thrombocytopenia and have large platelet, it means bone marrow megakaryocytes are making new platelets. Hence, high MPV with low PLT = regenerative thrombocytopenia.
49
What are the causes of regenerative thrombocytopenia?
- Platelet consumption/utilization - Platelet destruction
50
What are the number one breed that has the genetic disease relating to PLT?
Cavalier King Charles Spaniels (50%) with their lovely congenital macrothrombocytopenia.
51
What is PCT? What does it measure?
PCT = Proportion of whole blood occupied by platelets. This represents platelet mass.
52
When is the appropriate time to perform BMBT and what is the result tells you?
Buccal mucosal bleeding time is useful to perform to confirm primary hemostatic problem. They usually perform after CBC and normal PLT count. If the result is >4 mins, then it tells you your patient have thrombocytopenia, thrombopathia, vWD, vasculopathy.
53
How to evaluate vW factor? What does the result tell us?
- Use vWF antigen assay (vWF:Ag) - This is an ELISA assay that compares patient vWF amount to healthy dog pool vWF amount. Result is % activity. - If <50%, patient is positive for vWD. If <35%, patient is at risk of hemorrhage.
54
What are the subtypes of vWD? Which one is the most common?
- Type 1: decreased but still present vWF. Most common (shows in Doberman). - Type 2: inadequate vWF multimers. - Type 3: complete absence of vWF.
55
What are the major mechanisms of thrombocytopenia?
- Increased PLT consumption/utilization - Increase PLT destruction - Increase PLT sequestration - Decreased PLT production
56
What are the 2 hallmarks of magnitude of thrombocytopenia?
<20K = Spontaneous hemorrhage <50K = excessive surgical bleeding
57
What are the causes of increased platelet consumption? What hallmark do you see in increased PLT consumption? (Hint: a parameter in CBC)
- Severe trauma - Vasculitis - DIC - Sepsis - Viper envenomation Increase MPV = regenerative thrombocytopenia.
58
What are the causes of increased platelet destruction? What hallmark do you see in increased PLT consumption? (Hint: a parameter in CBC)
- ITP**** [a dog with PLT count <50K!!] - Infectious agent (tick-borne dz) Increase MPV = regenerative thrombocytopenia in some cases.
59
What is the signs for increased PLT sequestration?
- Normal MPV, normal PLT mass. - Mild thromobocytopenia. - NO petechia or ecchymosis - Will never result in spontaneous hemorrhage.
60
If you have low PLT due to bone marrow disease, will you see regenerative response?
NO.
61
What are the two types of platelet dysfunction disorders (thrombopathia)?
- Acquired: medication, uremic acid (CKD or diabetes), hypergammaglobulinemia. - Inherited: very rare.
62
What are the 4 mechanisms of thromobocytosis?
1) Excitation = splenic contraction, epinephrine response. 2) Inflammation (chronic) = sterile or infections 3) Iron deficiency anemia = GI blood loss, platelets try to patch up the wound in mucosa. 4) Neoplasia: paraneoplastic (other tumor drives platelet increase); essential thrombocytosis (megakaryocyte neoplasia).
63
What are the two species that have more platelets than other species?
Ruminants and mice have 2-3x the number of platelets than other species.

402 Exam 3 (2 decks)

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