Define The Following Terms Of Hematology-pathology Quiz

1. What is the next best step in the workup for a 21-year-old asymptomatic African-American woman with recurrent microscopic hematuria, normal renal ultrasonography, negative urine culture, and no casts present in the urine sediment?

Perform a kidney biopsy for further evaluation

Start empiric treatment with antibiotics for a possible urinary tract infection

Repeat urinalysis in one week

*Sickle cell screen (Induce sickling)
The patient most likely has sickle cell trait(Aa), which causes recurrent microscopic hematuria.In sickle cell trait, the percentage of sickle hemoglobin is 40% to 45%, and the remainder of hemoglobin is hemoglobin A.*There are no sickle cells in the peripheral smear in sickle cell trait,therefore, a sickle cell screen is required to induce sickling of RBCs containing sickle hemoglobin. However, the O2 tension in the renal medulla is low enough to induce sickling of RBCs in the peritubular capillaries. This causes microinfarctions in the renal medulla leading to hematuria.*There is also the potential for renal papillary necrosis and subsequent loss of both concentration and dilution.

The patient most likely has sickle cell trait(Aa), which causes recurrent microscopic hematuria. A sickle cell screen is required to induce sickling of RBCs containing sickle hemoglobin. This will help confirm the diagnosis and guide further management.

Explanation

The patient most likely has sickle cell trait(Aa), which causes recurrent microscopic hematuria. A sickle cell screen is required to induce sickling of RBCs containing sickle hemoglobin. This will help confirm the diagnosis and guide further management.

2. Why might a chronic alcoholic present with Pancytopenia?

Chronic alcohol inhibits bone marrow production of blood cells leading to Pancytopenia.

Chronic alcohol consumption directly damages blood cells causing Pancytopenia.

Chronic alcohol increases platelet production leading to Pancytopenia.

*Chronic alcohol>Cirrhosis>Portal hypertension>Congestive splenomegaly with too much blood getting stuck in spleen>Secondary Hypersplenism(Portal hypretension is MCC of hypersplenism)>Spleen sequesters RBCs,WBCs,Platelets>Too much of it>Pancytopenia.<Contrast this with Hyposplenia(For example after autosplenectomy in Sickle cell patient or After surgical removal of spleen) where you would see Basophillic Nuclear remnants(DNA remnant) in RBCs known as Howell-Jolly bodies.BOTH of these have been tested so know them

3. Female who complains of menorrhagia, sustained a minor cut and bleeding time was more then expected(more than 2-6 mins)...She received oral contraceptives. Her platelet count, PT, PTT are all normal...What is the likely diagnosis and treatment?

*She likely has Von willebrand disease-Most common inherited bleeding diathesis, it is autosomal dominant condition that involves lack of Factor 8, so PTT can be prolonged(In this patient it is not, remember that oral contraceptives increase release of vWF and factor 8, so it can be partially responsible), however the ONLY sign of this disease can be Prolonged bleeding time.

Thrombocytopenia - Treatment involves addressing the underlying cause and possible platelet transfusions.

Iron-deficiency anemia - Treatment involves iron supplements and identifying the source of bleeding.

Hemophilia A - Treatment involves replacing clotting factor VIII.

Von Willebrand disease is a common inherited bleeding disorder that primarily affects females and is characterized by prolonged bleeding time. The absence of Factor VIII in this disease can lead to prolonged bleeding times despite normal platelet counts and coagulation parameters. Treatment focuses on managing bleeding symptoms and may involve medications to increase clotting factor levels.

Explanation

Von Willebrand disease is a common inherited bleeding disorder that primarily affects females and is characterized by prolonged bleeding time. The absence of Factor VIII in this disease can lead to prolonged bleeding times despite normal platelet counts and coagulation parameters. Treatment focuses on managing bleeding symptoms and may involve medications to increase clotting factor levels.

4. Platelet Count Bleeding Time PT PTT in a young patient who recently has undergone wisdom tooth extraction developed severe bleeding from tooth socket after he rinsed his mouth with lukewarm water. What is the likely reason for the bleeding?

*ONLY PTT Will be increased, because patient likely has Hemophilia A-X linked condition where Factor VIII is deficient. lack of thrombin from the VIII:C deficiency prevented conversion of the fibrinogen to fibrin, producing a stable platelet thrombus held together by fibrin. When the patient rinsed his mouth out with lukewarm water, the temporary platelet plugs were dislodged causing serious bleeding..For mild hemophilia like this give Desmopression>Increases release of Factor VIII from ENDOTHELIAL cells.

PT will be increased due to a deficiency in clotting factors.

Platelet Count and Bleeding Time will be increased due to a platelet disorder.

Platelet Count, Bleeding Time, PT, and PTT will all be increased due to a vitamin K deficiency.

The patient is likely experiencing severe bleeding due to a deficiency in Factor VIII, resulting in an increase in PTT. This condition leads to a lack of thrombin from the Factor VIII deficiency, preventing conversion of fibrinogen to fibrin and causing unstable platelet plugs.

Explanation

The patient is likely experiencing severe bleeding due to a deficiency in Factor VIII, resulting in an increase in PTT. This condition leads to a lack of thrombin from the Factor VIII deficiency, preventing conversion of fibrinogen to fibrin and causing unstable platelet plugs.

5. In a classic Burkitt lymphoma case involving a mass in the JAW region of an African-American boy, which translocation is NOT typically associated with the disease?

Trisomy 21 (Down syndrome)

Translocation between chromosome 8 and 14 (Involves HEAVY chain gene locus)

Translocation between chromosome 9 and 22 (BCR-ABL fusion gene)

*ANSWER was translocation between 2-8(Involves KAPPA LIGHT chain gene locus)

Burkitt lymphoma is commonly associated with a translocation between chromosome 8 and 14 involving the HEAVY chain gene locus. However, in this specific case, the translocation involving the KAPPA LIGHT chain gene locus between chromosome 2 and 8 is more typical. The presence of BCR-ABL fusion gene from translocation between chromosome 9 and 22 is associated with chronic myelogenous leukemia, not Burkitt lymphoma. Trisomy 21, also known as Down syndrome, is a chromosomal disorder unrelated to Burkitt lymphoma.

Explanation

Burkitt lymphoma is commonly associated with a translocation between chromosome 8 and 14 involving the HEAVY chain gene locus. However, in this specific case, the translocation involving the KAPPA LIGHT chain gene locus between chromosome 2 and 8 is more typical. The presence of BCR-ABL fusion gene from translocation between chromosome 9 and 22 is associated with chronic myelogenous leukemia, not Burkitt lymphoma. Trisomy 21, also known as Down syndrome, is a chromosomal disorder unrelated to Burkitt lymphoma.

6. What changes are expected in platelet count, bleeding time, PT, and PTT with warfarin (contained in rat poison)?

Platelet count increased, bleeding time decreased, PT normal, PTT normal

Platelet count normal, bleeding time normal, PT decreased, PTT normal

*platelet count normal, bleeding time normal, PT increased, PTT increased,both PT and PTT are prolonged because factors 2 and 10 are affected by warfarin(those are vitamin K dependent coagulation factors), yet more factors 2,7,9,10 are all affected by warfarin as they all are vitamin K dependent, factor 7 is only involved in Extrinsic pathway and generally we use PT to monitor warfarin(very testable fact), however remember that even though PT changes more, PTT is affected by warfarin too.

Platelet count decreased, bleeding time increased, PT decreased, PTT decreased

Warfarin affects vitamin K-dependent factors (2, 7, 9, 10), resulting in increased PT and PTT due to the inhibition of factors 2 and 10. Factor 7, involved in the extrinsic pathway, is also affected by warfarin, leading to PT prolongation. While PT changes are more prominent, PTT is also affected by warfarin.

Explanation

Warfarin affects vitamin K-dependent factors (2, 7, 9, 10), resulting in increased PT and PTT due to the inhibition of factors 2 and 10. Factor 7, involved in the extrinsic pathway, is also affected by warfarin, leading to PT prolongation. While PT changes are more prominent, PTT is also affected by warfarin.

7. What changes in platelet count, bleeding time, PT, and PTT are expected with PRIMARY fibrinolysis, such as in a patient who has just undergone radical prostatectomy? Is the patient likely to have a positive D-dimer test?

The PT and PTT decrease due to increased coagulation during fibrinolysis

The platelet count decreases because of fibrinolysis

*Patient has primary fibrinolysis, which may occur in radical prostate surgery.In this setting, urokinase is released from the tissue causing activation of plasminogen and the release of plasmin.Plasmin degrades multiple coagulation factors (e.g., V, VIII, fibrinogen)>>This increases the PT and PTT, because factors V and VIII are in the final common pathway.The degradation products of fibrinogen interfere with platelet aggregation causing an increase in the bleeding time.The platelet count is not affected.*Test for fibrinogen degradation products is positive, however, d-dimer test is negative because fibrin clots are not present in primary fibrinolysis.all in all :platelet count normal, bleeding time increased, PT increased, PTT increased.

The patient is likely to have a negative D-dimer test in cases of primary fibrinolysis

8. History of menorrhagia, easy bruisability, bleeding from superficial scratches, and epistaxis all abating with oral contraceptives and recurring again when off of them is a classic scenario for Von Willebrand disease. What changes would you expect in PT, aPTT, bleeding time, and platelet count?

Platelet count normal, bleeding time normal, PT increased, PTT normal

Platelet count decreased, bleeding time increased, PT normal, PTT decreased

Platelet count decreased, bleeding time decreased, PT increased, PTT normal

*platelet count normal, bleeding time increased, PT normal, PTT increased.Remember vWF helps platelets to adhere to damaged endothelial cells.(So lack of vWF>Increased bleeding time)*It also normally prevents degradation of factor8, so deficiency of vWF>deficiency of factor 8>Prolongation of PT.*Contraceptives increase factor 8 release and thus removes most of her symptoms.

Von Willebrand disease is characterized by a deficiency in von Willebrand factor which helps platelets adhere to damaged endothelial cells. This results in normal platelet count, increased bleeding time, normal PT, and increased PTT. Contraceptives can alleviate symptoms by increasing factor 8 release.

Explanation

Von Willebrand disease is characterized by a deficiency in von Willebrand factor which helps platelets adhere to damaged endothelial cells. This results in normal platelet count, increased bleeding time, normal PT, and increased PTT. Contraceptives can alleviate symptoms by increasing factor 8 release.

9. INCREASED CENTRAL PALLOR of RBCs represents what?

NORMAL HEMOGLOBIN CONCENTRATION

INCREASED HEMOGLOBIN CONCENTRATION

INCREASED RBC COUNT

*DECREASED HEMOGLOBIN CONCENTRATION.

DECREASED RBC COUNT

Increased central pallor of RBCs means the red blood cells have less hemoglobin concentration, leading to a lighter color in the center of the cell.

Explanation

Increased central pallor of RBCs means the red blood cells have less hemoglobin concentration, leading to a lighter color in the center of the cell.

10. What is the likely progression in someone who ingested lot's of rat poison containing BRODIFACOUM, a long-acting 4-hydroxyCOUMARIN derivative?

It will give similar manifestations as WARFARIN overdose, basically you'll get BLEEDING DIATHESIS once old vitamin K dependent coagulation factors(2,7,9,10) are depleted(around 48 hours).
EMERGENCY treatment is FRESH FROZEN PLASMA(DIRECTLY give clotting factors/proteins) vitamin K will need DAYS to exert its effects.

It will result in rapid onset of gastrointestinal symptoms such as vomiting and diarrhea.

It will cause immediate paralysis due to neurotoxic effects of Brodifacoum.

It will lead to severe dehydration and electrolyte imbalances within a few hours post-ingestion.

Ingestion of rat poison containing BRODIFACOUM, a long-acting anticoagulant, will lead to delayed bleeding diathesis similar to WARFARIN overdose due to depletion of vitamin K dependent coagulation factors. Immediate paralysis, rapid gastrointestinal symptoms, and severe dehydration with electrolyte imbalances are not typical presentations in this context.

Explanation

Ingestion of rat poison containing BRODIFACOUM, a long-acting anticoagulant, will lead to delayed bleeding diathesis similar to WARFARIN overdose due to depletion of vitamin K dependent coagulation factors. Immediate paralysis, rapid gastrointestinal symptoms, and severe dehydration with electrolyte imbalances are not typical presentations in this context.

11. Why might FFP actually ENHANCE anticoagulative effects of HEPARIN?

Because it increases platelet aggregation, leading to stronger clot formation.

Because it contains ANTIthrombin 3.

Because it contains Vitamin K, which counteracts the effects of Heparin.

Because it inhibits the release of tissue plasminogen activator, decreasing fibrinolysis.

FFP contains antithrombin 3, which enhances the anticoagulative effects of Heparin by facilitating its ability to inhibit coagulation factors.

Explanation

FFP contains antithrombin 3, which enhances the anticoagulative effects of Heparin by facilitating its ability to inhibit coagulation factors.

12. What is the main difference between azurophilic and specific granules in hematopoiesis?

Neutrophils vs Eosinophils

Lymphocytes vs Monocytes

Platelets vs Red Blood Cells

PROmyelocytes vs Myelocytes

Azurophilic granules are found in promyelocytes, which are early precursor cells in hematopoiesis, while specific granules are characteristic of more mature myelocytes.

Explanation

Azurophilic granules are found in promyelocytes, which are early precursor cells in hematopoiesis, while specific granules are characteristic of more mature myelocytes.

13. What is the mechanism of Basophilic stippling caused by lead?

Retention of RNA not dna.*this retention of RNA is due to LEAD mediated INHIBITION Of 5" NucleotidASE activity.

Increased synthesis of DNA due to lead toxicity.

Enhanced degradation of RNA by lead exposure.

Activation of DNA repair mechanisms by lead poisoning.

Lead poisoning leads to the retention of RNA through the inhibition of 5' Nucleotidase activity, resulting in Basophilic stippling.

Explanation

Lead poisoning leads to the retention of RNA through the inhibition of 5' Nucleotidase activity, resulting in Basophilic stippling.

14. What is the most DIRECT mechanism of ineffective hematopoiesis and extravascular hemolysis leading to microcytic and hypochromic anemia in B-thalassemia?

Iron deficiency leading to impaired hemoglobin synthesis

Decreased production of B-chain hemoglobin in the liver

*DEATH of RBC PRECURSORS in Bone marrow>Ineffective hematopoiesis, this along with EXTRAvascular hemolysis is due to PRECIPITATION of UNpaired Alpha chains within RBC.(Unpaired cause no B-chain synthesis).vs
Most DIRECT effect of decreased B-chain synthesis is mIcrocytic/hypOchromic anemia.

Autoimmune destruction of RBCs in the spleen

In B-thalassemia, the most DIRECT mechanism of ineffective hematopoiesis and extravascular hemolysis causing microcytic and hypochromic anemia is the DEATH of RBC PRECURSORS in Bone marrow due to the PRECIPITATION of UNpaired Alpha chains within RBC. This results in no B-chain synthesis and leads to the observed effects.

Explanation

In B-thalassemia, the most DIRECT mechanism of ineffective hematopoiesis and extravascular hemolysis causing microcytic and hypochromic anemia is the DEATH of RBC PRECURSORS in Bone marrow due to the PRECIPITATION of UNpaired Alpha chains within RBC. This results in no B-chain synthesis and leads to the observed effects.

15. HYPERchromia(DECREASED central pallor of RBC) can be caused by what mutations?

Hemoglobin mutation

*it is characteristic for SPHEROCYTOSIS-so defect should be in gene that codes for RBC CELL MEMBRANE PROTEIN.*Possibilities:ANKYRINSPECTRINBand 3protein 4.2image ilegal

Glycolysis enzyme mutation

Bone marrow stem cell mutation

Spherocytosis is a condition characterized by spherical shaped red blood cells due to defects in RBC cell membrane proteins like ankyrin, spectrin, band 3, and protein 4.2. Mutations in hemoglobin, glycolysis enzymes, or bone marrow stem cells would not directly lead to hyperchromia with decreased central pallor of RBC.

Explanation

Spherocytosis is a condition characterized by spherical shaped red blood cells due to defects in RBC cell membrane proteins like ankyrin, spectrin, band 3, and protein 4.2. Mutations in hemoglobin, glycolysis enzymes, or bone marrow stem cells would not directly lead to hyperchromia with decreased central pallor of RBC.

16. What is the capital of France?

Dasd

Rome

Berlin

London

Paris is the capital of France, while London is the capital of the United Kingdom, Berlin is the capital of Germany, and Rome is the capital of Italy.

Explanation

Paris is the capital of France, while London is the capital of the United Kingdom, Berlin is the capital of Germany, and Rome is the capital of Italy.

17. Six hours after undergoing surgical excision of the distal colon for cancer, a 77-year-old man has decreased urine output. His urine output has been 10 mL/h during the past 3 hours. During the 4-hour operation, he lost 500 mL of blood and underwent transfusion of 1 unit of packed red blood cells. Hisinitial postoperative course wasuncomplicated. Two years ago, he had a myocardial infarction and underwent coronary artery bypass grafting. He has a 10-year history of hypertension well controlled with atenolol. Current medications include morphine and labetalol. He currently appears pale and diaphoretic. His temperature is 37°C (98.6°F), pulse is 85/min, respirations are 14/min, and blood pressure is 90/60 mm Hg. Pulse oximetry on 2 L/min of oxygen via nasal cannula shows an oxygen saturation of 89%. Cardiopulmonary examination shows no abnormalities. The abdomen is nondistended with mild tenderness over the incision. His hematocrit is 24%, serum sodium concentration is 140 mEq/L, and serum creatinine concentration is 2.1 mg/dL. The patient is switched to administration of 100% oxygen by a nonrebreathing face mask. The most appropriate next step in management is administration of which of the following?

D-Furosemide

F-0.45% Saline

E-PACKED RBCs

A-Bumetanide

The correct next step in management for a patient with decreased urine output after surgery and low hematocrit is administration of packed red blood cells to address any ongoing blood loss and improve oxygen-carrying capacity of the blood.

Explanation

The correct next step in management for a patient with decreased urine output after surgery and low hematocrit is administration of packed red blood cells to address any ongoing blood loss and improve oxygen-carrying capacity of the blood.

18. Why are babies with sickle cell disease asymptomatic at birth?

The symptoms of sickle cell disease do not appear until later in life.

Babies with sickle cell disease actually do experience symptoms at birth.

The concentration of hemoglobin S is too low

The immune system of babies with sickle cell disease suppresses any symptoms.

The structure of red blood cells is not affected in babies with sickle cell disease.

Babies with sickle cell disease are initially protected by the presence of fetal hemoglobin, which reduces the concentration of hemoglobin S and delays the onset of symptoms.

Explanation

Babies with sickle cell disease are initially protected by the presence of fetal hemoglobin, which reduces the concentration of hemoglobin S and delays the onset of symptoms.

19. What are the mechanism and manifestations of HbC formation?

Neutrally charged glutamate substituted by LYSINE > Octagonal crystal formation with HEMOLYSIS of RBCs > Moderate ANEMIA, Decreased affinity to oxygen.

Positively charged glutamate substituted by NEGATIVELY charged LYSINE > Pentagonal crystal formation with HYDRATION of RBCs > Severe HEMOLYTIC anemia, Increased affinity to oxygen.

Negatively charged glutamate substituted by LYSINE > Circular crystal formation with AGGLUTINATION of RBCs > No change in ANEMIA, Increased affinity to carbon dioxide.

Negatively charged glutamate substituted by POSITIVELY charged LYSINE>HExagonal crystal formation with DEHYDRATION of RBCs>Mild HEMOLYTIC anemia, NO change in affinity to oxygen.

20. What is the mechanism of left-sided shift of OBC in individuals with alpha thalassemia?

Formation of dimers of B-globins and tetramers of delta chains resulting in decreased oxygen affinity

*Defect in alpha chain synthesis>Formation of TETRAMERS of B-globins(hemoglobin H) and TETRAMERS of GAMMA chains(Barts), these tetramers result in INCREASED oxygen affinity(So high that it is comparable to myoglobin)>LEFT SHIFT In OBC.

Absence of alpha chains resulting in normal oxygen affinity

Increased synthesis of alpha chains leading to decreased oxygen affinity

21. Do pathologies that change HEMOGLOBIN content affect % saturation of Hemoglobin and proportion of O2 Dissolved oxygen in plasma(PO2)?

Yes, they both decrease in ANEMIA and increase in Polycythemia.

Only % saturation of Hemoglobin is affected in ANEMIA and Polycythemia.

NO EFFECT on PO2/%Saturation of Hb(Hence these are Unchanged in ANEMIA-Decreased Hb or POLYCYTHEMIA-INCREASED Hb), only thing that is altered is Total O2 content(DECREASED in ANEMIA and INCREASED In Polycythemia)

Proportion of O2 Dissolved oxygen in plasma is directly proportional to HEMOGLOBIN content.

Pathologies that change HEMOGLOBIN content do not directly impact the % saturation of Hemoglobin and proportion of O2 Dissolved oxygen in plasma(PO2). Instead, they influence the Total O2 content in the blood, which decreases in Anemia and increases in Polycythemia.

Explanation

Pathologies that change HEMOGLOBIN content do not directly impact the % saturation of Hemoglobin and proportion of O2 Dissolved oxygen in plasma(PO2). Instead, they influence the Total O2 content in the blood, which decreases in Anemia and increases in Polycythemia.

22. Does CO Poisoning affect Total O2 content of blood?

YES-DECREASES it.

NO-INCREASES it.

YES-INCREASES it.

NO-NO EFFECT on it.

Carbon monoxide (CO) has a higher affinity to hemoglobin than oxygen, which leads to decreased total O2 content in the blood when someone is affected by CO poisoning.

Explanation

Carbon monoxide (CO) has a higher affinity to hemoglobin than oxygen, which leads to decreased total O2 content in the blood when someone is affected by CO poisoning.

23. How do nitrites affect changes in the body related to oxygen carrying capacity?

Oxygen carrying capacity increases

Oxygen saturation increases

ALL decrease because nitrites OXIDIZE Fe2 into Fe3+ producing METHEMOGLOBINEMIA.

Oxygen delivery to tissues increases

Nitrites oxidize Fe2 into Fe3+ producing methemoglobinemia, which decreases oxygen carrying capacity, oxygen saturation, and oxygen delivery to tissues.

Explanation

Nitrites oxidize Fe2 into Fe3+ producing methemoglobinemia, which decreases oxygen carrying capacity, oxygen saturation, and oxygen delivery to tissues.

24. What is the description of glycogen in cori disease?

ABNORMAL Glycogen with Long Outer chain.

Normal Glycogen with VERY SHORT OUTER chain.

Normal Glycogen with Long Outer chain.

ABNORMAL Glycogen with VERY SHORT OUTER chain.

Cori disease is a type of glycogen storage disease characterized by ABNORMAL Glycogen with VERY SHORT OUTER chain. This abnormal glycogen buildup leads to various health issues in individuals with Cori disease.

Explanation

Cori disease is a type of glycogen storage disease characterized by ABNORMAL Glycogen with VERY SHORT OUTER chain. This abnormal glycogen buildup leads to various health issues in individuals with Cori disease.

25. What is the MOST common cause of Porphyria Cutanea Tarda (PCT)?

Excessive consumption of vitamin C.

Heavy metal toxicity.

Genetic mutation in heme biosynthetic pathway enzymes.

ACQUIRED deficiency of uroporphyrinogen decarboxylase.

Porphyria Cutanea Tarda (PCT) is most commonly caused by an acquired deficiency of uroporphyrinogen decarboxylase, which is essential for the heme biosynthetic pathway. Genetic mutations, excessive vitamin C intake, and heavy metal toxicity can also contribute to the development of PCT but are not the primary cause.

Explanation

Porphyria Cutanea Tarda (PCT) is most commonly caused by an acquired deficiency of uroporphyrinogen decarboxylase, which is essential for the heme biosynthetic pathway. Genetic mutations, excessive vitamin C intake, and heavy metal toxicity can also contribute to the development of PCT but are not the primary cause.

26. How can they describe defect in Sickle cell disease to confuse you?

Increase in the number of red blood cells

Substitution of hydrophilic amino acid(Glutamate) by hydroPHOBIC amino acid(Valine), note that this alteration happens in PRIMARY structure(AMINO ACID sequence) and then RESULTS in alteration of secondary/tertiary structures.

Addition of an extra chromosome

Mutation in the mitochondrial DNA

The correct description of the defect in Sickle cell disease involves a specific substitution of amino acids in the primary structure of hemoglobin. This alteration results in the formation of abnormal sickle-shaped red blood cells which can lead to various complications.

Explanation

The correct description of the defect in Sickle cell disease involves a specific substitution of amino acids in the primary structure of hemoglobin. This alteration results in the formation of abnormal sickle-shaped red blood cells which can lead to various complications.

27. Patient with heavy menstrual bleeding, prolonged bleeding time and PTT. Risonectin test shows poor platelet aggregation. Platelet count is normal. Why? What is the first-line treatment?

The patient might have a vitamin K deficiency leading to abnormal bleeding time and PTT.

*Patient likely has VWD(lack of vWF), this causes the defect in platelet adhesion and aggregation as upon endothelial damage it is vWF that platelets Gp1B binds.*Bleeding time is prolonged due to FUNCTIONAL deficiency of Factor 8(vWF normally protects factor 8 degradation-increasing its half-life),severe deficiency can cause decreased factor 8 levels leading to PTT(INTRINSIC pathway measure) Prolongation.*Risonectin test is abnormal because all it does is activation of Gp1B receptors on platelets, but again aggregation can NOT happen because there is no ligand for them(vWF), BUT when you add normal plasma(with vWF) then platelet aggregation becomes normal and that is total giveaway for vWD(Autosomal DOMINANT inheritance).They want you to know that synthetic ADH analog-DESMOPRESISN can be used for treatment as it stimulates vWF release from endothelium, HOWEVER they also want you to know that FIRST-line drug for vWD induced MENORRHAGIA in women is COMBINED ORAL contraceptives(not desmopressin).

Patient likely has hemophilia A (deficiency of Factor 8), which is causing the prolonged bleeding time and PTT.

Patient is likely experiencing idiopathic thrombocytopenic purpura (ITP) despite having normal platelet count.

The correct answer explains that the patient's symptoms are consistent with Von Willebrand Disease (VWD) and the first-line treatment for VWD induced menorrhagia is combined oral contraceptives. The incorrect answers provide alternative conditions that do not match the patient's presentation.

Explanation

The correct answer explains that the patient's symptoms are consistent with Von Willebrand Disease (VWD) and the first-line treatment for VWD induced menorrhagia is combined oral contraceptives. The incorrect answers provide alternative conditions that do not match the patient's presentation.