Hemostasis Flashcards
Disease States #79
Herparin induced thrombocytopenia (HIT) is an immune mediated complication associated with heparin therapy. Antibodies are produced against:
* ACLA
* PF4
* AT
* B2GP1
PF4
ACLA (anti-cardiolipin antibody) and B2GP1 (β-2-glycoprotein-1) are seen in antiphospholipid syndrome
Disease States #81
A 60-year-old man has a painful right knee and a slightly enlarged spleen. Hematology results include:
* Hemoglobin – 15g/dL
* Absolute neutrophil count – 10.0 x 10^3/μL
* Platelet count – 900 x 10^3/μL
* Uncorrected retic count – 1%
* Morphology – normal red cell morphology and indices, sl. increase in bands, rare metamyelocyte and myelocyte, giant and bizarre-shaped platelets
This is most compatible with:
* congenital spherocytosis
* rheumatoid arthritis with reactive thrombocytosis
* myelofibrosis
* idiopathic thrombocythemia (essential or primary)
Idiopathic Thrombocythemia (Essential or Primary)
Congential spherocytosis is characterized by an increased MCHC and reticulocyte count; Reactive thrombocytosis is not usually accompanied by abnormal platelets; Myelofibrosis is characterized by by abnormal RBC morphology and decreased platelets and reticulocytes.
Disease States #100
The platelet disorder in which the abnormality is due to a defect in platelet aggregation is:
* Glanzmann thrombasthenia
* von Willebrand disease
* Storage pool disease
* Bernard-Soulier syndrome
Glanzmann thrombasthenia
Laboratory Determinations #129
A patient presents with an aPTT of 62.5 seconds and the only factor decreased is factor XII. What is the clinical presentation of this patient?
* Negative bleeding history
* Prolonged PFA
* Decreased risk of thrombosis
* Epistaxis
Negative bleeding history
The ASCP Book lists the aPTT range as 25-35 seconds
Laboratory Determinations #122
What does the secondary wave of platelt aggregation seen with the biphasic low-dose ADP and epinephrine response represent?
* Increased binding to collagen
* Release of platelet granules
* Increased activation by collagen
* Formation of fibrin dimers
Release of platelet granules
Disease States #86
Which of the following characteristics are common between Hermansky-Pudlak and Chediak-Higashi syndromes?
* Giant inclusion granules in granulocytes
* Alpha granule storage pool defects
* Inclusions in macrophages
* Oculocutaneous albinism
Oculocutaneous albinism
Both Hermansky-Pudlak and Chediak-Higashi are due to defects in dense granule storage, where platelts store small molecules in order to initiate the secondary wave of aggregation. Inclusion granules are more common in Chediak-Higashi, while ceroidlike inclusions are more common in Hermansky Pudlak. Alpha-granule defects are not usually seen in either.
Disease States #91
TTP presents with a pentad of symptoms that does not include:
* Fever
* Anemia
* Thrombocytopenia
* Liver failure
Liver failure
The classic pentad of symptoms for TTP can be remembered with the insensitive “FAT RN” mnemonic (I can’t make this shit up omfg lmao): Fever, Anemia, Thrombocytopenia, Renal failure, Neurological symptoms. Clinically TTP can overlap with HUS.
Disease States #70
In patients who present with bleeding disorders caused by platelets, the most common type of bleeding is:
- Mucosal Bleeding
- Hemarthrosis
- Delayed Bleeding
- Deep Hematomas
Mucosal Bleeding
Disease States #73
von Willebrand factor mediates platelet adhesion by binding to platelet receptor:
* GPIb/IIa
* GPIb/GPIX/GPV
* GPIIb/GPIIa
* GPIb/GPIIIa/GPX
GPIb/GPIX/GPV membrane receptor
Studying Clarification Note: vWF binds to the GPIb receptor on the platelet, but the von Willebrand Factor itself forms a complex with GPIb/GPIX/GPV prior to that interaction
Disease States #74
The disease state that presents with quantitative platelet disorder is:
* von Willebrand disease
* Hemophilia A
* Glanzmann thrombasthenia
* May-Hegglin anomaly
May-Hegglin Anomaly
May-Hegglin anomaly is characterized by deceased platelet counts; vWD and hemophilia patients do not present with low platelet counts. Glanzmann patients present with normal platelet counts that do not function.
Disease States #50
A patient that has a lupus anticoagulant may bleed due to:
* Factor VIII deficiancy
* Drugs
* Antibodies to prothrombin
* Infection
Antibodies to prothrombin
Although lupus anticoagulants are most often associated with thrombosis, some patients (approximattely 30%) may experience bleeding due to the presence of anti-prothrombin (FII) antibodies.
Disease States #57
Bleeding doesn’t correlate well with factor levels in a deficiency of:
* Factor VIII
* Factor IX
* Factor XI
* Factor VII
Factor XI
Factor XI supplements or boosts the activation of Factor IX, so deficiencies of Factor XI are less severe clinically than deficiencies of Factor IX or Factor VIII
Bleeding still does correlate to FXI deficiencies though, just saying
Disease States #77
A 53 year-old man is in recovery following a triple bypass operation. Oozing is noted fro his surgical wound. The laboratory data shown in this table are obtained:
* Hemoglobin – 12.5g/dL
* Hematocrit – 37%
* Prothrombin Time – 12.3 seconds
* APTT – 34 seconds
* Platelet count – 40.0 x 10^3/μL
* Fibrinogen – 250mg/dL
The most likely cause of bleeding would be:
* Dilution of coagulation factors due to massive transfusion
* Intravascular coagulation secondary to microaggregates
* Hypofibrinogenemia
* Dilutional thrombocytopenia
Dilutional thrombocytopenia
Disease States #63
A patient with a clot presents with the results shown in this table:
* PT – 15.5 seconds
* aPTT – 50.3 seconds
* D-dimer – 1.62 mg/L
* Fibrinogen – 35 mg/dL
* Fibrinogen antigen – 268 mg/dL
The most likely diagnosis is:
* DIC
* Hypofibrinogenemia
* Dysfibrinogenemia
* Afibrinogenemia
Dysfibrinogenemia
Disease States #60
A 49-year-old male is screened pre-operatively. he has a postive family history for bleeding. The patient is of Ashkenazi Jewish descent. His results are as follows:
* PT – 11.5 seconds
* aPTT – 45.1 seconds
* 1:1 mixing study – patient = 28.1 seconds
Based on this history and the results of these tests, this patient’s likely diagnosis is a deficiency in factor:
* VIII
* IX
* XI
* XII
Factor XI
Disease States #62
A patient presents with a Factor VIII level of 2%. The vWF activity (ristocetin cofactor) is <1% with a vWF antigen of 3%. The most likely diagnosis is:
* Hemophilia A
* Hemophilia B
* Type II vWD
* Type III vWD
Type III vWD
Disease States #43
**A patient with the results shown in this table: **
* Thrombin time – 48 seconds
* Reptilase time – 34 seconds
These results are characteristic of:
* Dysfibrinogenemia
* Increased D-dimer
* Fibrin monomer-split product complexes
* Therapeutic heparinization
Dysfibrinogenemia
Disease States #40
A patient presents with bleeding 48 hours after tooth extraction. Results are shown in this table:
* PT – 11.5 seconds
* aPTT – 32.5 seconds
* Fibrinogen – 345 mg/dL
* Platelets – 324 x 10^3/μL
The cause of bleeding is most likely a deficiency in:
* Plasminogen
* Factor XIII
* α-2 antiplasmin
* Factor XII
Factor XIII
Physiology #7
The activation of plasminogen to plasmin resulting in the degradation of fibrin occurs by:
* PAI-1
* α-2 antiplasmin
* tPA
* α-2 macroglobulin
tPA
Physiology #18
Which of the following best represents the 3 steps of normal hemostasis (in order)?
* Decreased heart rate, adhesion of platelets, plug formation
* Platelet aggregation, formation of FXIII, fibrin plug
* Vasoconstriction, platelet aggregation, fibrin formation
* Vascular damage, stasis, endothelial injury
Vasoconstriction, platelet aggregation, fibrin formation
Physiology # 21
How does GPIb become activated in vivo and in vitro, respectively?
* Shear force, ristocetin
* Ristocetin, compression
* Activation of ADP receptor, ristocetin
* Binding vWF, epinephrine
Shear force, ristocetin
Physiology #6
The most potent plasminogen activator in the contact phase of coagulation is:
* Kallikrein
* Streptokinase
* HWMK
* Fibrinogen
Kallikrein
Physiology #2
Warfarin is classified as a Vitamin K antagonist. The factors that impacted by warfarin therapy is:
* VII, IX, and X
* I, II, V, and VII
* II, VII, IX, and X
* II, V, and VII
Factors II, VII, IX, and X
Physiology #1
Vasocontriction is caused by several regulatory molecules, which include:
* Fibrinogen and vWF
* ADP and EPI
* Thromboxane A2 and serotonin
* Collagen and actomyosin
Thromboxane A2 and serotonin
