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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
Purpura due to vasculitis Defective Body System Pathophysiology Clinical Symptoms Diagnostic Lab Tests and Results
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
26
Heparin induced Thrombocytopenia (HIT) Defective Body System Pathophysiology Clinical Symptoms Lab Tests
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
Disseminated Intravascular Coagulation (DIC) Defective Body System Pathophysiology Clinical Symptoms Diagnostic Lab Tests and Results
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
Aspirin ingestion Defective Body System Pathophysiology Clinical Symptoms Diagnostic Lab Tests and Results
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
Acute Immune Thrombocytopenia Purpura Defective Body System Pathophysiology Clinical Symptoms Diagnostic Lab Tests and Results
Defective Body System: Platelet disorder Pathophysiology: Immune mediated destruction of platelets Clinical Symptoms: Petechiae Diagnostic Lab Tests and results: Decreased platelet count
30
Bernard Soulier Disease Defective Body System Pathophysiology Clinical Symptoms Diagnostic Lab Tests and Results
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
Glansmann's Thrombasthenia Defective Body System Pathophysiology Clinical Symptoms Diagnostic Lab Tests and Results
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
Von Willebrand disease Defective Body System Pathophysiology Clinical Symptoms Diagnostic Lab Tests and Results
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
What is an agonist?
A substance that causes platelet activation
34
Agonists Strength, source, and platelet receptors ``` Collagen Thrombin Epinephrin ADP Serotonin Thromboxane PAF ```
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
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 ```
ADP: primary wave (aggregation) and secondary wave (secretion) Collagen: secretion Epinephrine: aggregation, second wave (secretion) Ristocetin: adhesion Ristocetin + vWF: adhesion
36
Template Bleeding Time ``` Purpose Principle Procedure Normal Reference Intervals Significance of Abnormal Results ```
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
Manual Platelet Studies ``` Purpose Principle Procedure Normal Reference Intervals Significance of Abnormal Results ```
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
Platelet Aggregation Studies Purpose Principle Procedure Normal Reference Intervals
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
Platelet Estimate (from a peripheral blood smear) Purpose Procedure Normal Reference Intervals Significance of Abnormal Results
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
Platelets ``` Production Distribution Lifespan Normal Reference Intervals Morphology ```
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
Megakaryocytes Distribution Lifespan Normal Reference Intervals Morphology
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
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
False decrease; analyzer does not count platelet in the clump
43
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
Falsely decreased (they are all in clot and not counted)
44
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
Platelets surround WBCs and don't get counted causing a falsely low count
45
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
Counted as different cell, falsely decrease count
46
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
False increase; RBC fragments are counted as platelets
47
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
No impact; aspirin impacts function not quantity
48
What is aspirin's "mode of action"?
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
What impact does aspirin have on platelet function?
Stops the production of Thromboxane A2 (TXA2) which is a platelet activation enhancer
50
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:
Would be prolonged because the activation is affected, therefore the platelet would struggle to form the platelet plug.
51
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:
The second wave of aggregation would not occur (where platelets respond to their own agonists) because the activation is inhibited
52
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:
It would be affected because TXA2 is not produced
53
Which of the following laboratory tests would be impacted by aspirin ingestion and what specific effect would it have on the results? Platelet count:
Not affected
54
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):
No impact because they evaluate clotting factors not platelets
55
Hemolytic Uremic Syndrome Pathophysiology Symptoms
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
Neonatal Alloimmune Thrombocytopenia
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
Posttransfusion Purpura
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
Thrombotic Thrombocytopenic Purpura
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
Increased Splenic Sequestration of Platelets
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
Dilutional Thrombocytopenia
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
Primary Thrombocytosis
Platelet count: >1,000,000/uL Pathophysiology: Essential Thrombocytosis, CML, Myeloproliferative diseases Labs: Platelet count increased, Abnormal platelet aggregation test
62
Secondary Thrombocytosis
Platelet count <1,000,000/uL Pathophysiology: surger, IDA, recovery from thrombocytopenia Lab: Platelet count, Diagnosis of underlying condition
63
Discuss the function of thromboxane A2 and prostacyclin in the regulation of the kinetics of platelets
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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