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Hemostasis > Platelets and the Vascular System > Flashcards

Platelets and the Vascular System Flashcards

1
Q

Describe the platelet maturation process, from CFU-Meg (of CFU-MK) to mature platelet.

A

The CFU-Meg (or CFU-MK) is a progenitor cell found in the bone marrow. Under the influence of humoral factors GM-CSF, IL-3 and TPO, it can differentiate into an immature megakaryocyte. Still in the BM, with further regulation from TPO, the megakaryocyte undergoes endomitosis and matures. This process takes about 4-5 days, after which the megakaryocyte enters the bone marrow sinus. Here, based on the regulation from TPO, the megakaryocyte’s cytoplasm breaks down along its demarcation membrane, producing many platelets which enter into circulation or into the spleen.

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2
Q

What is endomitosis? Is this process common to all cells, or unique to platelets?

A

Round of nuclear DNA synthesis without nuclear or cytoplasmic division

Unique to platelets

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3
Q

The four platelet zones

A

Peripheral zone
Structural zone
Organelle zone
membrane zone

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4
Q

Peripheral platelet zone

Function
Components
Membrane

A

Function: Adhesion and aggregation, contributes to platelets, overall neg charge and contain receptors

Components:
factor 5, von Willebrand factor and fibrinogen
Glycocalyx: proteins, glycoproteins and glycopolysaccharides

Membrane:
GP Ib/IX: receptor for von Willebrand factor and important for platelet adhesion

GP IIb/IIIa: receptor for Fibrinogen

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5
Q

Structural platelet zone

Function
Components

A

Function: Structure and Support

Components
• Microtubules (tubulin)
• Protein Network
o Actin 15-20% of platelet proteins
Globular (G) and Filamentus (F)—active form
o Other contractile proteins
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6
Q

Organelle platelet zone

Function
Components

A

Function: Secretion and Storage

Components:

  • Alpha and Delta Granules
  • ADP —Agonist for platelets
  • ATP —Agonist for cells other than platelets, Activates Ca+2 influx
  • Calcium—Platelet activation
  • Serotonin—Vasoconstriction; platelet agonist
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7
Q

Membrane Systems (platelet zone)

Function
Components

A

Functions: Secretion and Storage; Regulate Intracellular (Calcium)
Components:
• Open Canalicular system—connect the inside of platelet with membrane
• Dense Tubular system canals running within the cell, stores and regulates, prostaglanding and thromboxane synthesis

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8
Q

Steps of primary hemostasis

A

adhesion
aggregation
secretion
activation

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9
Q

Primary Hemostasis is measured by what?

A

Bleeding time
Platelet function test
Platelet aggregation test

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10
Q

Platelet role in adhesion

A

Platelet adheres to collagen from injured tissue with vWF as a bridge. Platelets have GPIb/IX receptors for vWF

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11
Q

Platelet role in aggregation

A
  • Changes occurs in shape (from disks to spiny spheres)
  • Metabolic biochem occurs with movement of intracellular calcium from dense bodes through the membrane to the cytoplasm. Phospholipase C and A2 and adenyl cyclase activate
  • GP IIb/IIIa receptor for fibrinogen appears
  • Membrane surface changes occur and allow coag factors to bind. Calcium, collagen and ADP are main agonists
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12
Q

Platelet role in secretion

A

The contents of the granules are secreted to the outside of the platelet through the open canalicular system after aggregation. Agonists attract more platelets

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13
Q

Platelet role in secondary hemostasis

A

Platelet contractile proteins causes the fibrin clot to shrink, which strengthens the clot. Platelets provide a surface for the reactions.

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14
Q

Describe the main functions of blood vessels in hemostasis.

A

Damaged blood vessels initiate hemostasis through vasoconstriction by interaction with thromboxane A2 and serotonin which are released from activated platelets. Heparin sulfate and thrombomodulin are released from the endothelial cells and inhibit the fibrin formation while vWF and tissue thromboplastin result in fibrin formation and platelet adhesion

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15
Q

Thrombocytopenia

A

deficiency of platelets in the blood <150 x 109/L

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16
Q

Thrombocytosis

A

disorder in which the body produces too many platelets. >400 x 109/L

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17
Q

Thrombophilia

A

tendency to form blood clots abnormally

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18
Q

Marfan Syndrome

Defective Body System
Pathophysiology
Clinical Symptoms
Diagnostic Lab Tests and Results

A

Defective Body System: Inherited Vascular disorder

Pathophysiology: Problem with Fibrillin
Abnormal structure/elasticity of vessels
Gene for fibrillin-1

Clinical Symptoms: Aortic aneurism, defects in mitral valve, death is common, long extremities hyper extendable joints

Diagnostic Lab Tests and results: Diagnosis by exclusion; bleeding time and platelet aggregation may be abnormal

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19
Q

Osteogenesis Imperfecta

Defective Body System
Pathophysiology
Clinical Symptoms
Diagnostic Lab Tests and Results

A

Defective Body System: Inherited Vascular disorder

Pathophysiology:
Patchy defective BM leading to brittle bones that fracture easily.
Gene for type 1 procollagens

Clinical Symptoms: Intercranial hemorrhage due to collapsed cranial bones, epistaxis, coughing up blood and spontaneous bruising

Diagnostic Lab Tests and results: Diagnosis by exclusion, platelet aggregation may be abnormal

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20
Q

Ehlers-Danlos Syndrome

Defective Body System
Pathophysiology
Clinical Symptoms
Diagnostic Lab Tests and Results

A

Defective Body System: Inherited Vascular disorder

Pathophysiology: Lack of collagen creating fragile vessels

Clinical Symptoms: Easy bruising, stretchable fragile skin, hyper extendable joints

Diagnostic Lab Tests and results: Diagnosis by exclusion; bleeding time may be abnormal

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21
Q

Hereditary Hemorrhagic Telangiectasia

Defective Body System
Pathophysiology
Clinical Symptoms
Diagnostic Lab Tests and Results

A

Defective Body System: Inherited Vascular disorder

Pathophysiology: No capillaries, arterioles connect directly to the venioles
Over dilation causes vessels to be thin and fragile and prone to rupture
Gene for endolin-1

Clinical Symptoms: Bleeding symptoms progress with age
Starts with Epistaxis and leads to more dangerous bleeding

Diagnostic Lab Tests and results: Diagnosis by exclusion, gene testing

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22
Q

Pseudoxanthoma Elasticum

Defective Body System
Pathophysiology
Clinical Symptoms
Diagnostic Lab Tests and Results

A

Defective Body System: Inherited Vascular disorder

Pathophysiology: Calcification of elastic tissue in skin and arteries

Clinical Symptoms: Appears 20-30 year old
Hemorrhage in GI, eyes, kidneys, nose, skin, easy bruising and petechia

Diagnostic Lab Tests and results: Diagnosis by exclusion

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23
Q

Purpura due to decreased connective tissue

Defective Body System
Pathophysiology
Clinical Symptoms
Diagnostic Lab Tests and Results

A

Defective Body System: Acquired Vascular disorder

Pathophysiology:

  • -Senile purpura: caused by ↓collagen with age, results in vessels prone to break
  • -Cushing syndrome: from supportive tissue that is weakened because of ↑ glucopolysaccharides that are present in condition or result from cortical steroid therapy
  • -Scurvy: deficiency in vit C, causes ↓collagen production resulting in vessels that are weakened

Clinical Symptoms: Bleeding, bruising and petechiae

Diagnostic Lab Tests and results: specific to cause

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24
Q

Purpura associated with paraprotein disorders

Defective Body System
Pathophysiology
Clinical Symptoms
Diagnostic Lab Tests and Results

A

Defective Body System: Acquired Vascular disorder

Pathophysiology: Paraproteins bind (deplete) calcium; paraprotein complexes deposited in vessel wall

Clinical Symptoms: Nonspecific bruising and petechia

Diagnostic Lab Tests and results: Specific to cause

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25
Q

Purpura due to vasculitis

Defective Body System
Pathophysiology
Clinical Symptoms
Diagnostic Lab Tests and Results

A

Defective Body System: Acquired Vascular disorder

Pathophysiology: Immune complexes bind to vessel wall, activating complement

Clinical Symptoms: Nonspecific bruising and petechia

Diagnostic Lab Tests and results: Specific to cause

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26
Q

Heparin induced Thrombocytopenia (HIT)

Defective Body System
Pathophysiology
Clinical Symptoms
Lab Tests

A

Defective Body System: Platelet disorder

Pathophysiology: Heparin/antibody/PF4 platelet complex initiates thrombosis, rapidly depleting platelet count

Clinical Symptoms: Thrombosis petechiae and/or bleeding

Diagnostic Lab Tests and results: Platelet count decreased
PTT increased (heparin present)
27
Q

Disseminated Intravascular Coagulation (DIC)

Defective Body System
Pathophysiology
Clinical Symptoms
Diagnostic Lab Tests and Results

A

Defective Body System: Acquired disorder of hemostasis

Pathophysiology: Consumption of coagulopathy
Systemic: circulating thrombin and unregulated platelets
Unregulated thrombin generation: depletion of I, II, V, VIII, XIII, platelet activation

Clinical Symptoms: Life threatening (50%)
Bleeding and clotting simultaneously
Acute: most common (80-90%) bleeding symptoms predominate with bleeds @ 3 or more sites
Chronic: thrombotic systems predominate leading to vessel occlusion and organ failure

Diagnostic Lab Tests and results: Platelet count decreased
PT, PTT, DD, TT elevated

28
Q

Aspirin ingestion

Defective Body System
Pathophysiology
Clinical Symptoms
Diagnostic Lab Tests and Results

A

Defective Body System: Platelet disorder

Pathophysiology: Aspirin inactivates cyclooxygenase, preventing the formation and release of ThromboxaneA2, and thus platelet secretion

Clinical Symptoms: Bleeding patients with underlying bleeding conditions or in cases of overdose

Diagnostic Lab Tests and results: Abnormal platelet aggregation test no secondary wave for ADP or epinephrine

29
Q

Acute Immune Thrombocytopenia Purpura

Defective Body System
Pathophysiology
Clinical Symptoms
Diagnostic Lab Tests and Results

A

Defective Body System: Platelet disorder

Pathophysiology: Immune mediated destruction of platelets

Clinical Symptoms: Petechiae

Diagnostic Lab Tests and results: Decreased platelet count

30
Q

Bernard Soulier Disease

Defective Body System
Pathophysiology
Clinical Symptoms
Diagnostic Lab Tests and Results

A

Defective Body System: Inherited Qualitative platelet disorder

Pathophysiology: Defective or deficient GPIb/IX receptor complex; results in platelet adhesion problems

Clinical Symptoms: Mild to severe bleeding in homozygotes

Diagnostic Lab Tests and results: abnormal platelet aggregation with ristocetin not corrected with vWF

31
Q

Glansmann’s Thrombasthenia

Defective Body System
Pathophysiology
Clinical Symptoms
Diagnostic Lab Tests and Results

A

Defective Body System: Inherited Qualitative platelet disorder

Pathophysiology: Defective or deficient GPIIb/IIIa receptor complex; results in platelet aggregation problems

Clinical Symptoms: Mild to severe bleeding in homozygotes

Diagnostic Lab Tests and results: Normal platelet count; abnormal platelet aggregation test (abnormal ADP, collage and epinephrine) increased bleeding time

32
Q

Von Willebrand disease

Defective Body System
Pathophysiology
Clinical Symptoms
Diagnostic Lab Tests and Results

A

Defective Body System: Inherited Secondary Hemostasis disorder

Pathophysiology: Genetic mutation that results in defective vWF processing or disruption of binding sites

Clinical Symptoms: mucosal and gum bleeding, epistaxis

Diagnostic Lab Tests and results:
Platelet aggregation test: Ristocetin is abnormal and Ristocetin + vWF is normal

33
Q

What is an agonist?

A

A substance that causes platelet activation

34
Q

Agonists
Strength, source, and platelet receptors

Collagen
Thrombin
Epinephrin
ADP
Serotonin
Thromboxane
PAF
A

Collagen - STRONG, Nonplatelet, GPIa/IIa, GPVI

Thrombin - STRONG nonplatelet, PAR1, PAR4

Epinephrin - weak, nonplatelet, A2 adrenergic receptor

ADP - weak, platelet, P2Y1, P2Y12

Serotonin - weak, platelet, 5HT24

Thromboxane - weak, platelet, TP

Platelet activating factor (PAF) - weak, platelet, PAFR

35
Q

List the common agonist reagents used in platelet aggregation testing, and which component of platelet function (adhesion, aggregation, secretion) it is evaluating.

ADP
Collagen
Epinephrine
Ristocetin
Ristocetin + vWF
A

ADP: primary wave (aggregation) and secondary wave (secretion)
Collagen: secretion
Epinephrine: aggregation, second wave (secretion)
Ristocetin: adhesion
Ristocetin + vWF: adhesion

36
Q

Template Bleeding Time

Purpose
Principle
Procedure
Normal Reference Intervals
Significance of Abnormal Results
A

Purpose: Evaluate the forming of the primary hemostatic plug

Principle: Measure the amount of time it takes to form the primary hemostatic plug

Procedure:
Dab filter paper on bleed every 30 seconds and count how many spots on paper

Normal Reference Intervals:
1-10 min

Significance of Abnormal Results:
↑ possible vascular or platelet problem
↓ not clinically significant

37
Q

Manual Platelet Studies

Purpose
Principle
Procedure
Normal Reference Intervals
Significance of Abnormal Results
A

Purpose: Quantitatively evaluate platelets

Principle: Count the number of platelets per a designated unit

Procedure (include calculation):
Manual (Hemocytometer) and Automated

Normal Reference Intervals:
150,000-400,000/uL

Significance of Abnormal Results:
↑ thrombocytosis
↓ Thrombocytopenia

38
Q

Platelet Aggregation Studies

Purpose
Principle
Procedure
Normal Reference Intervals

A

Purpose: Qualitatively evaluate platelets

Principle: Measures % transmittance in patient’s plasma after being mixed with agonist

Procedure:
Varying reagent agonists are added to whole blood sample; platelet aggregation monitored by aggregometry, producing a pattern or curve that is compared to a normal curve to determine the type of faulty platelet function

Normal Reference Curves:
ADP, Epinephrine — has two waves
Collagen, Ristocetin, Ristocetin + vWF – only one wave

39
Q

Platelet Estimate (from a peripheral blood smear)

Purpose
Procedure
Normal Reference Intervals
Significance of Abnormal Results

A

Purpose: screen peripheral blood for platelet quantity; verify automated platelet count

Procedure: Determine the average # of platelets per 100x field; multiply average by 20,000 to get /uL

Normal Reference Intervals: Should correlate with automated value

Significance of Abnormal Results: indicates problem with the automated analyzer

40
Q

Platelets

Production
Distribution
Lifespan
Normal Reference Intervals
Morphology
A

Production: Demarcation membranes form throughout megakaryocyte cytoplasm forming proplatelets that further breakdown into platelets

Distribution: 2/3 in active circulation, 1/3 sequestered in spleen

Lifespan: 9-12 days in circulation

Normal Peripheral Blood Reference Intervals: 150-400 x 109/L (150,000-450,000/uL)

Morphology: 2-3um; anuclear; granular; irregular (heterogeneous) shape

41
Q

Megakaryocytes

Distribution
Lifespan
Normal Reference Intervals
Morphology

A

Distribution: Bone Marrow

Lifespan: ~7 days in BM and eventually breaks down into platelets

Normal Bone Marrow Reference Intervals: ~1-3/lpf (10x) feather edge of smear

Morphology: (Stage 1&2) High N:C ratio; cytoplasm more blue; agranular, single lobed nucleus that may have nuclei; fine chromatin in nucleus
(Stage 3&4) Low N:C ratio; abundant, granular cytoplasm with a lavender color; multi-lobed nucleus with condensed chromatin

42
Q

Describe how (ex. falsely increase, falsely decrease, no impact) and why each of the following might impact an automated platelet count result.

Presence of EDTA-induced clumping

A

False decrease; analyzer does not count platelet in the clump

43
Q

Describe how (ex. falsely increase, falsely decrease, no impact) and why each of the following might impact an automated platelet count result.

A clotted EDTA sample

A

Falsely decreased (they are all in clot and not counted)

44
Q

Describe how (ex. falsely increase, falsely decrease, no impact) and why each of the following might impact an automated platelet count result.

A sample showing platelet satellitism

A

Platelets surround WBCs and don’t get counted causing a falsely low count

45
Q

Describe how (ex. falsely increase, falsely decrease, no impact) and why each of the following might impact an automated platelet count result.

A patient with many larger than normal platelets

A

Counted as different cell, falsely decrease count

46
Q

Describe how (ex. falsely increase, falsely decrease, no impact) and why each of the following might impact an automated platelet count result.

A patient with many RBC schistocytes present

A

False increase; RBC fragments are counted as platelets

47
Q

Describe how (ex. falsely increase, falsely decrease, no impact) and why each of the following might impact an automated platelet count result.

A patient that has taken aspirin

A

No impact; aspirin impacts function not quantity

48
Q

What is aspirin’s “mode of action”?

A

Aspirin interferes with prostaglandins. It irreversibly inhibits cyclo-oxygenase which is an enzyme needed to make Thromboxane A2 (TXA2). During platelet secretion, TXA2 is released to further activate the platelet.

The normal pathway of TXA2 synthesis:
Increased Phosopholipase A2 causes the release of increased amounts of Arachidonic Acid. Cyclo-oxidase converts Arachidonic Acid to PGG2; PGG2 is converted to TXA2 by Thromboxane synthase.

49
Q

What impact does aspirin have on platelet function?

A

Stops the production of Thromboxane A2 (TXA2) which is a platelet activation enhancer

50
Q

Which of the following laboratory tests would be impacted by aspirin ingestion and what specific effect would it have on the results?

Template bleeding time:

A

Would be prolonged because the activation is affected, therefore the platelet would struggle to form the platelet plug.

51
Q

Which of the following laboratory tests would be impacted by aspirin ingestion and what specific effect would it have on the results?

Platelet aggregation studies:

A

The second wave of aggregation would not occur (where platelets respond to their own agonists) because the activation is inhibited

52
Q

Which of the following laboratory tests would be impacted by aspirin ingestion and what specific effect would it have on the results?

Platelet function test:

A

It would be affected because TXA2 is not produced

53
Q

Which of the following laboratory tests would be impacted by aspirin ingestion and what specific effect would it have on the results?

Platelet count:

A

Not affected

54
Q

Which of the following laboratory tests would be impacted by aspirin ingestion and what specific effect would it have on the results?

Clotting times (ex. PT, aPTT):

A

No impact because they evaluate clotting factors not platelets

55
Q

Hemolytic Uremic Syndrome

Pathophysiology
Symptoms

A

Pathophysiology: verotoxin producing E coli (VTEC) or inherited, Likely due to toxin induced endothelial damage (primarily in renal glomeruli) that results in microvascular thrombi
Symptoms: Hemolytic anemia, acute renal failure that is more severe than TTP, thrombocytopenia, CNS involvement, microangiopathic hemolytic anemia, fever

56
Q

Neonatal Alloimmune Thrombocytopenia

A

HPA-1a is most common platelet antigen (97% population has this antigen)
Maternal IgG anti-HPA-1a—can cross placenta and attack baby’s platelets

57
Q

Posttransfusion Purpura

A

Rare, results in abrupt bleeding of mucous membranes and lasts 2-6 weeks
7-10 days post transfusion
The donor contains Anti-HPA-1a, when given, attacks the platelets of receiver

58
Q

Thrombotic Thrombocytopenic Purpura

A

Large vWF multimers attach to platelet surface—induce agglutination
Acquired or inherited deficiency of ADAMTS-13 (responsible for cleaving large vWF multimers)

Blood smear: acanthocyte, schistocytes, micro RBCs, and platelets

59
Q

Increased Splenic Sequestration of Platelets

A

Normally—spleen sequesters 1/3 of platelets from BM

Usually the platelet count doesn’t drop below 20 x 109/L therefore not life threatening

60
Q

Dilutional Thrombocytopenia

A

Caused by massive hemorrhage, occurs when patients recieve disproportionate amount of RBCs than platelets in transfusion
>10 units packed RBCs in 24 hours
Platelets and plasma proteins become depleted in proportion to amount of RBCs

61
Q

Primary Thrombocytosis

A

Platelet count: >1,000,000/uL

Pathophysiology: Essential Thrombocytosis, CML, Myeloproliferative diseases
Labs: Platelet count increased, Abnormal platelet aggregation test

62
Q

Secondary Thrombocytosis

A

Platelet count <1,000,000/uL

Pathophysiology: surger, IDA, recovery from thrombocytopenia
Lab: Platelet count, Diagnosis of underlying condition

63
Q

Discuss the function of thromboxane A2 and prostacyclin in the regulation of the kinetics of platelets

A

Arachidonic acid transforms into thromboxane A2 or prostacyclin depending on physiologic need

Thromboxane A2 is an aggregating agent and constricts the blood vessels
Prostacyclin is an anti-aggregating agent a strong platelet inhibitor and vasodilator

Hemostasis (3 decks)

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