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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
Q

What are the two tubular systems and their function?

A
  • 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.
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26
Q

What are the two types of granules? What each of them composed of?

A
  • Alpha granules: receptors + integrins; adhesion molecules; secondary hemostasis factors.
  • Dense (delta) granules: platelet activation factors; endothelial activity.
27
Q

What are the common thing between alpha and dense granules?

A

They both contain GP1b and GP2b2a.

28
Q

What are the roles of platelets in hemostasis?

A
  • Primary hemostasis: form platelet plug upon injury.
  • Secondary hemostasis: facilitate fibrin formation.
  • Strengthen clot formation.
29
Q

Describe the process of platelet adhesion?

A

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
Q

What are the factors/molecules that keep platelet quiet in its resting state?

A
  • Prostaglandin i2 (PGI2) - suppress PLT functions/activities
  • ADPase - degrade ADP (platelet activator)
  • Nitric Oxide (NO) - suppress PLT adhesion, activation, aggregation
31
Q

Name all the factors that can activate platelet.

A
  • Binding interactions: GP1b-vWF; GP6-collagen.
  • Soluble mediators: TXA2 (thromboxane A2); ADP; thrombin
32
Q

What is the result of platelet activation?

A
  • Shape change
  • Granule content secretion
  • TXA2 synthesis + release
  • Recruit other platelets
  • Aggregation
33
Q

How does given aspirin helps with a heart attack?

A

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
Q

Describe a platelet shape change once activated?

A

Shift from discoid, smooth surface to spheroid with cytoplasmic projections. Later, they shift to flat form to cover vascular defect.

35
Q

Describe what happens during platelet aggregation event?

A
  • Conformational change in GP2b3a to make it high affinity binding state to bind fibrinogen.
  • Fibrinogen cross link many platelets to form aggregation.
36
Q

What is the end product of aggregation?

A

The platelet plug = the end of primary hemostasis.

37
Q

What molecules help to dock critical coagulation factors to platelet plug surface?

A

Phosphatidylserine and locally released Calcium. This is the beginning of the coagulation cascade.

38
Q

What are the 2 hemostatic defect? What issues are each dealing with?

A
  • Primary hemostatic defect = issue with platelet numbers, platelet function, vWF, or endothelium.
  • Secondary hemostatic defect = issue with coagulation factors.
39
Q

What hemostatic disorder do petechia and ecchymosis considered as?

A

Primary (aka low volume hemorrhage)

40
Q

What is the marker for secondary hemostatic disorder (hint: volume)?

A

High volume bleeding into cavities.
Hemothorax, hemoabdomen, etc.

41
Q

Patient presented with hematuria, epistaxis, hematochezia, and hematemesis. What is your Ddx and issues are you looking at?

A
  • Primary hemostatic defects
  • Issues to test: thrombocytopenia, thrombopathia (abnormal PLT function), vW disease, vasculopathy (endothelium disfunction).
42
Q

Patients present with hemoabdomen, hemothorax, or hemathrosis. What is your Ddx and what issues are you looking at?

A
  • Secondary hemostatic defects
  • Coagulation cascade disorders
43
Q

What blood tube do you use to get platelet count from a CBC?

A

EDTA anticogulated blood on LTT.

44
Q

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?

A

Yes, blue top okay. Add 10% to platelet count.

45
Q

What is the main platelet metric we consider for increase or decrease PLT numbers?

A

Platelet count

46
Q

What are the consequences of platelet clumping?

A
  • Decrease platelet count
  • Increase mean platelet volume (MPV)
  • Pseudothrombocytopenia = occurs commonly with cats and horses.
47
Q

What do you do when your CBC machine tells you that your patient is thromobocytopenic?

A

Manual platelet count

48
Q

What does platelet size tell us?

A

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
Q

What are the causes of regenerative thrombocytopenia?

A
  • Platelet consumption/utilization
  • Platelet destruction
50
Q

What are the number one breed that has the genetic disease relating to PLT?

A

Cavalier King Charles Spaniels (50%) with their lovely congenital macrothrombocytopenia.

51
Q

What is PCT? What does it measure?

A

PCT = Proportion of whole blood occupied by platelets. This represents platelet mass.

52
Q

When is the appropriate time to perform BMBT and what is the result tells you?

A

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
Q

How to evaluate vW factor? What does the result tell us?

A
  • 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
Q

What are the subtypes of vWD? Which one is the most common?

A
  • Type 1: decreased but still present vWF. Most common (shows in Doberman).
  • Type 2: inadequate vWF multimers.
  • Type 3: complete absence of vWF.
55
Q

What are the major mechanisms of thrombocytopenia?

A
  • Increased PLT consumption/utilization
  • Increase PLT destruction
  • Increase PLT sequestration
  • Decreased PLT production
56
Q

What are the 2 hallmarks of magnitude of thrombocytopenia?

A

<20K = Spontaneous hemorrhage
<50K = excessive surgical bleeding

57
Q

What are the causes of increased platelet consumption? What hallmark do you see in increased PLT consumption? (Hint: a parameter in CBC)

A
  • Severe trauma
  • Vasculitis
  • DIC
  • Sepsis
  • Viper envenomation

Increase MPV = regenerative thrombocytopenia.

58
Q

What are the causes of increased platelet destruction? What hallmark do you see in increased PLT consumption? (Hint: a parameter in CBC)

A
  • ITP** [a dog with PLT count <50K!!]
  • Infectious agent (tick-borne dz)

Increase MPV = regenerative thrombocytopenia in some cases.

59
Q

What is the signs for increased PLT sequestration?

A
  • Normal MPV, normal PLT mass.
  • Mild thromobocytopenia.
  • NO petechia or ecchymosis
  • Will never result in spontaneous hemorrhage.
60
Q

If you have low PLT due to bone marrow disease, will you see regenerative response?

A

NO.

61
Q

What are the two types of platelet dysfunction disorders (thrombopathia)?

A
  • Acquired: medication, uremic acid (CKD or diabetes), hypergammaglobulinemia.
  • Inherited: very rare.
62
Q

What are the 4 mechanisms of thromobocytosis?

A

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
Q

What are the two species that have more platelets than other species?

A

Ruminants and mice have 2-3x the number of platelets than other species.

402 Exam 3 (2 decks)

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