Hematology — MCQs

A 4-year-old boy has appeared listless during the past week. He exhibits irritability when his arms or legs are touched. In the past 2 days, large ecchymoses have appeared on the right thigh and left shoulder. CBC shows hemoglobin, 9.3 g/dL; hematocrit, 28.7%; MCV, 96 mm3; platelet count, 45,000/mm3; and WBC count, 13,990/mm3. Examination of the peripheral blood smear shows blasts that lack peroxidase positive granules, but contain PAS-positive aggregates and stain positively for deoxynucleotidyl transferase negative (TdT-). Flow cytometry shows the phenotype of blasts to be CD19+, CD3-, and sIg-. Which of the following is the most likely diagnosis?

Q75Medium

What is the treatment of choice for severe ITP?

Q76Easy

All of the following are true regarding G-6PD deficiency except?

Q77Medium

A child presents with hypochromic microcytic anemia, with normal levels of free Erythrocyte Protoporphyrin. What is the most likely diagnosis?

Q78Medium

A 12-year-old male presented with a history of recurrent nose bleeds, easy bruising, frequent muscle hematoma formation, and prolonged bleeding following trivial trauma. On examination, certain skin lesions were seen along with jaundice, splenomegaly, lymphadenopathy, and joint and skin laxity. Lab findings revealed normal PT, prolonged aPTT, reduced ristocetin cofactor activity, and a normal factor VIII assay, normal platelet count and size, and normal platelet granules. What is the most probable diagnosis of the above condition?

Q79Medium

A 14-year-old boy presents with acute onset of right flank pain, which developed after he helped his father paint the ceiling of his bedroom. Physical examination demonstrates an area of ecchymosis in the right flank that is tender to palpation. The patient has a lifelong history of easy bruising. His brother shows the same tendency. The serum level of clotting factor VIII is less than 2% of normal. Which of the following is the most likely underlying mechanism for bleeding tendency in this patient?

Q80Medium

A newborn girl presents with severe Purpura Fulminans. Her elder sibling died of severe purpura fulminans at 1 year of age. Two other siblings are normal. What is the diagnosis?

Hematology Indian Medical PG Practice Questions and MCQs

Question 71: What is the normal reticulocyte count in a newborn?

A. 0.2-1.5%
B. 1-1.6%
C. 2.5-6% (Correct Answer)
D. 6-10.2%

Explanation: **Explanation:** The correct answer is **C. 2.5-6%**. **Understanding the Concept:** In a newborn, the reticulocyte count is physiologically elevated at birth [2], [3]. This is due to high levels of maternal and placental erythropoietin (EPO) and the relative intrauterine hypoxia the fetus experiences, which stimulates vigorous erythropoiesis [3]. In a healthy full-term neonate, the normal reticulocyte count ranges from **2% to 6%** (some texts cite up to 7%). This reflects an active bone marrow responding to the transition from fetal to neonatal life [2]. Within the first week of life (usually by day 4–7), as oxygen saturation increases and endogenous EPO production drops, the reticulocyte count falls significantly [1]. This suppression of erythropoiesis leads to a decline in hemoglobin levels known as physiologic anemia of infancy [1]. **Analysis of Options:** * **Option A (0.2-1.5%):** This is the normal range for **adults** and older children. In a newborn, such a low count would be considered inappropriately low (reticulocytopenia). * **Option B (1-1.6%):** This range is too low for the immediate neonatal period and represents the stabilized levels seen after the first week of life. * **Option D (6-10.2%):** While preterm infants may have higher counts, a range starting at 6% and going up to 10% is generally considered **pathological reticulocytosis** in a term neonate, suggesting hemolysis (e.g., Rh/ABO incompatibility) or acute blood loss. **Clinical Pearls for NEET-PG:** * **Preterm Infants:** Reticulocyte counts are higher in preterm infants (up to 10%) compared to term infants. * **Physiological Nadir:** The reticulocyte count reaches its lowest point around 2–3 months of age (coinciding with physiological anemia of infancy) [1]. * **Corrected Reticulocyte Count (CRC):** Always remember to interpret reticulocyte percentages in the context of the total Hemoglobin/Hematocrit to assess true bone marrow response. * **High-Yield Fact:** Persistent reticulocytosis beyond the first week of life should prompt an investigation for chronic hemolysis (like Hereditary Spherocytosis or G6PD deficiency).

Question 72: A serious coagulopathy characterized by severe thrombocytopenia and hemorrhage due to platelet trapping within the tumor is called?

A. Phace (S) Syndrome
B. Kasabach-Merrit Phenomenon (Correct Answer)
C. Kaposi's sarcoma
D. Hemangioma

Explanation: ### Explanation **Kasabach-Merritt Phenomenon (KMP)** is the correct answer. It is a life-threatening hematologic condition characterized by the combination of a rapidly enlarging vascular tumor, **profound thrombocytopenia**, and consumptive coagulopathy. **1. Why it is correct:** The underlying mechanism involves **platelet trapping** and activation within the abnormal architecture of specific vascular tumors. This leads to the consumption of platelets and clotting factors (DIC-like picture), resulting in severe hemorrhage. It is most commonly associated with **Tufted Angioma** or **Kaposiform Hemangioendothelioma**, rather than common infantile hemangiomas. **2. Why other options are incorrect:** * **PHACE(S) Syndrome:** This is a neurocutaneous syndrome involving **P**osterior fossa malformations, **H**emangiomas (large, segmental), **A**rterial anomalies, **C**ardiac defects, and **E**ye anomalies. It does not inherently involve platelet sequestration. * **Kaposi’s Sarcoma:** A spindle-cell tumor caused by HHV-8, typically seen in immunocompromised patients (AIDS). While it is a vascular tumor, it does not cause the systemic consumptive coagulopathy seen in KMP. * **Hemangioma:** While common infantile hemangiomas are benign vascular tumors, they **do not** cause Kasabach-Merritt Phenomenon. KMP is specific to more aggressive vascular neoplasms like Kaposiform Hemangioendothelioma. **3. NEET-PG High-Yield Pearls:** * **Classic Triad:** Large vascular tumor + Thrombocytopenia + Microangiopathic hemolytic anemia. * **First-line Treatment:** Systemic corticosteroids and **Sirolimus** (mTOR inhibitor) are currently preferred. * **Lab Findings:** Low platelets, low fibrinogen, and elevated D-dimer (consumptive coagulopathy). * **Avoid:** Platelet transfusions should be avoided unless there is active bleeding, as they may "fuel the fire" by being trapped in the tumor.

Question 73: Fanconi's anemia is a type of:

A. Constitutional anemia (Correct Answer)
B. Hemolytic anemia
C. Iron deficiency anemia
D. Autoimmune anemia

Explanation: **Explanation:** **Fanconi’s Anemia (FA)** is the most common cause of **inherited (constitutional) aplastic anemia**. It is an autosomal recessive (rarely X-linked) DNA repair disorder characterized by hypersensitivity to DNA cross-linking agents. The term "constitutional" refers to the fact that the condition is congenital and arises from an underlying genetic defect present from birth, leading to progressive bone marrow failure. **Analysis of Options:** * **Option A (Correct):** It is a constitutional anemia because it is a hereditary syndrome involving pancytopenia. It typically presents between 5–10 years of age with macrocytic anemia progressing to aplastic anemia. * **Option B (Incorrect):** Hemolytic anemias involve the premature destruction of RBCs (e.g., Spherocytosis, G6PD deficiency). FA is a failure of production (hypoplasia), not destruction. * **Option C (Incorrect):** Iron deficiency is a nutritional microcytic anemia. FA is a normocytic to macrocytic anemia caused by stem cell depletion. * **Option D (Incorrect):** Autoimmune anemias (like AIHA) involve antibody-mediated destruction. While some aplastic anemias are T-cell mediated (acquired), FA is strictly genetic. **High-Yield Clinical Pearls for NEET-PG:** * **Physical Findings:** Short stature, **absent/hypoplastic thumbs**, radius abnormalities, microcephaly, and **Café-au-lait spots**. * **Gold Standard Diagnosis:** **Chromosomal Breakage Analysis** (using Mitomycin C or Diepoxybutane). * **Malignancy Risk:** High predisposition to **AML** and squamous cell carcinomas (head and neck). * **Treatment:** Hematopoietic stem cell transplant (HSCT) is the definitive cure for hematologic manifestations.

Question 74: A 4-year-old boy has appeared listless during the past week. He exhibits irritability when his arms or legs are touched. In the past 2 days, large ecchymoses have appeared on the right thigh and left shoulder. CBC shows hemoglobin, 9.3 g/dL; hematocrit, 28.7%; MCV, 96 mm3; platelet count, 45,000/mm3; and WBC count, 13,990/mm3. Examination of the peripheral blood smear shows blasts that lack peroxidase positive granules, but contain PAS-positive aggregates and stain positively for deoxynucleotidyl transferase negative (TdT-). Flow cytometry shows the phenotype of blasts to be CD19+, CD3-, and sIg-. Which of the following is the most likely diagnosis?

A. Acute lymphoblastic leukemia (Correct Answer)
B. Acute myelogenous leukemia
C. Chronic lymphocytic leukemia
D. Chronic myelogenous leukemia

Explanation: **Explanation:** The clinical presentation and laboratory findings are classic for **Acute Lymphoblastic Leukemia (ALL)**, the most common malignancy in children. **1. Why the Correct Answer is Right:** * **Clinical Presentation:** The child presents with signs of bone marrow failure: anemia (listlessness), thrombocytopenia (ecchymoses), and bone pain (irritability when touched), which is caused by leukemic infiltration of the periosteum. * **Morphology & Cytochemistry:** The blasts are **PAS-positive** (characteristic of lymphoblasts) and **Peroxidase-negative** (ruling out AML). * **Immunophenotyping:** The presence of **CD19** (a B-cell marker) and the absence of surface immunoglobulin (**sIg-**) confirms a **Pre-B cell lineage**. While most ALL cases are TdT positive, the combination of CD19+, CD3-, and PAS positivity strongly points to ALL over any other option. **2. Why Incorrect Options are Wrong:** * **B. Acute Myelogenous Leukemia (AML):** AML blasts typically show **Myeloperoxidase (MPO)** positivity and may contain Auer rods. They would express myeloid markers (CD13, CD33) rather than CD19. * **C. Chronic Lymphocytic Leukemia (CLL):** CLL is a disease of the elderly (median age >60) and involves mature-appearing lymphocytes, not blasts. * **D. Chronic Myelogenous Leukemia (CML):** CML typically presents with massive splenomegaly and a spectrum of maturing myeloid cells (myelocytes, metamyelocytes) rather than a predominance of PAS-positive blasts. **3. NEET-PG High-Yield Pearls:** * **Most common childhood cancer:** ALL (Peak age: 2–5 years). * **Best Prognostic Factor:** Age 1–10 years and WBC count <50,000/mm³. * **Cytogenetics:** t(12;21) has a **good** prognosis; t(9;22) [Philadelphia chromosome] has a **poor** prognosis in ALL. * **Common Sites of Relapse:** Testes and CNS (due to the blood-brain/blood-testis barrier).

Question 75: What is the treatment of choice for severe ITP?

A. Bone Marrow Transplant (BMT)
B. Intravenous immunoglobulin (IV gammaglobulins) (Correct Answer)
C. Plasmapheresis
D. Steroids

Explanation: **Explanation:** Immune Thrombocytopenic Purpura (ITP) in children is typically a self-limiting condition. However, in cases of **severe ITP** (defined by significant mucosal bleeding or a platelet count <10,000/mm³), rapid elevation of the platelet count is necessary to prevent life-threatening complications like intracranial hemorrhage. **Why IVIG is the Treatment of Choice:** Intravenous Immunoglobulin (IVIG) is the preferred treatment for severe ITP because it provides the **fastest rise in platelet count** (usually within 24–48 hours). It works by saturating the Fc receptors on splenic macrophages, thereby preventing the destruction of antibody-coated platelets. **Analysis of Other Options:** * **Steroids (Option D):** While steroids are the first-line treatment for *mild to moderate* symptomatic ITP, they take longer (3–7 days) to increase platelet counts compared to IVIG. * **Plasmapheresis (Option C):** This is used to remove circulating toxins or autoantibodies in conditions like TTP or Goodpasture syndrome, but it has no established role in the routine management of ITP. * **Bone Marrow Transplant (Option A):** BMT is used for bone marrow failure syndromes (e.g., Aplastic Anemia) or malignancies, not for peripheral destructive processes like ITP. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause** of isolated thrombocytopenia in an otherwise healthy child is ITP. * **Indication for treatment:** Treatment is based on **bleeding severity**, not just the absolute platelet count. * **Anti-D therapy:** Can be used as an alternative to IVIG in Rh-positive, non-splenectomized patients. * **Chronic ITP:** Defined as thrombocytopenia persisting for >12 months. Second-line agents include Rituximab or TPO-receptor agonists (Eltrombopag).

Question 76: All of the following are true regarding G-6PD deficiency except?

A. A recessive X-linked trait
B. Females are commonly affected (Correct Answer)
C. Oxidative stress causes hemolysis
D. Protective against Plasmodium falciparum malariae

Explanation: **Explanation:** Glucose-6-Phosphate Dehydrogenase (G6PD) deficiency is the most common red cell enzyme defect worldwide. The correct answer is **Option B** because it is a false statement. **1. Why Option B is the correct answer (False statement):** G6PD deficiency follows an **X-linked recessive** inheritance pattern. This means the gene is located on the X chromosome. Males (XY) are hemizygous and therefore primarily affected. Females (XX) are typically asymptomatic carriers. For a female to be clinically affected, she must either be homozygous (rare) or have significant **"Lyonization"** (unfavorable X-inactivation). Thus, females are *not* commonly affected. **2. Analysis of other options:** * **Option A (True):** As stated, it is an X-linked recessive trait, mapping to the long arm of the X chromosome (Xq28). * **Option C (True):** G6PD is essential for maintaining the pool of reduced glutathione, which protects RBCs from oxidative damage. In its absence, oxidative stress (from infections, fava beans, or drugs like Primaquine/Dapsone) causes hemoglobin to denature and precipitate as **Heinz bodies**, leading to hemolysis. * **Option D (True):** G6PD deficiency provides a selective survival advantage against **Plasmodium falciparum** malaria. The parasite grows poorly in G6PD-deficient cells due to lower levels of NADPH and increased oxidative stress within the host cell. **High-Yield Clinical Pearls for NEET-PG:** * **Peripheral Smear:** Look for **Heinz bodies** (supravital stain) and **Bite cells** (degmacytes) formed by splenic macrophages pitting out denatured hemoglobin. * **Triggers:** Most common trigger is **Infection**. Classic drug triggers include **Primaquine, Nitrofurantoin, Dapsone, and Sulphonamides.** * **Diagnosis:** Quantitative spectrophotometric assay is the gold standard. **Note:** Do not test during an acute hemolytic episode as young reticulocytes have higher enzyme levels, potentially yielding a false-normal result.

Question 77: A child presents with hypochromic microcytic anemia, with normal levels of free Erythrocyte Protoporphyrin. What is the most likely diagnosis?

A. Iron deficiency anemia
B. Lead toxicity
C. Thalassemia (Correct Answer)
D. Anemia of chronic disease

Explanation: **Explanation:** The key to solving this question lies in understanding the heme synthesis pathway. **Free Erythrocyte Protoporphyrin (FEP)** is the precursor that combines with iron to form heme. If iron is unavailable or its utilization is blocked, FEP accumulates in the red blood cell. **1. Why Thalassemia is correct:** Thalassemia is a quantitative defect in **globin chain synthesis**, not heme synthesis. Since the machinery for producing protoporphyrin and the availability of iron are both normal, FEP levels remain **normal**. This is a classic biochemical marker used to differentiate Thalassemia from Iron Deficiency Anemia (IDA). **2. Why the other options are incorrect:** * **Iron Deficiency Anemia (IDA):** There is insufficient iron to bind with protoporphyrin. Consequently, "unbound" or Free Erythrocyte Protoporphyrin **increases**. * **Lead Toxicity:** Lead inhibits the enzyme *Ferrochelatase*, which prevents the insertion of iron into the protoporphyrin ring. This leads to a significant **increase** in FEP (specifically Zinc Protoporphyrin). * **Anemia of Chronic Disease (ACD):** Iron is trapped within macrophages (high ferritin) and is unavailable for erythropoiesis. Similar to IDA, the lack of available iron leads to **increased** FEP. **High-Yield Clinical Pearls for NEET-PG:** * **Mentzer Index:** (MCV/RBC count) < 13 suggests Thalassemia; > 13 suggests IDA. * **RDW:** Usually normal in Thalassemia trait but increased in IDA. * **Confirmatory Test:** Hb Electrophoresis (showing increased HbA2 > 3.5%) is the gold standard for Beta-Thalassemia trait. * **FEP** is also increased in Sideroblastic anemia (except the X-linked ALAS2 deficiency subtype).

Question 78: A 12-year-old male presented with a history of recurrent nose bleeds, easy bruising, frequent muscle hematoma formation, and prolonged bleeding following trivial trauma. On examination, certain skin lesions were seen along with jaundice, splenomegaly, lymphadenopathy, and joint and skin laxity. Lab findings revealed normal PT, prolonged aPTT, reduced ristocetin cofactor activity, and a normal factor VIII assay, normal platelet count and size, and normal platelet granules. What is the most probable diagnosis of the above condition?

A. von Willebrand disease (Correct Answer)
B. Bernard-Soulier syndrome
C. Hemophilia A
D. Platelet function defect

Explanation: **Explanation:** The clinical presentation and laboratory findings point towards **von Willebrand Disease (vWD)**, the most common inherited bleeding disorder. **1. Why von Willebrand Disease is Correct:** * **Clinical Picture:** vWD typically presents with mucosal bleeding (epistaxis) and easy bruising. However, severe forms (Type 3) or specific subtypes can mimic hemophilia with muscle hematomas and joint issues. The mention of **joint and skin laxity** suggests an association with connective tissue disorders (like Ehlers-Danlos), which can coexist with or exacerbate vWD symptoms. * **Lab Findings:** The hallmark of vWD is a **prolonged aPTT** (due to vWF’s role in stabilizing Factor VIII) and **reduced Ristocetin Cofactor Activity** (which measures vWF-dependent platelet adhesion). * **The "Normal Factor VIII" Catch:** While vWF usually stabilizes Factor VIII, in many mild-to-moderate cases of vWD, Factor VIII levels may remain within the low-normal range, whereas Ristocetin activity is significantly impaired. **2. Why Incorrect Options are Wrong:** * **Bernard-Soulier Syndrome:** While it shows reduced Ristocetin activity, it is characterized by **thrombocytopenia** and **giant platelets** (absent here). * **Hemophilia A:** This would explain the muscle hematomas and prolonged aPTT, but it would show **low Factor VIII** levels and **normal Ristocetin activity**. It does not typically cause mucosal bleeding (nose bleeds). * **Platelet Function Defect:** Glanzmann Thrombasthenia or storage pool diseases would have normal Ristocetin activity (except in specific rare variants) and normal aPTT. **Clinical Pearls for NEET-PG:** * **vWF Function:** 1. Platelet adhesion (via GpIb receptor); 2. Carrier for Factor VIII. * **Ristocetin Induced Platelet Aggregation (RIPA):** Decreased in vWD and Bernard-Soulier; *Increased* in Pseudo-vWD or Type 2B vWD. * **Treatment of Choice:** Desmopressin (DDAVP) for Type 1; vWF concentrate for Type 3.

Question 79: A 14-year-old boy presents with acute onset of right flank pain, which developed after he helped his father paint the ceiling of his bedroom. Physical examination demonstrates an area of ecchymosis in the right flank that is tender to palpation. The patient has a lifelong history of easy bruising. His brother shows the same tendency. The serum level of clotting factor VIII is less than 2% of normal. Which of the following is the most likely underlying mechanism for bleeding tendency in this patient?

A. Circulating antibodies directed against factor VIII
B. Decreased hepatic synthesis of multiple coagulation factors
C. Deficiency of vitamin K
D. Genetic defect involving the factor VIII gene (Correct Answer)

Explanation: ### Explanation **Correct Answer: D. Genetic defect involving the factor VIII gene** The clinical presentation is classic for **Hemophilia A**. The patient is a young male with a lifelong history of easy bruising, a positive family history (brother affected), and a factor VIII level <2% (Moderate Hemophilia). The acute flank pain and ecchymosis after physical exertion (painting the ceiling) suggest a **spontaneous or trauma-induced retroperitoneal or muscular hemorrhage**. Hemophilia A is an **X-linked recessive** disorder caused by various mutations (most commonly an **inversion of intron 22**) in the factor VIII gene. This genetic defect leads to deficient or dysfunctional factor VIII, impairing the intrinsic pathway of the coagulation cascade and resulting in a failure to generate adequate thrombin. **Why Incorrect Options are Wrong:** * **Option A:** Circulating antibodies (Inhibitors) usually develop as a complication *after* treatment with exogenous factor VIII or in autoimmune conditions, rather than being the primary underlying cause in a patient with a lifelong family history. * **Option B:** Decreased hepatic synthesis would affect multiple factors (II, VII, IX, X, Protein C/S). Isolated factor VIII deficiency is not typical of liver disease, as factor VIII is also produced by endothelial cells. * **Option C:** Vitamin K deficiency affects factors II, VII, IX, and X. Factor VIII levels remain normal in vitamin K deficiency. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** X-linked recessive (affects males; females are usually asymptomatic carriers). * **Severity:** * <1% activity: Severe (spontaneous hemarthrosis). * 1–5% activity: Moderate (bleeding with minor trauma). * >5% activity: Mild (bleeding only with surgery/major trauma). * **Lab Findings:** Prolonged **aPTT**, normal PT, normal bleeding time, and normal platelet count. * **Most Common Site of Bleeding:** Hinge joints (Knee > Elbow > Ankle). * **Mixing Study:** aPTT will correct with normal plasma (distinguishes deficiency from inhibitors).

Question 80: A newborn girl presents with severe Purpura Fulminans. Her elder sibling died of severe purpura fulminans at 1 year of age. Two other siblings are normal. What is the diagnosis?

A. Hemophilia A
B. Protein C deficiency (Correct Answer)
C. Immune Thrombocytopenic Purpura (ITP)
D. Von Willebrand disease (vWD)

Explanation: **Explanation:** The clinical presentation of a newborn with **Purpura Fulminans** and a family history of a sibling death due to the same condition strongly points toward **Homozygous Protein C Deficiency**. **1. Why Protein C Deficiency is correct:** Protein C is a natural anticoagulant that inactivates Factors Va and VIIIa. In the rare autosomal recessive homozygous state, there is a complete absence of Protein C. This leads to unchecked thrombin generation, resulting in microvascular thrombosis, skin necrosis (Purpura Fulminans), and disseminated intravascular coagulation (DIC) shortly after birth. The family history suggests an autosomal recessive inheritance pattern (affected siblings, normal parents). **2. Why other options are incorrect:** * **Hemophilia A:** An X-linked recessive disorder causing Factor VIII deficiency. It presents with deep tissue bleeds or hemarthrosis, not purpura fulminans or neonatal skin necrosis. * **Immune Thrombocytopenic Purpura (ITP):** Usually occurs in older children following a viral infection. While it causes petechiae/purpura, it does not cause the life-threatening thrombotic necrosis seen in Purpura Fulminans. * **Von Willebrand Disease (vWD):** The most common inherited bleeding disorder, typically presenting with mucosal bleeds (epistaxis, menorrhagia) rather than neonatal thrombosis. **Clinical Pearls for NEET-PG:** * **Management:** Acute treatment involves **Fresh Frozen Plasma (FFP)** or Protein C concentrate. Long-term management requires oral anticoagulation (Warfarin). * **Warfarin-Induced Skin Necrosis:** Patients with heterozygous Protein C deficiency are at risk for skin necrosis when starting Warfarin without heparin bridging. * **Differential Diagnosis:** Consider **Protein S deficiency** or **Antithrombin III deficiency** in neonatal thrombosis, though Protein C deficiency is the classic association with Purpura Fulminans.

Practice by Chapter

Anemias in Children

Practice Questions

Hemoglobinopathies

Practice Questions

Hemolytic Anemias

Practice Questions

Nutritional Anemias

Practice Questions

Thrombocytopenia

Practice Questions

Bleeding Disorders

Practice Questions

Thrombotic Disorders

Practice Questions

White Blood Cell Disorders

Practice Questions

Bone Marrow Failure Syndromes

Practice Questions

Blood Component Therapy

Practice Questions

Hemophilia and Von Willebrand Disease

Practice Questions

Evaluation of Bleeding Tendencies

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free

Hematology — MCQs

Hematology — MCQs

On this page

Practice by Chapter

Want unlimited practice?