CLINICAL PATHOLOGY | 2022

1
COAGULATION AND FIBRINOLYSIS
Please use at your own risk
FIBRINOGEN. IT IS USED TO CHARACTERIZE
2022 CANVAS FIBRINOGEN FUNCTION.
1. Which is the most potent inhibitor of activated FV- 5. What is generated by plasmin that cleaves the
TF complex? cross-linked fibrin clot and suggests that a clot is
a. Prostacyclin undergoing lysis in the circulation?
b. TFPI a. Fibrinogen
c. Amyloid beta protein precursor b. D-dimers
d. C1 esterase inhibitor c. Tissue factor
d. Thrombus
TFPI IS THE MOST POTENT INHIBITOR OF THE
FVIIA–TISSUE FACTOR COMPLEX. UNDER THE PRESENCE OF SOLUBLE D -DIMER INDICATES
PHYSIOLOGIC CONDITIONS, TFPI EXERTS ITS THAT FIRST THROMBIN HAS BEEN FORMED, THEN
INHIBITORY EFFECTS BY FORMING A QUATERNARY CLOTTING HAS OCCURRED, THEN THE CLOT HAS
COMPLEX WITH FVIIA, TF, AND FXA. BEEN CROSS-LINKED BY FXIIIA, AND FINALLY
2. What factor undergoes autoactivation when PLASMIN HAS BEEN FORMED AND HAS CLEAVED
THE INSOLUBLE, CROSS-LINKED FIBRIN CLOT.
exposed to collagen and leads to production of
thrombin? 6. Which of the following is the main serine protease
a. Factor XII inhibitor of coagulation enzymes in the plasma
b. Factor X serine protease inhibitor system?
c. Facyor VIII a. TFPI
d. Factor VI b. Scupa
c. AT
FXII PARTICIPATES IN IN VIVO THROMBUS d. TPA
FORMATION, PRESUMABLY BY AUTOACTIVATION
ON RELEASED POLYPHOSPHATES FROM ACTIVATED ANTITHROMBIN (ANTITHROMBIN III) IS THE MAIN
PLATELETS, VESSEL WALL, OR BACTERIA; SERINE PROTEASE INHIBITOR OF COAGULATION
EXTRACELLULAR RIBONUCLEIC ACID; AGGREGATED ENZYMES OF THE PLASMA SERINE PROTEASE
PROTEINS; OR EXPOSED COLLAGEN IN THE INHIBITOR SYSTEM.
INTRAVASCULAR COMPARTMENT IN FLOWING
BLOOD. 7. The inhibitor effect brought about by activated
protein C(APC) leads to the following effects,
3. Which test should be measured routinely in a EXCEPT:
bleeding patient and with cirrhosis? a. Blocks fibrinolysis
a. D-dimer b. Initiates inflammation
b. Fibrinogen assay c. Reduces thrombin formation
c. APTT d. Reduce thrombosis risk
d. PT
THUS ACTIVATED PROTEIN C REDUCES THROMBIN
DYSFIBRINOGENEMIAS ARE MOST COMMONLY FORMATION, STIMULATES FIBRINOLYSIS, AND
ACQUIRED IN ASSOCIATION WITH LIVER DISEASE. INITIATES INFLAMMATION TO REDUCE
PATIENTS WITH DYSFIBRINOGENEMIA ARE THROMBOSIS RISK.
USUALLY ASYMPTOMATIC OR HAVE MILD
BLEEDING, BUT IN SOME CASES, THROMBOSIS HAS 8. Which of the following characterizes
BEEN REPORTED, WITH OR WITHOUT A BLEEDING thrombospondin 5?
HISTORY . a. Also known as cartilage oligomeric
matrix protein
4. What test is NOT commonly ordered because of its b. It is a derivative of L arginine
limited utility in the laboratory for assessing c. It is a potent vasodilator
bleeding disorders? d. It is an intracellular protein and a
a. PT vasoconstrictor
b. APTT
c. Fibrinogen test THROMBOSPONDIN-5, ALSO KNOWN AS CARTILAGE
d. Thrombin time OLIGOMERIC MATRIX PROTEIN (COMP), IS AN
EXTRACELLULAR PROTEIN ABLE TO CONTROL
THE THROMBIN TIME MEASURES ONLY THE ABILITY VASCULAR TONE. COMP IS RELEASED BY A VARIETY
OF EXOGENOUS THROMBIN TO PROTEOLYZE (CLOT)

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COAGULATION AND FIBRINOLYSIS
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OF CARTILAGE AND MUSCLE TISSUES AND ALSO d. Factor V Deficiency
ACTIVATED PLATELETS
ABNORMAL ACTIVATED PARTIAL THROMBOPLASTIN
9. What does "Decryption of encrypted TF" mean? TIME (APTT) ALONE
a. Endothelial cell TF is the initial nidus in ASSOCIATED WITH BLEEDING: VIII, IX, AND XI
hemostasis and thrombosis DEFECTS
b. Activated macrophages express TF on
NOT ASSOCIATED WITH BLEEDING: XII,
their cell membrane in physiologic PREKALLIKREIN (PK), HIGH-MOLECULAR- WEIGHT
hemostasis
KININOGEN, LUPUS ANTICOAGULANTS
c. Microparticles released by leukocytes
involved in initiation of coagulation 3. In which of the following patients would Vit. K
d. Able to activate coagulation when cell deficiency most likely occur?
membrane properties are modified a. Hepatitis B-positive patients
b. Very ill patients under total parenteral
TF IS NOT FULLY ACTIVE ON INTACT CELLS; IT nutrition
BECOMES ABLE TO ACTIVATE COAGULATION WHEN c. Patient with DIC
CELL MEMBRANE PROPERTIES ARE MODIFIED. THIS d. Patient with sepsis
PROCESS IS CALLED “DECRYPTION” OF
“ENCRYPTED” TF, AND IT IS STILL NOT COMPLETELY IN CLINICAL PRACTICE, VITAMIN K DEFICIENCY IS
UNDERSTOOD. SEEN MOST OFTEN IN ACUTELY ILL PATIENTS ON
ANTIBIOTICS WHO HAVE SUBSISTED ON
10. Which of the following is NOT a characteristic of
PARENTERAL NUTRITION.
normal hemostasis?
a. It is well regulated. 4. A 5 year old male develops fever with severe
b. It is generalized. bleeding in the knee joint. Laboratory study shows
c. It is localized. serum level of Factor VIII is decreased but levels of
d. It is rapidly initiated. Factor XI are within normal limits. Give your
diagnosis.
HEMOSTASIS IS THE PHYSIOLOGIC PROCESS BY a. Henoch-Schonlein purpura
WHICH THE CLOTTING SYSTEM SEALS A VASCULA R b. Hemophilia B
INJURY TO LIMIT BLOOD LOSS; IT MUST BE QUICK, c. Von Willebrand Disease
LOCALIZED, AND WELL REGULATED. d. Hemophilia A

2022 BATCH DECREASED FACTOR VII: HEMOPHILIA A

DECREASED FACTOR IX: HEMOPHILIA B
1. AJ, a 56 year old male alcoholic has liver cirrhosis.
Which of the following would be an expected 5. What test is used to confirm a diagnosis of
laboratory finding with AJ’s condition? Disseminated Intravascular Coagulation?
a. Normal APTT and PT a. D-dimer
b. Normal APTT with prolonged PT b. APTT
c. Prolonged APTT with normal PT c. TT
d. Prolonged APTT and PT d. PT

COMBINED ABNORMAL APTT AND PT D-DIMERS ARE GENERATED BY PLASMIN THAT

MEDICAL CONDITIONS: ANTICOAGULANTS, CLEAVES THE CROSS-LINKED FIBRIN CLOT. IN THE
DISSEMINATED INTRAVASCULAR COAGULATION APPROPRIATE CLINICAL SETTING, IT IS USEFUL FOR
(DIC), LIVER DISEASE, VITAMIN K DEFICIENCY, A DIAGNOSIS OF DISSEMINATED INTRAVASCULAR
MASSIVE TRANSFUSION RARELY, COAGULATION (DIC), WHERE IT IS ELEVATED, AND
DYSFIBRINOGENEMIA; FACTOR X, V, AND II TO RULE OUT DEEP VEIN THROMBOSIS (DVT) AND
DEFECTS PULMONARY EMBOLISM (PE) IN PATIENTS WITH
LOW CLINICAL PROBABILITY, WHERE THE D-DIMER
2. RH, a 23-year old female, experienced postpartum IS NOT ELEVATED.
bleeding. Laboratory Tests: APTT- Prolonged, PT-
Normal. What is the MOST probable cause of her 6. SB, a23-year old female who developed profuse
bleeding? bleeding had sepsis following induced abortion.
a. Factor I Deficiency Platelet count is decreased, PT and APTT are both
b. Factor XII Deficiency prolonged. Most probable condition?
c. Factor XI Deficiency

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COAGULATION AND FIBRINOLYSIS
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a. Hereditary Hemorrhagic Disorders of after a motorcycle accident. What would be
Fibrinolysis affected in his hemostasis?
b. Factor XIII deficiency a. Platelet aggregation
c. Disseminated intravascular coagulation b. Platelet activation
d. Vitamin K deficiency c. Platelet dissolution
d. Platelet adhesion
COMBINED ABNORMAL APTT AND PT
MEDICAL CONDITIONS: ANTICOAGULANTS, FOLLOWING INJURY TO THE BLOOD VESSEL,
DISSEMINATED INTRAVASCULAR COAGULATION PLATELETS ADHERE TO EXPOSED
(DIC), LIVER DISEASE, VITAMIN K DEFICIENCY, SUBENDOTHELIUM BY A PROCESS (ADHESION)
MASSIVE TRANSFUSION RARELY, THAT INVOLVES THE INTERACTION OF A PLASMA
DYSFIBRINOGENEMIA; FACTOR X, V, AND II PROTEIN, VWF, AND A SPECIFIC GLYCOPROTEIN
DEFECTS COMPLEX ON THE PLATELET SURFACE, GPIB-IX- V),
DIC CAN OCCUR IN PATIENTS WITH SEPSIS, WHICH BINDS VWF PARTICULARLY UNDER
MALIGNANCY, OBSTETRIC COMPLICATIONS, OR CONDITIONS OF HIGH SHEAR STRESS.
MASSIVE TISSUE INJURY. THESE CHANGES RESULT
IN THE CLINICAL FEATURES OF USUALLY 9. Which of the following is the most common rare
WIDESPREAD BLEEDING (ESPECIALLY FROM hereditary coagulation factor deficiency?
PUNCTURE SITES, WOUNDS, AND SURGICAL SITES) a. Factor VII
AND LABORATORY FINDINGS OF PROLONGED PT, b. Factor IX
APTT, DECREASED FIBRINOGEN, ELEVATED D - c. Factor X
DIMERS, AND THROMBOCYTOPENIA. d. Factor VIII

7. Of the events in hemostasis which of the following THE MOST COMMON RICDS INCLUDE DEFICIENCIES
immediately and markedly reduces blood flow to OF FXI AND FVII, FOLLOWED BY FV, FX,
the injured area? FIBRINOGEN, AND FXIII .
a. Formation of the platelet plug
b. Primary hemostasis 10. Which laboratory test reflects Factor XIII
c. Activation of Tissue Factor deficiency?
d. Arteriolar vasoconstriction a. Normal APTT; Prolonged PT
b. Prolonged APTT and PT
THE DISRUPTED ENDOTHELIUM ALTERS LAMINAR c. Normal APTT and PT
BLOOD FLOW AT THE SITE OF INJURY; THEREBY, d. Prolonged APTT; Normal PT
PLATELETS UNDERGO SHAPE CHANGE
FROM DISCOID TO SPHERICAL AND PRODUCE FACTOR XIII DEFICIENCY CAN DETERMINE DELAYED
PSEUDOPODIA THAT WILL BREACH THE SITE OF BLEEDING, USUALLY 24 TO 36 HOURS AFTER
ENDOTHELIAL DAMAGE BY BINDING TO VWF VIA SURGERY OR TRAUMA; SPONTANEOUS BLEEDING
GPIB/IX/V RECEPTORS. ALSO OCCURS. COAGULATION ASSAYS SUCH AS PT,
THIS STEP IS CALLED PLATELET ADHESION PTT, AND TT ARE NORMAL. A REDUCED PLASMA
(ATTACHMENT OF PLATELETS TO A NONPLATELET FACTOR XIII ACTIVITY, DETERMINED WITH AN
SURFACE), WHICH IS FOLLOWED BY SECRETION. IMMUNOASSAY FOR FACTOR XIII, LEADS TO THE
DURING SECRETION, CONTENTS OF ALPHA AND DIAGNOSIS.
DENSE GRANULES FROM PLATELETS ARE RELEASED
ALONG WITH THE GENERATION OF THROMBOXANE 2019 BATCH
A2 (TXA2) VIA THE CYCLOOXYGENASE -1 (COX-1) 1. Abnormal PT and APTT may be due to which one of
PATHWAY. the following?
TXA2 CAUSES VASOCONSTRICTION AND ACTIVATES a. Disseminated intravascular coagulation
PLATELETS VIA THE TXA RECEPTOR. DURING THE b. Lupus anticoagulant
NEXT STEP OF PLATELET ACTIVATION, THE SIGNAL c. Dysfibrinogenemia
TRANSDUCTION WITHIN PLATELETS LEADS TO A d. Warfarin
CONFORMATIONAL CHANGE IN GPIIB/IIIA,
ALLOWING FIBRINOGEN (ACTS AS A LIGAND) TO
BRING ADJACENT PLATELETS TOGETHER, CAUSING
AGGREGATION (ATTACHMENT OF ONE PLATELET
TO ANOTHER).

8. Olaf was diagnosed with von Willebrand disease. He

sustained a 2-inch lacerated wound on his left leg
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 CLINICAL PATHOLOGY | 2022
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COAGULATION AND FIBRINOLYSIS
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ACUTE HEMORRHAGE – PROLONGED PT AND APTT

5. Causes of isolated prolonged aPTT include

a. Vitamin K deficiency
b. Severe Von Willebrand Disease
c. Immediately after acute hemorrhage
d. Fresh frozen plasma transfusion

ISOLATED PROLONGED APTT IS A COMMON

CLINICAL FINDING. FURTHER INVESTIGATION
SHOULD BE DICTATED BY A PERSONAL AND FAMILY
HISTORY OF BLEEDING IF THAT IS THE PRESENTING
2. The following describes platelet satellitism, except: SYMPTOM, WHEREAS IN A NONBLEEDING PATIENT
a. Occurs only in EDTA-anticoagulated blood IT IS ESSENTIAL TO CHECK PREVIOUS APTTS.
b. Platelets adhere to neutrophils, but may HOWEVER, THE BLEEDING TENDENCY MAY BE
also involve other normal cells MODIFIED BY ADDITIONAL DEFECTS SUCH AS
c. May not be clinically significant, but may HEMOPHILIA, VON WILLEBRAND DISEASE , AND
lead to low platelet count PLATELET FUNCTION DEFECTS.
d. Reversal of phenomenon after treatment 6. What is the advantage of using reptilase test vs
of an immune disease has been observed thrombin time?
a. It is used to better assess abnormalities of
PLATELET SATELLITISM IS A UNIQUE, UNCOMMON, plasminogen
IN VITRO PHENOMENON SEEN IN PERIPHERAL b. Having a normal reptilase test and a
BLOOD SMEARS PREPARED FROM EDTA -MIXED prolonged thrombin time usually
BLOOD. THIS IS SEEN IN THE FORM OF PLATELETS indicates heparin contamination
ADHERING TO POLYMORPHONUCLEAR LEUCOCYTES c. Reptilase is inhibited by the presence of
IMPARTING A ROSETTE -LIKE APPEARANCE. IT IS heparin
DEFINED AS ADHERENCE OF PLATELETS ON THE d. Prolonged reptilase test and thrombin
SURFACE OF POLYMORPHONUCLEAR LEUCOCYTES time indicate normal fibrinogen
AND IMPARTING A ROSETTE -LIKE APPEARANCE.
THERE IS NO DEFINITE CAUSAL ASSOCIATION WITH IN THE PRESENCE OF A PROLONGED THROMBIN
ANY DISEASE. TIME, THE REPTILASE TIME IS USEFUL IN
JOURNALS: SOME PATIENTS HAVE PERSISTENT DIAGNOSIS OF DYSFIBRINOGENEMIA,
PLATELET SATELLITISM EVEN AFTER THE HYPOFIBRINOGENEMIA, AND DOCUMENTING THE
SUCCESSFUL TREATMENT OF THE DISEASE. PRESENCE OF HEPARIN.
3. Causes of isolated prolonged PT include: 7. The following are causes of thrombocytopenia
a. Vitamin K deficiency except
b. Severe Von Willebrand Disease a. Infiltration of the bone marrow by
c. Immediately after acute hemorrhage malignancy
d. Fresh frozen plasma transfusion b. Chemotherapy via direct toxicity to
megakaryocytes
ISOLATED PROLONGED PT IS USUALLY DUE TO AN c. Ethanolism
FVII DEFICIENCY AND MAY ALSO BE PROLONGED d. Pregnancy
DUE TO MILD DEFICIENCIES OF COMMON
PATHWAY FII, FV, AND FX DEPENDING ON THE
REAGENT’S SENSITIVITY. MOST OF THESE PATIENTS
WITH ISOLATED PROLONGED PT/INR GENERALLY
HAVE VITAMIN K DEFICIENCY.

4. Causes of shortened PT include:

a. Vitamin K deficiency
b. Severe Von Willebrand Disease
c. Immediately after acute hemorrhage
d. Fresh frozen plasma transfusion

VITAMIN K DEFICIENCY – PROLONGED PT

VOL WILLEBRAND DSE – PROLONGED APTT
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COAGULATION AND FIBRINOLYSIS
Please use at your own risk
8. MW, a 28 y/o call center agent, went to see her ROTHROMBIN GENE MUTATION (OR FACTOR II
doctor for purpura and petechiae in her arms and MUTATION OR PROTHROMBIN G20210A) IS AN
legs for 3 to 4 days. Which of the following will you INHERITED CONDITION THAT INCREASES YOUR
include in your differential diagnosis?
PREDISPOSITION TO DEVELOP ABNORMAL BLOOD
a. Hemophilia A
b. Thrombocytopenia CLOTS IN THE VEINS (DEEP VEIN THROMBOSIS OR
c. Von Willebrand Disease DVT) AND LUNGS (PULMONARY EMBOLISM OR PE).
d. Vasculitis
10. WD, a 70 y/o male, has been on warfarin for 6 years
e. B,C and D only
for atrial fibrillation. The activity of which of the
following coagulation factors is diminished in this
patient?
a. Fibrinogen, VIII, IX & X
b. Prothrombin, VII, IX & X
c. I, V, IX & XI
d. II, VI, VII & XII
e. Proteins C & S

THE PT SERVES AS THE BASIS FOR THE

INTERNATIONAL NORMALIZED RATIO (INR) VALUE
HEMOPHILIA A SYMPTOMS: USED TO MONITOR ANTICOAGULATION WITH
NOSEBLEEDS WARFARIN OR OTHER VITAMIN-ANTAGONISTS.
WARFARIN ALSO INHIBITS THE ENZYMATIC
BLEEDING GUMS
PATHWAY NECESSARY FOR VITAMIN K
SWOLLEN AND STIFF JOINTS
UTILIZATION. THUS PATIENTS WILL HAVE REDUCED
COUGHING OR VOMITING OF BLOOD
CLOTTABLE FACTOR LEVELS FOR THE VITAMIN K –
BLOOD IN STOOL AND URINE
DEPENDENT FACTORS II, VII, IX, AND X .
HEAVY MENSTRUAL BLEEDING
PETECHIAE USUALLY DO NOT OCCUR IN PATIENTS 11. CD, an 8 y/o boy, suffers from hemophilia A. The
WITH HEMOPHILIA. THE REASON IS THAT coagulation factor he is deficient in belongs to:
PETECHIAE ARE MANIFESTATIONS OF CAPILLARY a. Contact group
BLOOD LEAKAGE, WHICH IS TYPICALLY THE RESULT b. Fibrinogen group
OF VASCULITIS OR ABNORMALITIES IN THE c. Prothrombin group
NUMBER OR FUNCTION OF PLATELETS. d. Fibrinolytic group
9. ES, a 24 y/o female, had recurrent deep venous e. Anticoagulation group
thrombosis of both legs. The following conditions
should be investigated EXCEPT: HEMOPHILIA A – FVIII DEFICIENCY
a. Acquired inhibitor to Factor VIII
b. Antiphospholipid antibody syndrome
c. Factor V Leiden
d. Protein C deficiency
e. Prothrombin G20210A mutation

ANTIPHOSPHOLIPID SYNDROME – COMMON

ACQUIRED CAUSE OF VENOUS THROMBOSIS
PEOPLE WITH FACTOR V LEIDEN THROMBOPHILIA
HAVE A HIGHER THAN AVERAGE RISK OF
DEVELOPING A TYPE OF BLOOD CLOT CALLED A
DEEP VENOUS THROMBOSIS (DVT).
12. AP was delivered with the help of forceps due to
PROTEIN C DEFICIENCY IS A DISORDER THAT failure of progress of labor. After delivery, the
INCREASES THE RISK OF DEVELOPING ABNORMAL midwife noticed that he developed a larged
BLOOD CLOTS; THE CONDITION CAN BE MILD OR hematoma on the scalp. Further history revealed
SEVERE. INDIVIDUALS WITH MILD PROTEIN C his maternal grandfather and uncle have repeated
DEFICIENCY ARE AT RISK OF A TYPE OF BLOOD episodes of bleeding into joints. The bleeding most
likely is a problem of:
CLOT KNOWN AS A DEEP VEIN THROMBOSIS (DVT)

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a. Primary hemostasis
b. Secondary hemostasis
c. Tertiary hemostatis
d. Consumption coagulopathy
13. Gh, a 65 y.o diabetic, was admitted to the ICU for
sepsis. Despite antibiotics, he went into shock and
started bleeding from the gums and
gastrointestinal tract. Clinical impression was
disseminated intravascular coagulation. In this
condition, the following is/are activated:
a. Coagulation cascade
b. Fibrinolytic system
c. Both
d. Neither
DIC IS A CLINICOPATHOLOGIC CONDITION IN
WHICH ACTIVATION OF THE COAGULATION AND
FIBRINOLYSIS SYSTEMS RESULTS IN THE
SIMULTANEOUS FORMATION OF THROMBIN A ND
PLASMIN WITH CONSUMPTION OF COAGULATION
FACTORS AND INHIBITORS OF THE SYSTEM,
RESULTING IN THE CLINICAL LABORATORY
PHENOTYPE OF PROLONGED PT, APTT, AND
THROMBOCYTOPENIA.
14. Inhibitor/s of clotting include:
a. Anti-plasmin
b. Anti-thrombin
c. Calcium
d. Coagulation factors
e. Phospholipids
NATURAL INHIBITORS OF CLOTTING FACTORS
INCLUDE ANTITHROMBIN III, PROTEIN S, AND
PROTEIN C. WHEN ACTIVATED, THESE PROTEINS
INACTIVATE SPECIFIC CLOTTING FACTORS,
PROVIDING A REGULATORY MECHANISM THAT
SERVES TO CONTROL THE COAGULATION RESPONSE
AND LIMIT THE EXTENSION OF THE CLOT.
15. TRUE statement/s regarding disorders of tertiary
hemostasis
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CLINICAL PATHOLOGY | 2022
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COAGULATION AND FIBRINOLYSIS
Please use at your own risk
a. Components affected are the coagulation
factors
b. Inheritance is usually autosomal dominant
c. Sites of bleeding include wounds and
genitourinary tract
d. Timing of bleeding is immediate
e. All of the above
16. What is the action of the blood vessels in
hemostasis immediately after an injury?
a. Platelet aggregation
b. Platelet adhesion
c. Thrombosis
d. Vasoconstriction
e. Vasodilation
THE DISRUPTED ENDOTHELIUM ALTERS LAMINAR
BLOOD FLOW AT THE SITE OF INJURY; THEREBY,
PLATELETS UNDERGO SHAPE CHANGE FROM
DISCOID TO SPHERICAL AND PRODUCE
PSEUDOPODIA THAT WILL BREACH THE SITE OF
ENDOTHELIAL DAMAGE BY BINDING TO VWF VIA
GPIB/IX/V RECEPTORS. THIS STEP IS CALLED
PLATELET ADHESION (ATTACHMENT OF PLATELETS
TO A NONPLATELET SURFACE), WHICH IS
FOLLOWED BY SECRETION. DURING SECRETION,
CONTENTS OF ALPHA AND DENSE GRANULES FROM
PLATELETS ARE RELEASED ALONG WITH THE
GENERATION OF THROMBOXANE A2 (TXA2) VIA
THE CYCLOOXYGENASE -1 (COX-1) PATHWAY. TXA2
CAUSES VASOCONSTRICTION AND ACTIVATES
PLATELETS VIA THE TXA RECEPTOR.
NOT: ACTION OF BLOOD VESSELS ANG TANONG,
NOT PLATELETS KAYA HINDI PLATELET ADHESION
ANG SAGOT
17. Which factors are involved in the initial activation
of the coagulation system and require contact with
a negatively charged surface for their activation?
a. Factors II, V, VII, X
b. Factors XII, XI, PK, HK
c. Factors II, VII, IX, X
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COAGULATION AND FIBRINOLYSIS
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d. Factors I, V, VIII, XIII
Pangit ng ratio ko sa huli pero yan na yon. HAHAHA

Goodluck, doctors!

18. What activates the extrinsic pathway?

a. Contact with tissue factor
b. Exposure to negatively charged surfaces
c. Factor XIIA
d. Intrinsic pathway

19. Homeostasis depends on the balance of:

a. Blood flow, platelet & coagulation cascade
b. Coagulation, fibrinolytic &
anticoagulation systems
c. Contact, prothrombin and fibrinogen
groups of coagulation factors
d. Vascular injury, vasoconstriction and
thrombosis

L (2022)