Hematopoiesis — MCQs
A 20-year-old male presented with fatigue, weakness, and jaundice. What is the most likely diagnosis?
What type of anaemia is primarily associated with leukaemia?
Where do primitive red blood cells first originate during early embryonic development?
What is the most immediate hematological adaptation that occurs during high-altitude exposure to improve oxygen delivery to tissues?
NO acts on platelets through what mechanism?
Erythropoietin is secreted by which of the following organs?
Cortisol increases all of the following components except:
True statement about cerebrospinal fluid is
Which hormone is secreted by the "Delta cells" of the stomach?
What is the inheritance pattern of the ABO blood group system and the HLA system?
Hematopoiesis Indian Medical PG Practice Questions and MCQs
Question 1: A 20-year-old male presented with fatigue, weakness, and jaundice. What is the most likely diagnosis?
- A. Acute lymphoblastic leukemia
- B. Chronic myeloid leukemia
- C. Chronic lymphocytic leukemia
- D. Acute myeloid leukemia (Correct Answer)
Explanation: ***Acute myeloid leukemia*** - Presents with **fatigue** and **weakness** due to bone marrow infiltration and resultant cytopenias, typical in this age group [1]. - Often shows **myeloblasts** on peripheral blood smear, confirming the diagnosis [2]. *Chronic myeloid leukemia* - Usually occurs in **older adults** and characterized by **elevated white blood cell counts** with a predominance of mature neutrophils. - Symptoms like fatigue may arise, but there are distinct **Philadelphia chromosome** findings and typically a **longer symptom duration**. *Acute lymphoblastic leukemia* - More common in **younger children** and often associated with **lymphadenopathy** and **thrombocytopenia**, rather than fatigue alone. - Characteristically shows **lymphoblasts** in the blood, which are not mentioned in this patient's presentation. *Chronic lymphocytic leukemia* - Typically presents in adults over **50 years** and is characterized by **lymphocytosis** and often asymptomatic in early stages. - Fatigue may occur but lacks the acute presentation and findings seen in **acute leukemias**. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 607-608. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 621-622.
Question 2: What type of anaemia is primarily associated with leukaemia?
- A. Aplastic anaemia
- B. Iron deficiency anaemia
- C. Megaloblastic anaemia
- D. Myelophthisic anaemia (Correct Answer)
Explanation: ***Myelophthisic anaemia*** - This condition arises from the **displacement of normal hematopoietic tissue** in the bone marrow by abnormal cells, like those seen in leukaemia, leading to **extramedullary hematopoiesis**. - Marrow infiltration causes **pancytopenia** and often results in the presence of **immature granulocytes** and **nucleated red blood cells** in the peripheral blood (leukoerythroblastosis). *Iron deficiency anaemia* - This type of anaemia is caused by insufficient iron for **hemoglobin synthesis**, often due to chronic blood loss or inadequate dietary intake. - While leukaemia patients can develop iron deficiency due to bleeding, it is not the **primary type of anaemia** directly resulting from the marrow infiltration by leukaemic cells. *Megaloblastic anaemia* - Characterized by the production of abnormally large, immature red blood cells, primarily due to **vitamin B12** or **folate deficiency**. - There is no direct causal link between leukaemia and the development of megaloblastic anaemia as a **primary haemato-pathological mechanism**. *Aplastic anaemia* - Characterized by **pancytopenia** due to bone marrow failure with hypocellular marrow, not marrow infiltration. - While both leukaemia and aplastic anaemia can present with cytopenias, aplastic anaemia shows a **hypocellular marrow** whereas leukaemia shows a **hypercellular marrow** with infiltration by malignant cells.
Question 3: Where do primitive red blood cells first originate during early embryonic development?
- A. Liver
- B. Yolk sac (Correct Answer)
- C. Bone marrow
- D. Spleen
Explanation: ***Yolk sac*** - The **yolk sac** is the primary site of **hematopoiesis** during the first few weeks of embryonic development. - Primitive erythroid cells (red blood cells) originate here to supply the developing embryo with oxygen. *Liver* - The **liver** takes over as the main hematopoietic organ from about the 6th week of gestation, after the yolk sac [1]. - While it produces various blood cells, it is not the *first* site of primitive red blood cell formation. *Bone marrow* - **Bone marrow** becomes the primary site of hematopoiesis during the **fetal period** (around the 20th to 24th week) and continues throughout postnatal life [2]. - It is not involved in the initial production of primitive red blood cell formation in early embryogenesis. *Spleen* - The **spleen** plays a minor role in fetal hematopoiesis, mainly producing lymphoid cells and some myeloid cells, and can take on myeloid functions if the bone marrow is compromised. - It is not the initial site of red blood cell production in the early embryo.
Question 4: What is the most immediate hematological adaptation that occurs during high-altitude exposure to improve oxygen delivery to tissues?
- A. Increased red blood cell mass
- B. Reduced erythropoietin production
- C. Increased white blood cell count
- D. Increased 2,3-BPG levels (Correct Answer)
Explanation: ***Increased 2,3-BPG levels*** - **2,3-Bisphosphoglycerate (2,3-BPG)** is an organic phosphate that binds to hemoglobin, reducing its affinity for oxygen and thereby facilitating oxygen release to tissues. - This is a **rapid adaptation** in response to hypoxia at high altitudes, occurring within hours to days, providing an immediate improvement in oxygen delivery. *Increased red blood cell mass* - An increase in **red blood cell mass (polycythemia)** is a more chronic adaptation, typically taking weeks to months to develop in response to sustained hypoxia. - While it ultimately improves oxygen-carrying capacity, it is not the most immediate hematological adaptation. *Reduced erythropoietin production* - High-altitude exposure actually leads to **increased erythropoietin (EPO) production** by the kidneys due to tissue hypoxia. - This increased EPO stimulates erythropoiesis, leading to the delayed increase in red blood cell mass. *Increased white blood cell count* - An **increased white blood cell count (leukocytosis)** is primarily associated with infection, inflammation, or stress, not with the physiological response to high-altitude hypoxia for improving oxygen delivery. - It does not directly contribute to the oxygen-carrying capacity of the blood.
Question 5: NO acts on platelets through what mechanism?
- A. Adenosine
- B. cGMP (Correct Answer)
- C. cAMP
- D. TXA2
Explanation: ***cGMP (inhibits platelet activation)*** - **Nitric oxide (NO)** diffuses into platelets and activates **guanylate cyclase**, leading to an increase in intracellular **cyclic guanosine monophosphate (cGMP)**. - Elevated **cGMP** levels then activate protein kinase G, which phosphorylates various proteins involved in platelet signaling, ultimately inhibiting **platelet activation**, adhesion, and aggregation. *cAMP (modulates platelet function through other pathways)* - While **cAMP** also plays a role in inhibiting platelet aggregation, it is primarily generated through the activation of **adenylyl cyclase** by agents like **prostacyclin (PGI2)**, not directly by NO. - NO's direct effect on platelets is mediated by **cGMP**, not **cAMP**. *Adenosine (vasodilator)* - **Adenosine** is a nucleoside known for its **vasodilatory** properties and can also influence platelet function, but it is not the primary mechanism by which NO acts on platelets. - **Adenosine** exerts its effects by activating specific **purinergic receptors** on the platelet surface, distinct from NO's intracellular signaling pathway. *TXA2 (a mediator of platelet aggregation and vasoconstriction)* - **Thromboxane A2 (TXA2)** is a potent **pro-aggregatory** and **vasoconstrictive** eicosanoid produced by platelets through the **cyclooxygenase pathway**. - NO's action on platelets is to *antagonize* the effects of **TXA2**, promoting **platelet inhibition** rather than mediating it.
Question 6: Erythropoietin is secreted by which of the following organs?
- A. Muscle
- B. Kidney (Correct Answer)
- C. Liver
- D. Heart
Explanation: ***Kidney*** - The **kidneys** are the primary site of erythropoietin production in adults, particularly the **peritubular interstitial cells**. - Erythropoietin's main function is to stimulate **red blood cell production** in the bone marrow in response to hypoxia. *Muscle* - Muscles are involved in movement and metabolism but do not produce **erythropoietin**. - They primarily store glycogen and generate force through contraction. *Liver* - The liver produces erythropoietin during **fetal development** but contributes minimally to its production in adulthood. - Its main functions include metabolism, detoxification, and protein synthesis. *Heart* - The heart is responsible for **pumping blood** throughout the body and does not produce **erythropoietin**. - It primarily consists of cardiac muscle tissue.
Question 7: Cortisol increases all of the following components except:
- A. Monocytes
- B. RBCs
- C. Platelets
- D. Eosinophils (Correct Answer)
Explanation: ***Eosinophils*** - Cortisol causes **eosinopenia** (a decrease in eosinophils) by increasing their sequestration in tissues and promoting their apoptosis. - This effect is a classic indicator of stress and can be observed in conditions of elevated endogenous or exogenous cortisol. *Monocytes* - Cortisol typically causes a **mild monocytosis** (increase in circulating monocytes), although this effect can vary. - It impacts the trafficking and differentiation of monocytes, leading to their transient increase in the bloodstream. *RBCs* - Cortisol can lead to a slight **increase in red blood cell (RBC) count** or hemoglobin concentration. - This effect is partly due to hemoconcentration and partly by promoting erythropoiesis. *Platelets* - Cortisol generally causes a **thrombocytosis** (increase in platelet count). - This effect is thought to be mediated by various factors, including cytokine interactions and direct effects on megakaryopoiesis.
Question 8: True statement about cerebrospinal fluid is
- A. More in ventricle than in subarachnoid space
- B. Maximum secreted by choroid plexus (Correct Answer)
- C. Flows from lateral ventricles to 3rd ventricle through aqueduct of sylvius
- D. CSF formation and absorption are equal at 68 mm CSF pressure
Explanation: ***Maximum secreted by choroid plexus*** - The **choroid plexus**, located within the ventricles, is the primary site of cerebrospinal fluid (CSF) production, responsible for approximately **70-80%** of its secretion. - Cells of the choroid plexus actively transport ions and solutes, drawing water into the ventricular system to form CSF. *More in ventricle than in subarachnoid space* - The majority of CSF volume, approximately **120-150 mL**, is found in the **subarachnoid space** surrounding the brain and spinal cord, not within the ventricles. - The ventricles, while producing CSF, serve more as a conduit for its circulation. *Flows from lateral ventricles to 3rd ventricle through aqueduct of sylvius* - CSF flows from the lateral ventricles to the third ventricle through the **foramina of Monro (interventricular foramina)**, not the aqueduct of Sylvius. - The **aqueduct of Sylvius (cerebral aqueduct)** connects the third ventricle to the fourth ventricle. *CSF formation and absorption are equal at 68 mm CSF pressure* - CSF formation and absorption typically achieve equilibrium at a pressure of approximately **130 mm H2O (or about 10 mmHg)** in a recumbent adult, not 68 mm. - Fluctuations outside this range can indicate issues with CSF circulation or absorption.
Question 9: Which hormone is secreted by the "Delta cells" of the stomach?
- A. Cholecystokinin
- B. Gastrin-releasing peptide
- C. Somatostatin (Correct Answer)
- D. Secretin
Explanation: ***Somatostatin*** - **Delta cells (D cells)** in the stomach and pancreas secrete **somatostatin**, a potent inhibitory hormone. - Somatostatin **inhibits the release of gastrin**, histamine, secretin, cholecystokinin, and gastric acid secretion, acting as a "universal off switch." *Cholecystokinin* - **Cholecystokinin (CCK)** is primarily secreted by **I cells** in the duodenum and jejunum. - Its main functions include stimulating gallbladder contraction and pancreatic enzyme secretion. *Gastrin-releasing peptide* - **Gastrin-releasing peptide (GRP)**, also known as **bombesin**, is a neuropeptide released from **enteric neurons**. - It stimulates the release of **gastrin** from G cells. *Secretin* - **Secretin** is secreted by **S cells** in the duodenum in response to acidic chyme entering the small intestine. - Its primary role is to stimulate the pancreas to release **bicarbonate-rich fluid** to neutralize gastric acid.
Question 10: What is the inheritance pattern of the ABO blood group system and the HLA system?
- A. Pseudodominance
- B. Autosomal dominant
- C. Autosomal recessive
- D. Codominant (Correct Answer)
Explanation: ### Explanation **Correct Option: D (Codominant)** The ABO blood group and the Human Leukocyte Antigen (HLA) system are classic examples of **codominance**. In codominance, both alleles in a heterozygous individual are fully expressed, and neither masks the other. * **ABO System:** The $I^A$ and $I^B$ alleles are codominant. If an individual inherits $I^A$ from one parent and $I^B$ from the other, their phenotype is AB, expressing both A and B antigens on the RBC surface. (Note: Both $I^A$ and $I^B$ are dominant over the $i$ allele). * **HLA System:** HLA genes (located on Chromosome 6) are the most polymorphic genes in humans. An individual expresses HLA antigens from both maternal and paternal haplotypes simultaneously on the cell surface. This is critical for immune recognition and organ transplant matching. **Why other options are incorrect:** * **A. Pseudodominance:** This occurs when a recessive allele is expressed because the dominant allele is missing (e.g., due to deletion), commonly seen in X-linked disorders in males. * **B & C. Autosomal Dominant/Recessive:** These follow Mendelian patterns where one allele masks the other. In ABO, while A and B are dominant over O, they do not mask each other, making "Codominant" the more specific and accurate description. **High-Yield Facts for NEET-PG:** 1. **Multiple Allelism:** The ABO system is also an example of multiple allelism (three alleles: A, B, and O). 2. **Bombay Phenotype:** A rare condition where the H-substance is missing; these individuals phenotypically appear as Type O regardless of their genotype. 3. **HLA Association:** HLA-B27 is strongly associated with Ankylosing Spondylitis; HLA-DR3/DR4 is associated with Type 1 Diabetes Mellitus. 4. **Chromosome 9:** The locus for the ABO gene is on the long arm of Chromosome 9.
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