BLOOD – 2020

Reiter’s syndrome, now more accurately called Reactive Arthritis, is a systemic autoimmune condition that typically develops after certain infections, especially involving the gastrointestinal or genitourinary tracts (e.g., Shigella, Salmonella, Chlamydia, Campylobacter).

It is part of the seronegative spondyloarthropathies, and often associated with the HLA-B27 genetic marker.

Classic Triad of Reiter’s Syndrome:

1. Arthritis – asymmetric, typically involving large joints like knees or ankles.

2. Conjunctivitis – mild eye redness, irritation, sometimes uveitis.

3. Urethritis – dysuria or urinary discomfort, often sterile (no bacteria).

👉 A common mnemonic:

“Can’t see, can’t pee, can’t climb a tree.”

✅ Correct Answer:

Arthritis, conjunctivitis, urethritis

❌ Why the Other Options Are Incorrect:

• Conjunctivitis, arthritis, cervicitis:
  Cervicitis can occur, but urethritis is the core diagnostic feature in both sexes.

• Arthritis, oophoritis, thyroiditis:
  Oophoritis and thyroiditis are not typical of reactive arthritis.

• Thyroiditis, tonsillitis, conjunctivitis:
  These are unrelated conditions and not seen together in Reiter’s syndrome.

• Cervicitis, arthritis, pancreatitis:
  Pancreatitis has no role in this syndrome; again, urethritis is the hallmark.

Cancer stem cells (CSCs) are a small subpopulation of tumor cells with the ability to:

• Self-renew

• Differentiate into various tumor cell types

• Regenerate the tumor even after treatment

They are thought to play a key role in tumor relapse, resistance, and metastasis.

Now, why are cancer stem cells less susceptible to chemotherapy?

🔄 Key Reason: Most CSCs are in the G₀ phase (quiescent)

• Chemotherapy drugs primarily target rapidly dividing cells, especially those in the S, G₂, or M phases of the cell cycle.

• CSCs are often in the G₀ phase, a dormant, non-dividing state.

• Since they are not actively proliferating, they evade the cytotoxic effects of standard chemotherapy agents.

• After treatment, these quiescent cells can re-enter the cell cycle, leading to tumor regrowth or recurrence.

✅ Correct Answer:

Cells are mostly in G₀ phase

❌ Why the Other Options Are Incorrect:

• Because of tumor debulking:
  Debulking is a surgical strategy to remove part of the tumor, not related to the inherent resistance of CSCs.

• Because of distant metastasis of tumor:
  Metastasis makes treatment more complex but doesn’t explain why CSCs themselves resist chemotherapy.

• Growth rate equals that of adjacent normal cells:
  CSCs actually tend to divide less frequently, which is part of their resistance mechanism.

• Because of local tumor invasion:
  Local invasion relates to tumor aggressiveness, not chemotherapy resistance of individual cells.

HbH disease is a form of α-thalassemia caused by the deletion of three α-globin genes (out of the four present — two on each chromosome 16).

🧬 Pathophysiology:

• With three α genes deleted, the body cannot produce enough α-globin chains.

• This leads to an excess of β-globin chains, which form unstable β₄ tetramers known as HbH.

• HbH is ineffective for oxygen transport, and it precipitates inside RBCs, leading to hemolysis.

🩸 Clinical features:

• Moderately severe anemia

• Splenomegaly

• Iron overload, often due to chronic hemolysis and transfusions

• It is not as severe as β-thalassemia major (Cooley’s anemia), which usually requires lifelong transfusions.

✅ Correct Answer:

Caused by the deletion of three α-globin genes

❌ Why the Other Options Are Incorrect:

• Iron overload is usually seen:
  True in the long term, but not the most defining or initial feature. Iron overload can also occur in many hemolytic anemias and with transfusions, so it’s not specific.

• Anemia is moderately severe:
  This is true, but it’s less specific than the gene deletion, which is the key identifying feature of HbH disease.

• Results because of gene deletion:
  Also true, but not specific enough. HbH specifically involves deletion of three α-globin genes.

• Not as severe as β-thalassemia major:
  True, but again, this is a relative comparison, not a defining characteristic.

Carcinogens are agents capable of causing cancer by inducing genetic mutations or epigenetic changes that disrupt normal cell regulation.

They are broadly classified into:

• Chemical carcinogens (e.g., benzene, aflatoxins)

• Physical carcinogens (e.g., UV light, ionizing radiation)

• Biological carcinogens (e.g., HPV, EBV)

Now let’s focus on chemical carcinogens, which can be:

1. Direct-acting — do not require metabolic conversion to become active (e.g., alkylating agents).

2. Indirect-acting (procarcinogens) — require metabolic activation, usually by cytochrome P-450 enzymes in the liver, to become ultimate carcinogens.

✅ Correct Answer:

Most of the known carcinogens are metabolized by cytochrome P-450

❌ Why the Other Options Are Incorrect:

• No promotor is required for direct acting chemical carcinogen:
  Incorrect phrasing. In multistep carcinogenesis, initiators (like carcinogens) and promoters (which are not carcinogenic but enhance proliferation) work together. But this statement is misleading — the concept of promoters applies regardless of the carcinogen being direct or indirect.

• All carcinogens are some form of ionic radiation:
  Completely false. Not all carcinogens are radiation-based. Many are chemical or biological.

• All carcinogens are manmade:
  False. Many are naturally occurring, such as aflatoxin (from Aspergillus) and UV radiation from the sun.

• Man cannot manufacture carcinogens:
  Also false. We manufacture many carcinogenic compounds, including some chemotherapy drugs (e.g., cyclophosphamide), industrial chemicals, and tobacco-related products.

Pleomorphic adenoma is the most common benign tumor of the salivary glands, particularly the parotid gland. The term “pleomorphic” refers to its mixed cellular composition, and “adenoma” implies a benign epithelial origin.

It is classified as a benign mixed tumor because it contains:

• Epithelial components (glandular tissue)

• Mesenchymal-like components (cartilage, myxoid, or even bone-like areas)

Despite this mixed appearance, all components are believed to originate from a single germ layer (epithelial origin) that undergoes divergent differentiation.

Key features of pleomorphic adenoma:

• Painless, slow-growing mass

• Most commonly arises in the parotid gland

• Has a tendency to recur if not fully excised due to its irregular borders

• Rarely, it can undergo malignant transformation into carcinoma ex pleomorphic adenoma

✅ Correct Answer:

Benign mixed tumor

❌ Why the Other Options Are Incorrect:

• Mixed malignant tumor:
  Pleomorphic adenoma is benign, not malignant. Malignant transformation is rare and not implied by the diagnosis.

• Benign epithelial cell tumor:
  Only partially correct — this option misses the mesenchymal-like component, which defines it as a mixed tumor.

• Painful, fast-growing inflammation:
  Incorrect — pleomorphic adenoma is typically painless and slow-growing, and not inflammatory in nature.

• Malignant tumor:
  It is benign by definition. Malignant transformation is a separate condition.

Pernicious anemia is a specific type of megaloblastic anemia caused not by a lack of vitamin B₁₂ in the diet, but by impaired absorption of vitamin B₁₂ due to deficiency of intrinsic factor (IF).

Here’s how it works:

• Intrinsic factor is a glycoprotein secreted by parietal cells in the stomach.

• It binds to vitamin B₁₂ in the small intestine, facilitating its absorption in the terminal ileum.

• In pernicious anemia, the body produces autoantibodies against:

  • Intrinsic factor itself, or

  • Parietal cells that produce intrinsic factor

• Without IF, even if B₁₂ is present in the diet, it cannot be absorbed, leading to:

  • Megaloblastic anemia

  • Neurological symptoms (due to demyelination)

It is considered an autoimmune condition, often associated with other autoimmune diseases.

✅ Correct Answer:

Deficiency of intrinsic factor

❌ Why the Other Options Are Incorrect:

• Inadequate diet:
  May lead to nutritional B₁₂ or folate deficiency, but not pernicious anemia, which is specifically autoimmune and absorption-related.

• Folic acid antagonists:
  Like methotrexate, cause folate deficiency, leading to megaloblastic anemia — but again, not pernicious anemia.

• Vegetarianism:
  Can lead to dietary B₁₂ deficiency (since B₁₂ is animal-derived), but this is not autoimmune and is not called pernicious anemia.

• Hemodialysis:
  Can cause anemia of chronic disease and loss of water-soluble vitamins, but it is not a cause of pernicious anemia.

To understand bleeding disorders, it helps to classify the underlying causes:

• Platelet abnormalities (number or function) → lead to mucocutaneous bleeding (e.g., petechiae, gum bleeding).

• Coagulation factor deficiencies → cause deep bleeding (e.g., joint bleeds, hematomas).

• Hypercoagulable states → lead to thrombosis, not bleeding.

Now let’s analyze the key option:

A low platelet count (thrombocytopenia) is most directly associated with bleeding.

Platelets are essential for forming the primary hemostatic plug. Without adequate numbers:

• Blood vessel injury can’t be sealed.

• Bleeding time increases.

• Minor traumas may lead to spontaneous bleeding, bruising, or internal hemorrhage.

✅ Correct Answer:

Low platelet count

❌ Why the Other Options Are Incorrect:

• High platelet count:
  Known as thrombocytosis — may actually promote clotting, not bleeding. Rarely, very high counts may cause dysfunctional platelets, but bleeding is uncommon.

• Prolonged bed rest or immobilization:
  Promotes venous stasis and thrombosis, not bleeding.

• Protein S deficiency:
  Protein S is a natural anticoagulant. Its deficiency leads to increased clotting, not bleeding.

• Protein C deficiency:
  Similar to Protein S — it increases risk of thrombosis, not hemorrhage.

Neutrophils are key phagocytic cells of the innate immune system and contain two main types of cytoplasmic granules:

1. Azurophilic (primary) granules — contain early, potent enzymes:

   • Myeloperoxidase (MPO)

   • Elastase

   • Proteinase 3

   • Defensins

2. Specific (secondary) granules — appear later during maturation and have a different protein profile:

   • Lysozyme

   • Lactoferrin

   • Collagenase

   • NADPH oxidase components

Among the choices listed, the substance found in the specific (secondary) granules of neutrophils is:

✅ Correct Answer:

Lysozyme

❌ Why the Other Options Are Incorrect:

• Cationic proteins:
  These are typically found in eosinophil granules (e.g., major basic protein), not neutrophils.

• Myeloperoxidase:
  A hallmark of azurophilic (primary) granules, not specific granules.

• Elastase:
  Also found in primary granules, used to degrade tissue matrix during inflammation.

• Proteinase:
  Generic term, but proteinase 3 specifically is in primary granules, not secondary.

In acute inflammation, leukocytes (mainly neutrophils early on) must travel from the bloodstream to the site of injury or infection. This migration occurs in a well-orchestrated, multi-step process involving:

1. Margination – Leukocytes move to the periphery of blood flow in post-capillary venules.

2. Rolling – Leukocytes loosely bind and roll along the endothelium via selectins.

3. Adhesion – Firm attachment of leukocytes to the endothelium via integrins.

4. Diapedesis (Transmigration) – Leukocytes squeeze through endothelial gaps into tissue.

5. Chemotaxis – Leukocytes actively move through the tissue toward the injury site in response to chemical gradients (e.g., IL-8, C5a, LTB₄, bacterial products).

Out of these, the term that specifically describes the directed movement of leukocytes toward the site of injury is:

✅ Correct Answer:

Chemotaxis

❌ Why the Other Options Are Incorrect:

• Rolling:
  Early step — leukocytes tumble along the endothelial surface using weak bonds, not actual migration toward the injury.

• Adhesion:
  Step where leukocytes firmly attach to endothelium — again, not movement through tissue.

• Margination:
  Describes leukocytes drifting to the edges of blood flow, a preparatory step before rolling.

• Diapedesis:
  Also called transmigration — the process of crossing the endothelium, not moving through tissues to the stimulus.

Thalassemia is a group of inherited disorders characterized by reduced or absent synthesis of alpha or beta globin chains of hemoglobin. This leads to microcytic hypochromic anemia, ineffective erythropoiesis, and hemolysis.

To diagnose thalassemia, the key is to identify abnormal hemoglobin types or proportions — particularly HbA₂, HbF, and any variant hemoglobins (like HbE, HbS, etc.). The best and most specific method to do this is:

🧪 Hemoglobin electrophoresis

• This technique separates different types of hemoglobin based on their electric charge and migration in a gel under an electric field.

• It allows detection of:

  • Increased HbA₂ and HbF → seen in beta-thalassemia trait

  • Absent or decreased HbA → seen in beta-thalassemia major

  • Other abnormal hemoglobins like HbS, HbC, etc.

✅ Correct Answer:

Hemoglobin electrophoresis

❌ Why the Other Options Are Incorrect:

• Estimation of shape hemoglobin molecules:
  This is not a standard or meaningful test — hemoglobin’s shape is not clinically estimated in thalassemia diagnosis.

• Hemoglobin chromatography:
  Useful in some labs, but less common and less standardized than electrophoresis for detecting thalassemia patterns.

• Measurement of iron:
  Important to rule out iron deficiency anemia, which also causes microcytosis — but not diagnostic for thalassemia.

• Measurement of mean corpuscular volume (MCV):
  In thalassemia, MCV is low (microcytosis), but this finding is non-specific — it also occurs in iron deficiency anemia.

An anaphylactic reaction is a severe, immediate Type I hypersensitivity reaction, usually triggered by allergens like peanuts, bee venom, or penicillin. It is mediated by IgE antibodies, which are bound to mast cells and basophils. Upon re-exposure to the allergen, these cells degranulate, releasing a cocktail of potent mediators.

Among these, the most immediate and critical mediator is histamine.

🧪 Key Roles of Histamine in Anaphylaxis:

• Vasodilation → causes hypotension and shock

• Increased vascular permeability → leads to edema and swelling (e.g., angioedema)

• Bronchoconstriction → causes wheezing and respiratory distress

• Stimulation of nerve endings → causes itching (pruritus) and flushing

Histamine is the reason why epinephrine is life-saving — it counteracts bronchoconstriction and vasodilation caused by histamine.

✅ Correct Answer:

Histamine

❌ Why the Other Options Are Incorrect:

• Slow-reacting substance of anaphylaxis (SRS-A):
  This is an older term used to describe a group of leukotrienes (C₄, D₄, E₄). While these sustain the reaction (especially bronchoconstriction), they are not the major initial mediator.

• Eosinophils:
  Involved more in late-phase allergic responses and parasitic infections, not the acute phase of anaphylaxis.

• Serotonin:
  Important in rodents and some animals, but not a major player in human anaphylaxis.

• Leukotriene:
  Potent and involved in prolonged effects (e.g., bronchospasm), but histamine acts faster and is the key initial trigger.

Macro-ovalocytes are large, oval-shaped red blood cells seen on a peripheral blood smear, and they are a hallmark feature of megaloblastic anemia.

Here’s why:

• Megaloblastic anemia is caused by impaired DNA synthesis, typically due to vitamin B₁₂ or folate deficiency.

• This defect affects rapidly dividing cells, including erythrocyte precursors in the bone marrow.

• As a result, the cells:

  • Grow larger than normal (macrocytic)

  • Show defective nuclear maturation

  • Appear oval-shaped due to abnormal cytoskeletal development

Peripheral smear findings:

• Macro-ovalocytes

• Hypersegmented neutrophils

• Sometimes, mild anisopoikilocytosis (variation in size and shape)

✅ Correct Answer:

Megaloblastic anemia

❌ Why the Other Options Are Incorrect:

• Iron deficiency anemia:
  Produces microcytic, hypochromic red cells — not macro-ovalocytes. Cells are smaller, paler, and sometimes pencil-shaped.

• G6PD deficiency:
  Leads to hemolysis with features like bite cells and Heinz bodies — not macro-ovalocytes.

• Hereditary spherocytosis:
  Characterized by spherocytes — small, round, densely-staining RBCs without central pallor, not large oval cells.

• Sickle cell anemia:
  Shows sickled, crescent-shaped RBCs, and possibly target cells, not macro-ovalocytes.

Kala-azar, also known as visceral leishmaniasis, is a systemic protozoal infection that affects internal organs like the spleen, liver, and bone marrow. It’s primarily caused by Leishmania donovani, and is transmitted to humans by the bite of the female sand-fly (Phlebotomus).

Key clinical features include:

• Prolonged fever

• Massive splenomegaly

• Hepatomegaly

• Pancytopenia

• Hyperpigmentation of the skin (hence the name “kala-azar” meaning “black fever”)

The parasite exists in two forms:

• Promastigote: in the sand-fly vector

• Amastigote: in human macrophages (diagnosed via bone marrow or splenic aspirate)

Kala-azar is prevalent in parts of India, Bangladesh, Sudan, Brazil, and East Africa.

✅ Correct Answer:

L. donovani

❌ Why the Other Options Are Incorrect:

• T. cruzi:
  Causes Chagas disease, not kala-azar. It is transmitted by the reduviid bug, not the sand-fly.

• L. tropica:
  Causes cutaneous leishmaniasis, which affects the skin and not visceral organs.

• L. braziliensis:
  Causes mucocutaneous leishmaniasis, particularly in South America, affecting nasal and oropharyngeal tissues.

• L. mexicana:
  Also causes cutaneous leishmaniasis, mostly in Central America and parts of Mexico.

In histopathology, “loss of polarity” is a classic microscopic feature of malignant tumors — and it refers to the disorganized architecture and misaligned orientation of cancer cells compared to normal epithelial cells.

Let’s unpack this:

• In normal epithelium, cells are polarized — meaning they have a definite orientation:

  • The nucleus is usually basally located.

  • The apical surface faces the lumen.

  • Cell junctions and cytoskeletal elements are tightly regulated.

• In malignancy, this orderly structure breaks down. Cells grow in disorganized sheets or clusters, and their orientation becomes random or haphazard.

  • Nuclei may face in various directions.

  • Apical and basal surfaces are indistinct.

  • This contributes to loss of tissue function and invasiveness.

This is distinct from pleomorphism, mitotic activity, or nuclear-cytoplasmic ratio, though those are also common in cancer.

✅ Correct Answer:

Markedly disturbed orientation of cancer cells

❌ Why the Other Options Are Incorrect:

• Formation of tumors against normal cells:
  Vague and not a defined histologic term. Doesn’t describe polarity or orientation.

• Pleomorphism:
  Refers to variation in size and shape of cells and nuclei — a separate feature of anaplasia, not about orientation.

• More than 10 mitoses/10 high power fields:
  Indicates high mitotic activity, a marker of rapid proliferation, but not related to polarity.

• Altered nuclear cytoplasmic ratio of cancer cells:
  True for malignancy (usually increased nuclear size), but again, it doesn’t describe cell orientation.

Malaria is caused by Plasmodium species, which are transmitted to humans via the bite of an infected female Anopheles mosquito. The form injected into humans is the sporozoite, which enters the bloodstream and travels quickly to its target organ.

The exo-erythrocytic cycle (also called the pre-erythrocytic cycle) refers to the phase before the parasite invades red blood cells.

• Once sporozoites reach the liver, they invade hepatocytes.

• Inside the liver cells, they undergo asexual replication (schizogony) to produce merozoites.

• These merozoites are then released into the bloodstream, where they begin the erythrocytic cycle by infecting red blood cells.

This liver stage is crucial for parasite amplification and occurs silently before clinical symptoms begin.

✅ Correct Answer:

Liver

❌ Why the Other Options Are Incorrect:

• Spleen:
  Involved later in filtering parasitized RBCs and mounting immune responses — not part of the exo-erythrocytic stage.

• Bone marrow:
  Plays a role in erythropoiesis and is affected in severe malaria, but it’s not the site where sporozoites replicate.

• Lymph node:
  Involved in immune responses, but has no role in the parasite’s life cycle.

• Heart:
  Not involved in malaria’s pathogenesis or parasite development.

Human T-cell Leukemia Virus Type 1 (HTLV-1) is a retrovirus that primarily infects and transforms CD4⁺ T-lymphocytes. It is the first human retrovirus discovered and is known to cause a rare but aggressive malignancy called adult T-cell leukemia/lymphoma (ATLL).

Let’s break it down:

• HTLV-1 integrates into the host genome and causes clonal proliferation of infected CD4⁺ T-cells, leading to malignant transformation.

• The virus expresses a regulatory protein called Tax, which promotes T-cell proliferation, inhibits tumor suppressor pathways, and activates NF-κB signaling — all of which contribute to leukemogenesis.

• Apart from malignancy, HTLV-1 is also associated with HTLV-1–associated myelopathy/tropical spastic paraparesis (HAM/TSP), a neuroinflammatory condition.

Importantly, although CD2 is a marker found on T-cells and NK cells, HTLV-1 specifically targets CD4⁺ T-cells, not all CD2⁺ cells.

✅ Correct Answer:

CD4⁺ T-cells

❌ Why the Other Options Are Incorrect:

• Neutrophils:
  These are innate immune cells primarily involved in bacterial infections and acute inflammation. HTLV-1 has no direct effect on neutrophils.

• Mast cells:
  Involved in allergic responses and parasitic infections. Not a target of HTLV-1.

• CD2⁺ T-cells:
  CD2 is a surface molecule on both CD4⁺ and CD8⁺ T-cells, but it’s not specific. HTLV-1 preferentially targets CD4⁺ T-cells, making this option too broad.

• Macrophages:
  Though they play a role in immune regulation and antigen presentation, HTLV-1 does not target them for transformation.

This question taps into the mechanisms of acute inflammation, particularly the role of histamine, a key vasoactive amine released by mast cells, basophils, and platelets in response to injury or allergens.

Histamine contributes to two hallmark signs of inflammation:

1. Vasodilation – leads to redness and warmth.

2. Increased vascular permeability (vascular leakage) – leads to swelling (edema).

Now, how does histamine increase permeability?

Histamine acts very rapidly (within minutes) on the post-capillary venules, causing:

• Contraction of endothelial cells, which creates gaps between them.

• These intercellular gaps allow plasma proteins and fluid to leak out into the interstitial tissue, producing exudate.

This reversible endothelial cell contraction is a transient process (typically lasting 15–30 minutes) and is a key early event in inflammation.

✅ Correct Answer:

Contraction of endothelial cells

❌ Why the Other Options Are Incorrect:

• Endothelial cell necrosis and detachment:
  This occurs in severe injuries (e.g., burns, infections), not during histamine release. It causes prolonged permeability but is not histamine-mediated.

• Increased transcytosis:
  This is a vesicle-mediated transport of proteins across endothelial cells, regulated by VEGF, not histamine.

• Increased hydrostatic pressure:
  This occurs in congestive heart failure or venous obstruction, leading to transudate (not exudate), and has no connection to histamine.

• Increased margination of leukocytes:
  This is a consequence of vascular changes (e.g., slowing of blood flow) and not a cause of vascular leakage. Histamine may contribute indirectly, but it does not cause margination.

Hemolytic disease of the newborn (HDN) due to Rh incompatibility is a classic example of Type II hypersensitivity, also known as cytotoxic hypersensitivity.

Let’s walk through the mechanism:

• In Rh incompatibility, an Rh-negative mother carries an Rh-positive fetus.

• During the first pregnancy, fetal red blood cells (RBCs) may enter the maternal circulation during delivery or placental separation.

• The mother’s immune system sees the Rh (D) antigen as foreign and begins to form IgG antibodies against it.

• These IgG antibodies can cross the placenta in subsequent pregnancies and attack the fetal Rh-positive RBCs.

• This leads to hemolysis of fetal RBCs, resulting in anemia, jaundice, and in severe cases, hydrops fetalis or death.

In Type II hypersensitivity:

• Antibodies bind to antigens on cell surfaces (like RBCs).

• This leads to complement activation, opsonization, and cell lysis.

• The reaction is targeted and cytotoxic, not generalized.

✅ Correct Answer:

Cytotoxic

❌ Why the Other Options Are Incorrect:

• Complement mediated:
  While complement is involved in Type II hypersensitivity, it’s not a type itself. It’s a mechanism, not a classification.

• Anaphylactic:
  This is Type I hypersensitivity — immediate, IgE-mediated reactions like asthma, urticaria, or peanut allergy. Not involved in HDN.

• Contact type:
  Refers to Type IV hypersensitivity, like poison ivy or TB skin test — delayed, T-cell mediated, not antibody-mediated.

• Immune complex mediated:
  This is Type III hypersensitivity, where antigen-antibody complexes deposit in tissues, leading to inflammation (e.g., serum sickness, SLE). Not RBC-specific.

Burkitt’s lymphoma is a highly aggressive B-cell non-Hodgkin lymphoma that is strongly associated with Epstein-Barr virus (EBV), particularly in endemic regions of Africa.

Endemic (African) Burkitt’s Lymphoma:

• Primarily affects children

• Commonly involves the jaw or facial bones

• Nearly 100% EBV-positive in endemic cases

• Malaria may act as a cofactor by suppressing immune surveillance

Microscopy hallmark:

• “Starry sky” appearance due to macrophages scattered among densely packed malignant lymphocytes

Why the correct answer is right:

• EBV infects B-cells via the CD21 receptor, promoting transformation and uncontrolled proliferation.

• In endemic areas, this leads to Burkitt’s lymphoma, especially with chronic immune stimulation by malaria.

Why the other options are incorrect:

• Leukemia:
  EBV is not a known cause of leukemia. Leukemia involves bone marrow and peripheral blood rather than discrete tumors.

• Peripheral T-cell lymphoma:
  This is a rare, T-cell origin malignancy and not commonly linked to EBV in children.

• Diffuse large B-cell lymphoma:
  While EBV may be involved in some cases, especially in elderly or immunocompromised, this is not the characteristic tumor seen in African children.

• Mastocytosis:
  A rare myeloproliferative disorder involving mast cells, not associated with EBV.

In wound healing, epithelialization refers to the migration and proliferation of epithelial cells to cover a wound.

Timeline in Suture Wounds:

• Although epithelial cells begin migrating within hours of injury, complete epithelialization of suture wounds typically occurs around 72 hours (3 days).

• This timeframe allows for the cells to cover the wound fully, restoring the integrity of the skin barrier.

• The exact timing can vary depending on factors like wound size, location, and patient health, but 72 hours is the generally accepted period for full epithelial coverage in surgical wounds.

Why Other Options Are Less Accurate:

• 24 to 48 hours may be early stages of epithelial migration but not full coverage.

• 96 hours might be too long for routine surgical wounds.

• 36 hours is an intermediate phase but less commonly cited as complete epithelialization time.

Graft rejection is primarily a result of the recipient’s immune system recognizing the transplanted tissue as foreign and mounting an immune response against it.

Key Players in Graft Rejection:

• Cytotoxic T cells (CD8+ T cells):
  These cells recognize foreign antigens presented on the graft’s MHC class I molecules. Upon activation, they directly kill graft cells by releasing cytotoxic molecules like perforin and granzymes, causing tissue damage and rejection.

• CD4+ T cells (Helper T cells):
  They help coordinate the immune response by activating other immune cells, including cytotoxic T cells and B cells, but do not directly cause cell death.

• B cells:
  Produce antibodies that can mediate graft rejection via antibody-mediated mechanisms, especially in hyperacute rejection, but they are not the primary cause of acute graft rejection.

• Macrophages:
  Involved in inflammation and tissue remodeling, but not the primary agents causing graft rejection.

Why Cytotoxic T Cells Are the Main Cause:

• They are the main effectors of cellular immunity responsible for the destruction of graft tissue.

• Their activation leads to acute rejection, which is the most common form of graft rejection.

Why Other Options Are Less Correct:

• Macrophages:
  Play a supportive role but do not directly kill graft cells.

• CD4+ cells:
  Assist in the immune response but are not the main executors.

• B cells:
  Important for antibody-mediated rejection but not the primary cellular killers.

• None of these:
  Incorrect, as cytotoxic T cells are key in graft rejection.

Apoptosis, or programmed cell death, is a mechanism to eliminate damaged or abnormal cells, including potentially cancerous cells. However, cancer cells typically acquire the ability to evade apoptosis, allowing them to survive and proliferate unchecked.

Why None of the Given Stages Is Correct:

• The cell cycle stages (G1, S, G2, M) are phases of cell division.

• Apoptosis can be triggered at various checkpoints if DNA damage or cellular stress is detected.

• However, cancer cells often bypass these apoptotic signals, so there isn’t a specific, reliable stage during the cell cycle where cancer cells undergo apoptosis.

• Instead, apoptosis is usually inhibited or defective in cancer cells, which contributes to tumor growth.

Why Other Options Are Incorrect:

• Before M (mitosis):
  Cells may arrest and undergo apoptosis if errors are detected, but cancer cells often resist this.

• After G1, After S, At restriction point:
  These are cell cycle checkpoints where DNA damage can lead to apoptosis in normal cells, but cancer cells evade this fate.

Metastasis is the process by which cancer cells spread from the primary tumor to distant sites. There are several well-recognized routes for this spread:

1. Local invasion:
   Cancer cells infiltrate surrounding tissues directly.

2. Seeding of cavities (transcoelomic spread):
   Tumor cells shed into body cavities like the peritoneum or pleura, implanting on serosal surfaces (common in ovarian cancer).

3. Lymphatic spread:
   Cancer cells enter lymphatic vessels and spread to regional lymph nodes, typical for many carcinomas.

4. Hematogenous spread:
   Tumor cells invade blood vessels and spread through the bloodstream, common in sarcomas and some carcinomas (e.g., liver, lungs).

Why “None of these” is Correct:

All the options listed are common and well-established pathways of metastatic spread. Therefore, none of the options provided is not a common pathway.

Why Other Answers Are Incorrect:

Each listed pathway is a recognized and frequent mode of metastasis, so none can be excluded as uncommon.

The immune system has both innate and adaptive components. This question focuses on innate immunity, particularly its role in early defense against tumor cells and virus-infected cells.

Why NK Cells Are the Correct Answer:

• Natural Killer (NK) cells are a part of the innate immune system.

• They do not require prior sensitization to recognize and kill abnormal cells.

• NK cells:

  • Detect cells with low or absent MHC I molecules (often the case with tumor or virus-infected cells).

  • Use cytotoxic granules (like perforin and granzymes) to induce apoptosis.

• They act immediately, without needing antigen presentation or prior activation—this is crucial for first-line defense.

Why the Other Options Are Incorrect:

• Cytotoxic T-lymphocytes (CD8+ T cells):

  • Part of the adaptive immune system.

  • Require antigen presentation via MHC I and prior exposure to become activated.

• CD4+ T cells:

  • Also adaptive.

  • Function as helper cells (not direct killers) that coordinate immune responses.

• CD8+ T cells:

  • This is another name for cytotoxic T-lymphocytes. Same reasoning applies—they need prior antigen exposure.

• B-lymphocytes:

  • Produce antibodies after activation.

  • Also part of adaptive immunity, and require antigen exposure and help from CD4+ T cells.

To answer this, let’s understand mucin antigens and how they’re used in identifying cancers.

What is MUC-1?

• MUC-1 is a high molecular weight glycoprotein (a type of mucin) expressed on the apical surface of epithelial cells in various tissues.

• In normal tissue, it’s highly glycosylated and helps protect epithelial surfaces.

• In malignant tissues, like breast and ovarian carcinomas, MUC-1 becomes:

  • Overexpressed

  • Abnormally glycosylated

  • Redistributed across the entire cell membrane (losing polarity)

This makes MUC-1 a targetable antigen and a diagnostic marker in both ovarian and breast cancers.

Why the Other Options Are Incorrect:

• Carcinoembryonic Antigen (CEA):
  Seen mainly in colorectal, pancreatic, and lung cancers. It’s not specific to breast or ovarian tumors.

• CA19-9:
  Primarily elevated in pancreatic and biliary tract cancers, not commonly associated with breast or ovarian cancers.

• CA-125:
  A classic marker for ovarian cancer, but not typically elevated in breast cancer. It’s not shared across both.

• None of these:
  Incorrect—MUC-1 is definitely expressed in both ovarian and breast cancers.

Warfarin is an oral anticoagulant that works by inhibiting vitamin K-dependent clotting factors—specifically Factors II, VII, IX, and X, along with proteins C and S. These factors are mostly involved in the extrinsic and common coagulation pathways.

Why PT/INR is Used:

• Prothrombin Time (PT) measures the extrinsic pathway, especially sensitive to Factor VII, which has the shortest half-life among the vitamin K-dependent factors.

• Because lab PT values can vary, results are standardized using the International Normalized Ratio (INR).

• INR is essential for monitoring warfarin therapy to ensure the patient is in the therapeutic range (typically INR 2.0–3.0 for most indications).

Why the Other Options Are Incorrect:

• Activated Partial Thromboplastin Time (aPTT):
  Measures the intrinsic pathway, mainly used to monitor heparin, not warfarin.

• Bleeding Time:
  Assesses platelet function and vascular integrity, but not useful for monitoring anticoagulants like warfarin.

• Complete Blood Picture (CBC):
  Gives information on red cells, white cells, and platelets—but doesn’t reflect clotting function or anticoagulation status.

• None of these:
  Incorrect—PT/INR is absolutely the correct and standard test for monitoring warfarin.

The body is host to trillions of microorganisms that live on or within various tissues and organs without causing disease — this is known as normal flora or commensal microbiota. These organisms often protect against pathogens, aid digestion, and stimulate the immune system.

However, some body compartments are sterile, and the presence of microorganisms in these areas is considered abnormal and pathological.

Why “Blood” Is Correct:

• Blood is a sterile environment in healthy individuals.
• The presence of microbes in the blood (bacteremia, viremia, fungemia) is always considered abnormal and often signifies systemic infection (e.g., sepsis, endocarditis).
• Unlike mucosal surfaces or skin, the bloodstream should never host colonizing flora.

Why the Other Options Are Incorrect (They Do Have Normal Flora):

Vagina:

• Populated by Lactobacillus species, which produce lactic acid to maintain an acidic pH and inhibit pathogens.

Colon:

• Extremely dense with microbial life; dominated by anaerobes like Bacteroides, as well as E. coli, Clostridium, and many others.

Distal urethra:

• Contains low levels of normal flora, including Staphylococcus epidermidis, Enterococcus, and Lactobacillus; this is more pronounced in females due to proximity to the vaginal and perianal flora.

Skin:

• Colonized by Staphylococcus epidermidis, Propionibacterium, and Corynebacterium; these organisms help prevent colonization by pathogens.

Dental caries result from the demineralization of tooth enamel and dentin due to acid production by bacteria in dental plaque. The primary culprit? Streptococcus mutans.

Why Streptococcus mutans?

• A gram-positive cocci, facultatively anaerobic.
• It:
  • Adheres to enamel using dextran-based biofilms (formed from dietary sucrose)
  • Ferments sugars, producing lactic acid
  • Lowers pH in the local environment, leading to enamel demineralization
• It thrives in acidic environments, perpetuating the cycle of decay.

It is the most significant initiator of dental caries, particularly early-stage enamel lesions.

Why the Other Options Are Incorrect:

Staphylococcus epidermidis:

• A skin commensal organism; not involved in dental caries.

Neisseria gonorrhoeae:

• A sexually transmitted pathogen affecting the genital tract and occasionally oropharyngeal tissues, but not implicated in caries.

Candida albicans:

• A fungus associated with oral thrush and angular cheilitis, particularly in immunocompromised individuals or denture wearers.
• Not a key agent in caries formation.

Prevotella melaninogenica:

• An anaerobic gram-negative rod associated with periodontal disease, not dental caries.
• Plays a role in inflammatory gum diseases, not enamel erosion.

It is not just due to decreased intake — it’s a cytokine-driven metabolic derangement, primarily involving inflammation-induced catabolism.

TNF-α (Tumor Necrosis Factor-alpha):

• Sometimes nicknamed “cachectin” for its prominent role in cachexia.
• Produced by macrophages, tumor cells, and other immune cells.
• Promotes:
  • Lipolysis and proteolysis
  • Decreased appetite
  • Increased basal metabolic rate
  • Muscle wasting and fat loss
• Induces IL-1 and IL-6, further amplifying catabolic pathways.

So, TNF-α is central to the pathophysiology of cancer cachexia.

Why the Other Options Are Incorrect:

IL-2:

• Promotes T-cell proliferation and activation.
• Important in cell-mediated immunity, but not involved in cachexia.

IL-5:

• Involved in eosinophil activation and IgA class switching.
• Plays a role in allergic responses, not cachexia.

TGF-β (Transforming Growth Factor-beta):

• Has immunosuppressive and fibrogenic effects.
• Involved in tumor progression and wound healing, but not in the development of cachexia.

CCL-5 (RANTES):

• A chemokine involved in leukocyte recruitment, especially T cells and eosinophils.
• It plays a role in inflammation and HIV pathogenesis, but not in cancer-related wasting.

Iron deficiency anemia is the most common type of anemia worldwide. It typically results from chronic blood loss, inadequate dietary intake, or malabsorption. The lack of iron impairs hemoglobin synthesis, leading to distinct changes in red blood cell (RBC) morphology.

In Severe Iron Deficiency Anemia, You Typically See:

• Microcytosis (small RBCs)
• Hypochromia (pale RBCs due to low hemoglobin content)
• Anisocytosis (variation in RBC size)
• Poikilocytosis (variation in RBC shape) — this is especially characteristic in severe cases

Poikilocytosis reflects defective erythropoiesis due to prolonged iron deficiency, leading to misshapen red cells such as:

• Target cells
• Tear drop cells
• Pencil cells

Why the Other Options Are Incorrect:

Macrocytosis:

• Seen in megaloblastic anemias (e.g., vitamin B12 or folate deficiency), not iron deficiency.
• RBCs are large, not small.

Elliptocytosis:

• Typically associated with hereditary elliptocytosis, a genetic RBC membrane disorder.
• Not a feature of iron deficiency.

Hyperchromia:

• Would indicate increased hemoglobin concentration, which is contrary to IDA, where hypochromia is the hallmark.
• In IDA, cells are pale (hypochromic) due to less hemoglobin.

Schistocytosis:

• Refers to fragmented RBCs, seen in microangiopathic hemolytic anemias like DIC, TTP, HUS.
• Not related to iron deficiency.

Thrombocytopenia refers to a low platelet count, typically defined as <150,000/µL. Platelets are essential for primary hemostasis, forming the initial platelet plug at sites of vessel injury. When platelet levels are low, small vessel bleeding becomes prominent.

Typical Clinical Features of Thrombocytopenia:

These result from defective primary hemostasis, leading to bleeding that is often:

• Mucocutaneous in nature
• Superficial and occurs immediately after trauma

Common manifestations include:

• Petechiae (pinpoint skin hemorrhages)
• Ecchymosis (larger skin bruises)
• Easy bruising
• Epistaxis (nosebleeds)
• Menorrhagia in women
• Gum bleeding

Why “Bleeding in Joints” Is the Correct (Incorrect) Option:

• Hemarthrosis (bleeding into joints) is a hallmark of coagulation factor deficiencies, especially Hemophilia A (Factor VIII deficiency) and Hemophilia B (Factor IX deficiency).
• It reflects defective secondary hemostasis, which is responsible for stabilizing the clot via the coagulation cascade.
• It is not characteristic of thrombocytopenia.

Why the Other Options Are Incorrect (i.e., they are features of thrombocytopenia):

Petechial hemorrhages:

• Classic finding in platelet disorders. Results from capillary leakage due to poor platelet plug formation.

Ecchymosis:

• Larger areas of skin discoloration from bleeding, often seen when platelet counts are very low.

Bruises:

• Common in thrombocytopenia due to minimal trauma causing superficial bleeding.

Epistaxis:

• Frequent nosebleeds are common due to mucosal capillary fragility and impaired platelet function.

Inflammation is the body’s defense response to infection or injury. A key step in the inflammatory process is chemotaxis — the directed movement of immune cells (especially neutrophils) toward the site of injury or infection.

What is Chemotaxis?

• It is the process by which leukocytes are attracted to chemical signals at the site of inflammation.
• These chemoattractants help leukocytes navigate through tissues toward pathogens or damaged cells.

Leukotriene B4 (LTB4):

• A lipid mediator derived from arachidonic acid via the lipoxygenase pathway.
• Powerful chemoattractant and activator of neutrophils.
• Increases neutrophil adhesion, degranulation, and ROS production.

Bacterial Products:

• Especially N-formylated peptides like fMLP (formyl-methionyl-leucyl-phenylalanine), released by bacteria.
• Recognized by pattern recognition receptors on neutrophils, leading to chemotaxis.

Together, LTB4 and bacterial peptides are key chemotactic agents, making them the correct answer.

Why the Other Options Are Incorrect:

Prostaglandin:

• These lipid mediators (like PGE2, PGI2) are involved in vasodilation, pain, and fever, not chemotaxis.

Leukotriene C4, D4, E4:

• These are slow-reacting substances of anaphylaxis (SRS-A).
• They are involved in bronchoconstriction, vasoconstriction, and increased vascular permeability, but not chemotaxis.

Substance P:

• A neuropeptide involved in pain transmission and vasodilation, but it does not guide leukocyte migration.

Histamine:

• Increases vascular permeability and causes vasodilation, facilitating immune cell entry into tissues.
• However, it does not direct cells toward the site (i.e., it’s not chemotactic).

To answer this question, it’s important to understand how tumors are named and classified based on tissue origin and behavior (benign vs. malignant).

Key Principles:

• Benign tumors: These are non-invasive, well-differentiated, and do not metastasize. Their names usually end in “-oma.”
• Malignant tumors: These invade surrounding tissues, may metastasize, and often show poor differentiation. While most malignant tumors of mesenchymal origin are called sarcomas and of epithelial origin are called carcinomas, there are exceptions in naming.

Why the Correct Answer Is Right:

Mesothelioma

This is a malignant tumor arising from the mesothelial lining of body cavities, most commonly the pleura. It is strongly associated with asbestos exposure. Despite ending in “-oma,” mesothelioma is malignant by nature. It is aggressive, with a poor prognosis, and is an exception to the usual naming convention.

Why the Other Options Are Incorrect:

Osteoma

This is a benign bone tumor. It often arises in the skull or facial bones and grows slowly. It does not invade surrounding tissue or metastasize.

Chondroma

This is a benign cartilaginous tumor, usually occurring in small bones of the hands and feet. It’s well-circumscribed and non-aggressive.

Leiomyoma

This is a benign tumor of smooth muscle, commonly seen in the uterus (fibroids). Although they can cause significant symptoms, they do not behave malignantly.

Fibroma

This is a benign tumor of fibrous connective tissue. It’s slow-growing, well-differentiated, and non-invasive.

The classic signs of inflammation were first described by Celsus and later expanded by Galen. These include redness (rubor), heat (calor), swelling (tumor), pain (dolor), and loss of function (functio laesa). Each of these signs represents a different physiological change that occurs in response to tissue injury or infection.

Increase in temperature is typically due to vasodilation and increased blood flow to the affected area. It is readily appreciable through simple palpation. Clinically, it’s quite easy to detect by comparing the affected area to surrounding skin.

Loss of function, while a key pathophysiological feature, is often subtle and not immediately obvious without further examination or history-taking. For example, a swollen, inflamed joint may have decreased range of motion, but this has to be assessed deliberately. In internal organs, such as the lungs or liver, loss of function may require specialized testing or imaging. This makes it the least easily detected of the cardinal signs.

Tenderness is a very common and overt symptom. When the inflamed area is palpated, it often elicits a pain response from the patient. It’s highly sensitive and easily elicited during a clinical exam.

Swelling is caused by increased vascular permeability and accumulation of fluid in the tissue. It is often visible to the naked eye or palpable, especially in superficial tissues.

Pain is often the most distressing and prominent symptom for patients. It is a frequent presenting complaint and very noticeable without any need for special testing.

So, while all five are hallmark signs of inflammation, loss of function stands out as the one that requires more active assessment and may not be immediately evident, especially in less obvious or internal conditions.

Hemophilia A is a hereditary bleeding disorder caused by a deficiency of clotting factor VIII, an essential cofactor in the intrinsic pathway of the coagulation cascade.

Key Features:

• X-linked recessive inheritance → Primarily affects males

• Factor VIII works with activated factor IX (IXa) to convert factor X to Xa.

• Deficiency leads to defective clot formation and prolonged bleeding.

• Common presentations: spontaneous bleeding, hemarthrosis (bleeding into joints), and prolonged bleeding after trauma/surgery

Why the correct answer is right:

• Hemophilia A = Factor VIII deficiency

• It’s the most common type of hemophilia

Why the other options are incorrect:

• Thrombocytopenia:
  This is a low platelet count, unrelated to clotting factors.

• Polycythemia:
  Refers to increased red blood cell mass, not a bleeding disorder.

• Von Willebrand disease:
  Caused by deficiency or defect in von Willebrand factor (vWF), which may indirectly lower factor VIII levels but is not the same as hemophilia A.

• Hemophilia B:
  Caused by factor IX deficiency, not VIII. Also known as Christmas disease.

Leukemia is a malignant neoplasm of the hematopoietic stem cells, particularly those in the myeloid or lymphoid lineages. It involves uncontrolled proliferation of immature white blood cells (blasts) that accumulate in the bone marrow and spill into the blood, crowding out normal hematopoietic cells.

Key characteristics:

• Can originate from:

  • Myeloid lineage → e.g., AML (acute myeloid leukemia), CML (chronic myeloid leukemia)

  • Lymphoid lineage → e.g., ALL (acute lymphoblastic leukemia), CLL (chronic lymphocytic leukemia)

• Results in:

  • Anemia (↓ RBCs)

  • Thrombocytopenia (↓ platelets)

  • Neutropenia or dysfunctional leukocytes

Why the correct answer is right:

• Leukemia refers specifically to malignant proliferation of white cell precursors—either myelogenous or lymphogenous—making it the most precise and accurate term for cancer of these blood cells.

Why the other options are incorrect:

• Thrombocytosis:
  This means increased platelet count, often reactive (e.g., infection, inflammation), not necessarily malignant and not involving white cells.

• Leukopenia:
  Refers to a decrease in white blood cell count. It is often a symptom, not a cancer.

• Anemia:
  Refers to low red blood cell levels. Again, this is a manifestation, not a cancer.

• Leukemoid reaction:
  This is a benign, exaggerated response to infection or stress, where WBC counts may mimic leukemia—but with no clonal malignancy or bone marrow replacement.

Normal somatic cells have a finite number of divisions due to the progressive shortening of telomeres—the protective caps at the ends of chromosomes. When telomeres become too short, the cell enters senescence or apoptosis to prevent genomic instability.

Cancer cells bypass this replicative limit by reactivating or upregulating the enzyme telomerase. Telomerase adds repetitive nucleotide sequences to the ends of chromosomes, maintaining telomere length even after many rounds of cell division.

Why this is crucial:

• Allows immortality of cancer cells

• Seen in over 85–90% of human cancers

• Contributes to genomic stability in rapidly dividing tumor cells

Why the correct answer is right:

• Telomerase prevents telomere shortening, allowing indefinite cell division—a key hallmark of cancer (“limitless replicative potential”).

Why the other options are incorrect:

• Cellular senescence:
  This is the opposite—a protective mechanism that limits cell division to prevent malignant transformation.

• Mitotic catastrophe:
  A form of cell death due to aberrant mitosis—not a mechanism cancer uses to survive.

• Increase in apoptosis:
  Cancer cells typically evade apoptosis, not promote it.

• Increased IGF resulting in angiogenesis:
  While IGF (insulin-like growth factor) may play a role in tumor growth and angiogenesis, it does not explain the limitless replicative ability of cancer cells. That’s the job of telomerase.

Oncofetal antigens are proteins that are normally expressed during fetal development but are re-expressed in certain tumor cells. These antigens are not typically found in significant amounts in healthy adult tissues, making them valuable tumor markers in oncology.

🔍 Why are they important?

During fetal development, these proteins play normal roles in growth and differentiation. However, in cancer, the re-expression of these genes reflects a return to a less differentiated, more proliferative state—hallmarks of malignancy.

🧪 Examples of Oncofetal Antigens:

• Alpha-fetoprotein (AFP):

  • Normally produced by the fetal liver.

  • Elevated in hepatocellular carcinoma and yolk sac tumors.

• Carcinoembryonic antigen (CEA):

  • Normally expressed in fetal gut, liver, and pancreas.

  • Elevated in colorectal, pancreatic, and gastric cancers.

❌ Why the other options are incorrect:

• Fraternal antigens:
  Not a recognized term in immunology or oncology.

• Oncofetal maternal antigens:
  Incorrect term—maternal refers to the mother, while oncofetal antigens originate from fetal and tumor cells.

• Neonatal antigens:
  Refers to antigens in the newborn period, not necessarily re-expressed in tumors.

• Cryptic antigens:
  These are normally hidden from the immune system and may become exposed due to cell damage but are not specific to fetal or tumor states.

🔹 Why Mast cells is correct:

Anaphylactic shock is a severe, life-threatening allergic reaction classified as a Type I hypersensitivity reaction. It is mediated by IgE antibodies that are bound to the surface of mast cells and basophils.

Upon exposure to an allergen (like a drug injection), the allergen cross-links IgE antibodies on mast cells, triggering them to rapidly degranulate and release:

• Histamine

• Leukotrienes

• Prostaglandins

• Cytokines

These mediators cause:

• Vasodilation (leading to hypotension),

• Increased vascular permeability (causing edema),

• Bronchoconstriction (leading to airway compromise),

• Hives, flushing, and shock.

Mast cells are therefore the primary effector cells in anaphylaxis.

❌ Why the other options are incorrect:

• B-lymphocytes
  They are involved in antibody production but do not directly cause anaphylaxis.

• Macrophages
  Participate in phagocytosis and chronic inflammation, but are not responsible for the immediate hypersensitivity reaction.

• Plasma cells
  These are differentiated B-cells that produce antibodies, including IgE, but they do not release inflammatory mediators.

• Antigen-presenting cells (APCs)
  Like dendritic cells or macrophages, APCs are involved in initiating immune responses, but are not directly responsible for anaphylactic symptoms.

🔹 Why T-cell is correct:

T-cells (or T-lymphocytes) are thymus-derived immune cells that are central to cell-mediated immunity. Their precursors originate in the bone marrow, but they mature in the thymus, where they undergo selection to recognize self-MHC and avoid self-antigens.

They participate in a wide range of cell-mediated immune reactions, including:

• Cytotoxic T cells (CD8⁺): Kill virus-infected and tumor cells.

• Helper T cells (CD4⁺): Activate macrophages, B cells, and cytotoxic T cells via cytokine release.

• Regulatory T cells: Suppress immune responses and maintain tolerance.

T-cells do not produce antibodies, but they are essential in direct immune responses, unlike B-cells which are involved in humoral immunity.

❌ Why the other options are incorrect:

• Monocyte
  A phagocytic cell that differentiates into macrophages in tissues; not thymus-derived and not specialized for cell-mediated immunity.

• Natural killer cell
  Part of the innate immune system, kills infected and tumor cells without prior sensitization, but is not thymus-derived.

• Plasma cell
  A terminally differentiated B-cell that secretes antibodies — central to humoral immunity, not cell-mediated.

• Polymorphonuclear cell
  Refers to neutrophils, which are also part of the innate immune system, involved in phagocytosis, not adaptive cell-mediated immunity.

🔹 Why 4 is correct:

The alpha-globin gene is unique because it is present in two copies on each chromosome 16, totaling four genes (αα/αα) in a normal individual. These genes are essential for producing the alpha chains of hemoglobin.

Alpha thalassemia occurs when one or more of these four genes are deleted or mutated. The severity of the disease depends on how many alpha genes are lost:

Thus, the clinical spectrum of alpha thalassemia is defined by the number of affected genes out of the 4 total.

❌ Why the other options are incorrect:

• 5, 3, 2, 1
  These numbers do not reflect the total number of alpha globin genes in a normal person. The correct and relevant number for alpha thalassemia variations is 4.

🔹 Why Opsonization is correct:

Opsonization is the process by which pathogens or antigen-antibody complexes are marked (“tagged”) for enhanced phagocytosis.

Key players in opsonization:

• C3b, a complement protein, binds to the surface of pathogens or immune complexes.

• Fc region of IgG antibodies can also act as opsonins.

Phagocytic cells such as macrophages and neutrophils have C3b receptors (CR1) and Fc receptors, which recognize these tags and facilitate efficient engulfment and destruction of the target.

Thus, C3b acts as an opsonin, significantly increasing the efficiency of phagocytosis.

❌ Why the other options are incorrect:

• Cytolysis
  Refers to the destruction of cells, especially through complement membrane attack complexes (MAC), not enhanced phagocytosis.

• Chemotoxin
  Not a standard term. Possibly a confusion with chemotaxis, which refers to cell movement toward chemical signals like C5a, but not relevant to phagocytosis tagging.

• Anaphylatoxin
  C3a and C5a are called anaphylatoxins because they trigger histamine release and inflammation, not opsonization.

• Lysis of bacteria
  Involves direct destruction of bacteria (e.g., via MAC), whereas opsonization involves marking for phagocytosis, not direct lysis.

The most common cause of a defect in leukocyte function is bone marrow suppression. This is because most leukocytes (especially neutrophils) are produced in the bone marrow. Any condition that impairs bone marrow function — such as chemotherapy, radiation therapy, aplastic anemia, or certain infections — can lead to quantitative and qualitative defects in leukocytes, reducing both their number and their effectiveness.

Key Points:

• Bone marrow suppression decreases leukocyte production, particularly neutrophils, leading to neutropenia.
• Fewer functional leukocytes mean impaired host defense mechanisms, especially against bacterial and fungal infections.
• It is acquired and far more common than inherited defects.

Why the Other Options Are Incorrect:

• Inherited defect in leukocyte adhesion: Refers to Leukocyte Adhesion Deficiency (LAD) — rare.
• Inherited defect in phagolysosome function: Seen in Chediak-Higashi syndrome, a rare autosomal recessive disorder.
• Chediak-Higashi syndrome: Specifically involves lysosomal trafficking defects; very uncommon.
• Inherited defect in microbial activity: Typically refers to Chronic Granulomatous Disease (CGD) — also rare.

These inherited conditions are significant but far less common than acquired defects like bone marrow suppression.

Thrombocytopenia refers to a condition where the platelet count is abnormally low, impairing the blood’s ability to clot. While minor bleeding episodes like gum or nose bleeding are common, the most dangerous and potentially fatal complication is intracranial bleeding.

Why is intracranial bleeding so fatal?

• The skull is a rigid structure — even a small amount of bleeding can increase intracranial pressure rapidly.
• This pressure can lead to brain herniation, coma, and death if not promptly treated.
• Unlike external bleeding, it’s often silent initially, making early detection difficult and increasing the risk of fatal outcomes.

Why the Other Options Are Incorrect:

• Needle prick: Minor and rarely serious — easily managed with pressure.
• Gum bleeding: Common but not life-threatening.
• Gastro-intestinal bleeding: Can be serious but typically detectable and treatable if medical attention is sought early.
• Nose bleeding (epistaxis): Common and usually controllable unless combined with another bleeding disorder.

Thrombocytopenia refers to a condition where the platelet count is abnormally low, impairing the blood’s ability to clot. While minor bleeding episodes like gum or nose bleeding are common, the most dangerous and potentially fatal complication is intracranial bleeding.

Why is intracranial bleeding so fatal?

• The skull is a rigid structure — even a small amount of bleeding can increase intracranial pressure rapidly.
• This pressure can lead to brain herniation, coma, and death if not promptly treated.
• Unlike external bleeding, it’s often silent initially, making early detection difficult and increasing the risk of fatal outcomes.

Why the Other Options Are Incorrect:

• Needle prick: Minor and rarely serious — easily managed with pressure.
• Gum bleeding: Common but not life-threatening.
• Gastro-intestinal bleeding: Can be serious but typically detectable and treatable if medical attention is sought early.
• Nose bleeding (epistaxis): Common and usually controllable unless combined with another bleeding disorder.

An important and defining feature of acute inflammation is changes in the microvasculature (small blood vessels such as arterioles, capillaries, and venules). These changes are responsible for the cardinal signs of inflammation — redness, heat, swelling, pain, and loss of function.

Key microvascular changes in acute inflammation include:

Vasodilation – increased blood flow to the area (causing redness and heat).

Increased vascular permeability – allows plasma proteins and leukocytes to exit the bloodstream and enter tissues (causing swelling).

Endothelial activation – expression of adhesion molecules for leukocyte rolling, adhesion, and transmigration.

These responses are crucial to deliver immune cells and proteins to eliminate the offending agents (e.g., pathogens or damaged cells).

Why the Other Options Are Incorrect:

• Accumulation of B-cells: This is more characteristic of chronic inflammation, which involves lymphocytes and macrophages.
• Decreased blood flow: Acute inflammation begins with increased blood flow (vasodilation), not decreased.
• Transmigration of plasma and red blood cells: While plasma leaks out, RBCs generally do not transmigrate; they may passively escape only in severe injury.
• Activation of RBCs: Red blood cells do not have immune functions; they are not involved in eliminating pathogens.

G6PD deficiency is an X-linked recessive enzymatic disorder that makes red blood cells more vulnerable to oxidative stress. Glucose-6-phosphate dehydrogenase (G6PD) plays a critical role in the pentose phosphate pathway, which generates NADPH — a molecule essential for maintaining glutathione in its reduced form.

Mechanism of Hemolysis:

• Without sufficient NADPH, red blood cells can’t effectively neutralize reactive oxygen species.
• Oxidative damage leads to the denaturation of hemoglobin, which aggregates into Heinz bodies — clumps of damaged hemoglobin seen on special stains.
• These Heinz bodies attach to the red cell membrane, damaging it and marking the cell for destruction, especially by splenic macrophages, leading to hemolysis.

Why the Other Options Are Incorrect:

• Spherocytosis: A defect in membrane proteins like spectrin or ankyrin causes spherical red cells—not related to oxidative stress or Heinz bodies.
• Spectrin deficiency: This causes hereditary spherocytosis, not G6PD deficiency.
• Excess of alpha globin chains: This is characteristic of beta-thalassemia, where unpaired alpha chains damage red cells.
• Hemosiderosis: Refers to iron overload from chronic transfusions, not a cause of hemolysis itself.

Among all the immunoglobulins, IgG is the only antibody class that can cross the placenta from mother to fetus. This transport is facilitated by specific Fc receptors (FcRn) on placental cells, which actively move IgG from maternal circulation into the fetal bloodstream.

Why is this important?

• IgG transfer provides the newborn with passive immunity during the first few months of life.
• This includes protection against common pathogens the mother has immunity to, such as measles, rubella, or influenza.

Why the Other Options Are Incorrect:

• IgA: Found predominantly in mucosal secretions (e.g., breast milk, saliva); it does not cross the placenta.
• IgM: The largest antibody (pentameric), making it too big to cross the placental barrier.
• IgE: Involved in allergic reactions and parasitic defense; does not cross the placenta.
• IgD: Primarily a receptor on B cells; it has no significant presence in circulation and does not cross the placenta.

A scar formed during pathological wound healing is characterized by fibrosis, which refers to the excessive accumulation of fibrous connective tissue, mainly composed of collagen. This process is a response to chronic injury or inflammation and leads to tissue that is dense, stiff, and non-functional compared to normal tissue.

Why is it Fibrotic?

• Fibrotic tissue results from the overactivation of fibroblasts and the deposition of extracellular matrix proteins, especially collagen.
• It lacks the normal structure and function of the original tissue.
• Fibrotic scars are a hallmark of diseases such as pulmonary fibrosis, cirrhosis, and keloids.

Why the Other Options Are Incorrect:

• Collagen: This is a major component of the scar but does not describe its overall nature.
• Necrotic tissue: This refers to dead or dying tissue, usually removed before healing begins—scars are formed from living fibrous tissue.
• Dead tissue: A scar is made of live fibroblasts and collagen, not dead cells.
• Elastic: Scar tissue is typically inelastic and stiff, unlike the normal tissue it replaces.

In β-thalassemia major, patients suffer from severe anemia due to defective production of β-globin chains. To manage this, regular blood transfusions are necessary, which unfortunately lead to iron overload.

There are two key contributors to this iron overload:

1. Chronic blood transfusions: Each unit of blood contains iron, and the human body has no natural mechanism to excrete excess iron. Over time, repeated transfusions significantly increase total body iron.

2. Low hepcidin levels: Hepcidin is a hormone produced by the liver that regulates iron absorption in the intestines and iron release from macrophages. In β-thalassemia, hepcidin levels are pathologically low, leading to increased dietary iron absorption in addition to the iron from transfusions.

These two mechanisms act synergistically to produce iron overload, which can result in organ damage (e.g., heart, liver, endocrine glands) if not managed with iron chelation therapy.

❌ Why the other options are incorrect:

• Elevated hepcidin levels: This would actually reduce iron absorption and mitigate iron overload—not cause it.

• Increased hemolysis: While present, it doesn’t significantly contribute to iron overload compared to transfusions and low hepcidin.

• Chronic blood transfusion: True, but this option ignores the compounding role of low hepcidin, making it incomplete.

• Low hepcidin levels: Also correct but incomplete on its own—doesn’t account for the transfusional iron load.

This clinical scenario describes a thermal injury (burn) that results in erythema (redness) and the formation of blisters. These findings are characteristic of serous inflammation, a type of acute inflammation.

🔬 What is serous inflammation?

• Definition: A form of acute inflammation where there is outpouring of thin, watery, protein-poor fluid derived from plasma or mesothelial cell secretions.

• Classic examples:

  • Blisters from burns (like in this case)

  • Blisters from viral infections (e.g., herpes simplex)

  • Early phase of inflammation in body cavities (pleura, peritoneum)

❌ Why the other options are incorrect:

• Ulceration: Involves loss of surface epithelium. This case shows blisters, not ulcerated tissue.

• Granulomatous inflammation: A chronic inflammatory process involving macrophages and giant cells. Seen in tuberculosis, sarcoidosis—not burns.

• Inflammation: Too general a term; does not specify type.

• Fibrinoid inflammation: Usually associated with immune reactions in blood vessels, such as in immune vasculitis or severe hypertension. It involves fibrin deposition, not blister formation.

Serum ferritin is considered the most reliable and specific non-invasive diagnostic test for iron deficiency anemia (IDA). Ferritin is a protein that stores iron inside cells and releases it when needed. The level of serum ferritin reflects the body’s iron stores.

• In iron deficiency anemia, serum ferritin levels are low, often before other abnormalities become apparent.

• It is non-invasive because it only requires a blood sample.

• Low serum ferritin is highly specific for iron deficiency, especially when the patient has no other conditions that elevate ferritin (like inflammation or infection).

❌ Why the other options are incorrect:

• Total iron-binding capacity (TIBC): This increases in IDA but is less specific and usually used along with ferritin and serum iron for full iron panel evaluation.

• Lipid profile: Measures cholesterol and triglycerides; not related to iron status.

• Complete blood count (CBC): Helps suggest anemia and its morphology (e.g., microcytic), but does not confirm iron deficiency as the cause.

• HbA1c: Measures long-term blood glucose control; used in diabetes management, not anemia diagnosis.

When the complement system is activated as part of the innate immune response, it leads to the recruitment of neutrophils to the site of infection or injury. Here’s how:

• Complement activation produces C3a and C5a, which are anaphylatoxins.

• These molecules increase vascular permeability and act as chemotactic factors, attracting neutrophils to the inflamed tissue.

• Neutrophils are the first responders to acute inflammation, where they phagocytose pathogens and release enzymes that help control infection.

Thus, an acute increase in neutrophils is a hallmark of acute inflammation mediated by complement.

❌ Why the other options are incorrect:

• Basophils: Involved more in allergic responses, not the primary cells recruited by complement.

• Eosinophils: More involved in parasitic infections and allergies.

• T-lymphocytes: Key players in adaptive immunity, not immediate responders in complement-mediated inflammation.

• B-lymphocytes: Produce antibodies but are not acutely increased due to complement activity.

Anti-neuronal antibodies are a feature that can be observed in Systemic Lupus Erythematosus (SLE), particularly when patients exhibit neurological symptoms like seizures, psychosis, or other neuropsychiatric manifestations. In SLE, these antibodies can contribute to neuropsychiatric lupus, which includes a variety of neurological disorders. However, anti-neuronal antibodies are not exclusive to SLE, and their presence in other conditions such as Bannwarth’s syndrome (a form of Lyme disease) can be more prominent in certain clinical contexts.

• SLE is an autoimmune disease where the body’s immune system attacks its own tissues, leading to a wide range of symptoms, including those affecting the central nervous system (CNS). In this context, anti-neuronal antibodies are associated with the disease’s neuropsychiatric manifestations, but they are not a hallmark feature of SLE.

Why other options are incorrect:

1. Psoriasis – This is a chronic skin condition and does not typically involve anti-neuronal antibodies.

2. Bannwarth’s syndrome – While anti-neuronal antibodies can be detected in this condition, it is more closely associated with Borrelia infection, making it less directly relevant in the context of this question.

3. Autoimmune hepatitis – Affects the liver and is not linked to the production of anti-neuronal antibodies.

4. Rheumatoid arthritis – This is an autoimmune disease affecting joints, and anti-neuronal antibodies are not commonly associated with it.

Serum sickness is a Type III hypersensitivity reaction, which is also known as an immune complex-mediated hypersensitivity. In this reaction, the immune system forms immune complexes by binding antibodies (usually IgG) with antigens. These immune complexes then deposit in tissues such as the skin, kidneys, joints, and blood vessels, leading to inflammation and tissue damage. The immune complexes can activate the complement system, which recruits inflammatory cells like neutrophils, causing further damage to the tissues.

Serum sickness most commonly occurs after the administration of non-human serum proteins, such as those used in antivenoms or monoclonal antibodies. It can also occur following some vaccines or medications. Symptoms of serum sickness include fever, rash, joint pain, and swelling, and these typically develop 7 to 10 days after exposure to the antigen.

🔬 Why the Other Options Are Incorrect:

1. Type I Hypersensitivity:

   • Type I hypersensitivity involves IgE-mediated reactions, such as those seen in allergic reactions (e.g., hay fever, asthma, anaphylaxis). It is characterized by immediate responses due to the release of histamine from mast cells and basophils.

2. Type II Hypersensitivity:

   • Type II hypersensitivity is antibody-mediated cytotoxicity, where antibodies (mainly IgG or IgM) bind to antigens on the surface of cells, leading to cell destruction. An example would be hemolytic anemia or transfusion reactions.

3. Type IV Hypersensitivity:

   • Type IV hypersensitivity is cell-mediated, involving T cells rather than antibodies. It is responsible for delayed-type hypersensitivity reactions such as contact dermatitis (e.g., poison ivy), tuberculosis skin test reactions, and graft-versus-host disease.

4. Type III and IV Hypersensitivity:

   • Although serum sickness is a Type III reaction, this option is not accurate because Type III alone is the correct classification.

This patient has a known diagnosis of rheumatoid arthritis (RA), and her symptoms of splenomegaly, anemia, and neutropenia suggest a possible complication of RA known as Felty’s syndrome.

Felty’s syndrome is a rare but recognized complication of rheumatoid arthritis and is characterized by:

• Splenomegaly (enlarged spleen)

• Neutropenia (low neutrophil count)

• Anemia (typically normocytic anemia)

Patients with Felty’s syndrome may also have recurrent infections due to the neutropenia, and this condition is more commonly seen in individuals with long-standing, severe RA. The mechanism is believed to be immune-mediated destruction of neutrophils and splenic sequestration.

🔬 Why the Other Options Are Incorrect:

1. Malaria:

   • While malaria can cause splenomegaly due to parasitic invasion, the patient’s history of rheumatoid arthritis, NSAIDs, and steroid use makes this diagnosis less likely. Additionally, malaria would likely present with other systemic symptoms such as fever and chills, which are absent in this case.

2. Viral fever:

   • Viral infections can occasionally cause splenomegaly, but viral fever is typically associated with acute fever and viral prodromes, which are not mentioned in this case. The anemia and neutropenia in the context of RA and steroid use make viral fever an unlikely cause.

3. Septicemia:

   • Septicemia can cause splenomegaly, but it is usually associated with signs of acute infection, such as fever, tachycardia, and hypotension, which are not described here. The absence of an obvious infection makes this diagnosis less likely.

4. Drug-induced:

   • Certain medications, including NSAIDs and steroids, can cause blood count abnormalities like anemia or neutropenia. However, these drugs do not typically cause splenomegaly unless there is an underlying immune condition like Felty’s syndrome. While drug-induced anemia and neutropenia could be a consideration, the combination of these features with splenomegaly strongly points toward Felty’s syndrome.

β-thalassemia major (also called Cooley’s anemia) is a severe, transfusion-dependent anemia caused by mutations leading to absent or severely reduced beta-globin chain synthesis. It presents in early infancy, typically around 6 months of age, when fetal hemoglobin (HbF) levels begin to decline.

🩺 Treatment Overview:

• Chronic transfusions are essential for survival but lead to iron overload.

• Iron chelation therapy is used to manage iron accumulation.

• Curative treatment: The only definitive cure is allogeneic bone marrow (stem cell) transplantation, especially when performed early in life before organ damage occurs due to iron overload.

❌ Why the Other Options Are Incorrect:

• “Iron overload is due to high levels of hepcidin”
  🔴 Incorrect — In β-thalassemia major, hepcidin levels are low, not high. Low hepcidin leads to increased iron absorption from the gut, contributing to iron overload along with repeated blood transfusions.

• “Manifests itself in-utero”
  🔴 Incorrect — Unlike α-thalassemia major (which can cause hydrops fetalis), β-thalassemia major does not manifest in-utero. Symptoms typically appear several months after birth as HbF declines.

• “With transfusions alone, survival into the sixth or seventh decade is possible”
  🔴 Incorrect — While transfusions can prolong life significantly, long-term survival into the 60s or 70s with transfusions alone is rare due to complications from iron overload and secondary organ damage unless chelation and supportive care are excellent.

The term “bactericidal” refers to any biocide or antimicrobial agent that kills bacteria. The suffix “-cidal” comes from Latin “cida”, meaning “killer” or “to kill.” Therefore, bactericidal agents directly eliminate bacteria rather than merely inhibiting their growth.

Examples of Bactericidal Agents:

• Penicillins (by disrupting bacterial cell walls)

• Fluoroquinolones (by targeting DNA replication enzymes)

• Aminoglycosides

These agents are particularly useful in severe infections or immunocompromised patients, where killing the pathogen is preferable to merely slowing its growth.

❌ Why the Other Options Are Incorrect:

• Bacteriostatic: Inhibits bacterial growth, but does not kill the bacteria. The immune system must clear the infection.

• Antibacteriotic: Not a scientifically recognized term in microbiology.

• Cleaning: A general process of removing dirt or contaminants; may or may not kill microbes.

• Insecticide: Kills insects, not bacteria.

Leukocyte Adhesion Deficiency (LAD) is a rare autosomal recessive innate immune disorder characterized by:

• Defective adhesion and migration of neutrophils to sites of infection

• Caused by mutations in integrins, particularly CD18, which are required for leukocyte adhesion and transmigration across endothelium

🚨 Key Clinical Features of LAD:

• Recurrent bacterial infections, especially of the skin and mucosal surfaces

• Delayed separation of the umbilical cord

• Absence of pus formation despite infections

• High neutrophil count in blood (neutrophilia), because neutrophils cannot exit the bloodstream to reach the infection site

• Consanguinity increases the risk due to autosomal recessive inheritance

❌ Why the Other Options Are Incorrect:

Hemophilia:

• A bleeding disorder, not an immune defect

• Involves coagulation factors, not innate immunity

Wiskott-Aldrich Syndrome:

• X-linked recessive, affects adaptive immunity

• Presents with eczema, thrombocytopenia, and recurrent infections

• Would not fit a female child, since it’s rare in females unless skewed X-inactivation

Systemic Lupus Erythematosus (SLE):

• An autoimmune disease, not a primary immune deficiency

• More common in older females and involves adaptive immunity dysregulation

Common Variable Immunodeficiency (CVID):

• Primarily affects B-cell differentiation

• Typically presents later in childhood or adolescence, not in early infancy

Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease characterized by the production of a wide array of autoantibodies, many of which are directed against nuclear components.

The hallmark of SLE is the formation of antinuclear antibodies (ANAs). These antibodies target various components inside the nucleus, such as:

• Double-stranded DNA (anti-dsDNA)
• Histones
• Smith antigen (anti-Sm)
• Ribonucleoproteins (RNPs)

These nuclear proteins and nucleic acids form immune complexes when bound by autoantibodies. These immune complexes circulate and deposit in tissues (like the kidneys, skin, joints), leading to inflammation and organ damage, which are the hallmark features of SLE.

Anti-dsDNA and anti-Sm are considered highly specific for SLE and are important diagnostic markers.

Why the other options are incorrect:

Nerves

SLE can cause neurological symptoms, but it is not due to antibodies directly targeting nerves. The symptoms are usually due to vascular inflammation or immune complex deposition, not direct autoimmunity against nerve tissue.

Lymphocytes

Lymphocytes are involved in the autoimmune process but are not the primary targets of autoantibodies in SLE.

Myocytes

Muscle inflammation (myositis) can occur in some autoimmune diseases (e.g., polymyositis), but SLE autoantibodies are not primarily directed against muscle cells.

RBCs

Autoimmune hemolytic anemia can occur in SLE, but the central and defining autoantibody targets are nuclear components, not RBCs per se. RBC involvement is secondary.

The special propensity to collect in tissues undergoing allergic reactions is demonstrated by which of the following types of WBCs?

Correct Answer:

Eosinophils

Detailed Explanation:

Eosinophils are a type of granulocytic white blood cell that play a central role in allergic reactions, parasite defense, and certain chronic inflammatory conditions.

They are characterized by:

• Bilobed nuclei
• Large cytoplasmic granules that stain bright red or pink with eosin (hence the name)
• Granules rich in cytotoxic proteins like major basic protein, eosinophil cationic protein, and peroxidases, which are toxic to parasites and host tissues

In allergic reactions, such as asthma or atopic dermatitis, eosinophils are recruited to affected tissues by cytokines like IL-5, which is secreted by Th2 helper T-cells. Once there, they contribute to inflammation and tissue remodeling.

Thus, eosinophils have a special propensity to accumulate in tissues where allergic inflammation is occurring, such as the lungs in asthma or skin in eczema.

Why the other options are incorrect:

Neutrophils

These are the first responders in acute bacterial infections and are excellent at phagocytosing bacteria. They are not specifically associated with allergic responses, although they may appear in chronic inflammation.

Macrophages

Macrophages are derived from monocytes and are involved in chronic inflammation, tissue repair, and antigen presentation. They do not have a special affinity for allergic tissues.

Lymphocytes

These include B-cells, T-cells, and NK cells. While Th2 lymphocytes play a role in promoting eosinophil activation via cytokines like IL-5, lymphocytes themselves do not preferentially collect in allergic tissues.

Platelets

Platelets are not white blood cells. They are cell fragments involved in clotting and have no special role in allergic tissue infiltration.

Reiter’s syndrome, now more commonly called reactive arthritis, is an autoimmune condition that arises after an infection, usually from the gastrointestinal tract (like Shigella, Salmonella, or Campylobacter) or the genitourinary tract (commonly Chlamydia trachomatis). It is classified as a seronegative spondyloarthropathy, typically associated with the HLA-B27 genetic marker.

The classical triad that defines Reiter’s syndrome includes:

• Arthritis: Often asymmetric and involving large joints such as the knees, ankles, or feet. It may be migratory and can include enthesitis (inflammation at tendon insertion sites).
• Conjunctivitis: Mild, non-purulent inflammation of the conjunctiva, usually transient but a key feature in the diagnosis.
• Urethritis: Inflammation of the urethra, leading to symptoms like dysuria or a urethral discharge.

This triad is classically summarized as:

“Can’t see, can’t pee, can’t climb a tree.”

Why the other options are incorrect:

Conjunctivitis, arthritis, cervicitis – Although cervicitis can occur in reactive arthritis, especially in women, it is not a part of the defining triad. Urethritis is the more consistent and classic manifestation.

Arthritis, oophoritis, thyroiditis – Oophoritis and thyroiditis are unrelated to Reiter’s syndrome. These are more indicative of endocrine or reproductive autoimmune disorders, not a reactive post-infectious arthritis.

Thyroiditis, tonsillitis, conjunctivitis – This option misrepresents the typical features of Reiter’s syndrome. Tonsillitis may precede some autoimmune conditions like rheumatic fever, but not reactive arthritis. Thyroiditis is also not involved.

Cervicitis, arthritis, pancreatitis – Pancreatitis is not associated with Reiter’s syndrome. While cervicitis and arthritis may co-occur, the hallmark features of conjunctivitis or urethritis are missing from this combination.

Cell signaling is essential for regulating growth, differentiation, immunity, and repair. There are several types of signaling based on where the signal comes from and who receives it:

📢 Autocrine signaling:

• In autocrine signaling, a cell secretes signaling molecules (like growth factors or cytokines) that bind to receptors on its own surface.

• This means the cell is both the sender and the receiver of the signal.

• This type of signaling is important in:

  • Cell growth and survival (e.g., cancer cells often use autocrine loops to promote uncontrolled growth)

  • Immune response regulation

  • Embryonic development

✅ Correct Answer:

Cell responding to signalling molecules that they themselves secreted

❌ Why the Other Options Are Incorrect:

• Cell responding to signalling molecules that are secreted by far away cells:
  That describes endocrine signaling, where hormones are secreted into the bloodstream and act on distant targets.

• Cell responding to signalling molecules brought by blood:
  Again, this is endocrine signaling, not autocrine.

• Cell responding to signalling molecules brought by lymphatics:
  Lymphatics may help transport immune-related signals, but this does not define autocrine signaling.

• Cell responding to signalling molecules that are secreted by adjacent cells:
  This is paracrine signaling, where cells affect neighboring cells.

Blood grouping involves two key antigen systems:

1. ABO system — based on presence of A and B agglutinogens (antigens).

2. Rh system — based on presence or absence of the D antigen, also called agglutinogen D.

In the Rh system:

• If a person has the D antigen on the surface of their red blood cells, they are Rh-positive.

• If they lack the D antigen, they are Rh-negative.

This is critical in:

• Pregnancy: Rh incompatibility can lead to hemolytic disease of the newborn.

• Transfusions: Giving Rh-positive blood to an Rh-negative person can trigger an immune response.

So, an Rh-positive individual possesses agglutinogen D on their red blood cells.

✅ Correct Answer:

Agglutinogen D

❌ Why the Other Options Are Incorrect:

• Agglutinin D:
  This would be the antibody against D antigen — found in Rh-negative individuals after sensitization, not in Rh-positive individuals.

• Agglutinogen A:
  Part of the ABO system, not related to Rh.

• Agglutinogen B:
  Also part of the ABO system, unrelated to Rh status.

• Agglutinin AB:
  Not a real term — people do not produce antibodies against both A and B unless they are blood group O, but again, this is ABO, not Rh-related.

Hemoglobin (Hb) is the oxygen-carrying protein in red blood cells. Each molecule can bind 4 molecules of oxygen, and this ability is quantified when calculating the oxygen-carrying capacity of blood.

The key value you need to know:

1 gram of pure hemoglobin can combine with approximately 1.34 ml of oxygen (O₂) when fully saturated.

This number is crucial in understanding:

• Arterial oxygen content (CaO₂)

• Oxygen delivery to tissues

• Clinical interpretation of anemia, hypoxia, and oxygen therapy

This value is constant and is used in the oxygen content formula:

CaO₂=(1.34×Hb×SaO₂)+(0.003×PaO₂)\text{CaO₂} = (1.34 \times \text{Hb} \times \text{SaO₂}) + (0.003 \times \text{PaO₂})CaO₂=(1.34×Hb×SaO₂)+(0.003×PaO₂)

✅ Correct Answer:

1.34 ml of oxygen

❌ Why the Other Options Are Incorrect:

• 13.4 ml of carbon dioxide:
  Wrong gas and incorrect volume — hemoglobin does carry some CO₂, but this is not the standard metric.

• 134 ml of oxygen:
  Too high — this would imply 100 grams of Hb.

• 13.4 ml of oxygen:
  This is the oxygen carried by about 10 grams of hemoglobin, not 1 gram.

• 1.34 ml of carbon dioxide:
  Hemoglobin does bind CO₂ (as carbaminohemoglobin), but not in this quantified oxygen-equivalent way.

Neutrophils are the most abundant type of white blood cell (WBC) in the adult human peripheral blood and play a key role in innate immunity, particularly in fighting bacterial infections.

In a normal differential WBC count, neutrophils typically make up:

• 60–70% of total leukocytes in adults.

They are the first responders to infection or inflammation and are involved in:

• Phagocytosis

• Release of granules (e.g., myeloperoxidase)

• Formation of neutrophil extracellular traps (NETs)

A significantly high count (neutrophilia) may indicate bacterial infection, while a low count (neutropenia) may predispose to infections.

✅ Correct Answer:

60 – 70%

❌ Why the Other Options Are Incorrect:

• 20 – 30%:
  Too low for neutrophils. This range is more typical for lymphocytes in adults.

• 0 – 10%:
  Far too low. Could correspond to basophils or eosinophils, not neutrophils.

• 30 – 40%:
  Still too low. May represent a mixed picture or childhood lymphocyte-dominant profile.

• 80 – 90%:
  Too high. May occur in extreme neutrophilic leukocytosis, but not normal.

Iron homeostasis in the human body is tightly regulated, because both iron deficiency and iron overload can be harmful. Importantly, the body has no natural mechanism to actively excrete excess iron, so iron loss is typically passive and occurs via:

• Shedding of skin and intestinal cells

• Minor bleeding (e.g., menstruation)

Now, for rapid depletion of iron stores, the only significant mechanism is through substantial blood loss.

Why?

• Most of the body’s iron (~70%) is found in hemoglobin inside red blood cells.

• When blood is lost (e.g., due to trauma, menstruation, GI bleeding, or donation), iron is lost along with hemoglobin.

• The loss can quickly outpace the body’s ability to recycle iron from senescent RBCs, especially if bleeding is chronic or acute.

✅ Correct Answer:

Blood loss

❌ Why the Other Options Are Incorrect:

• High altitude:
  Increases erythropoiesis due to low oxygen, which may increase iron demand, but it doesn’t directly cause iron loss.

• Weight loss:
  Might reflect poor nutrition, but does not inherently deplete iron rapidly.

• High calcium absorption:
  Calcium competes with iron for absorption in the gut, but this affects iron uptake, not rapid depletion of existing stores.

• Vigorous exercise:
  Can cause minor losses through sweat or gastrointestinal microbleeding in endurance athletes, but not significant or rapid iron depletion in most people.

Innate immunity is the first line of defense in the immune system — it is non-specific, immediate, and does not require prior exposure to a pathogen. It includes physical, chemical, and cellular barriers that act to prevent the entry or spread of microbes.

The skin is one of the most critical components of this system. Here’s why:

• Physical barrier: The skin’s stratified squamous epithelium prevents microbial invasion.

• Chemical barrier: Sweat and sebaceous secretions contain antimicrobial peptides, like defensins and lysozyme.

• Resident microbiota: Compete with pathogens for space and nutrients.

So, among the options listed, skin best represents a major component of innate immunity — it’s a literal frontline barrier.

✅ Correct Answer:

Skin

❌ Why the Other Options Are Incorrect:

• T-cells:
  Part of adaptive (acquired) immunity — specifically cell-mediated immunity. They require antigen presentation and take time to activate.

• Plasma cells:
  These are differentiated B-cells that secrete antibodies — again, part of the adaptive immune response.

• Antibodies:
  While they provide humoral defense, they are products of adaptive immunity, generated after antigen exposure.

• B-cells:
  These are responsible for humoral adaptive immunity, producing antibodies in response to specific pathogens.

In adults, the bone marrow is the primary site of hematopoiesis, including the formation of red blood cells (erythropoiesis).

Key Facts:

• Red blood cells originate from hematopoietic stem cells (HSCs).

• The myeloid lineage pathway gives rise to erythroid precursors, including:

  • Proerythroblast → Basophilic erythroblast → Polychromatic erythroblast → Orthochromatic erythroblast → Reticulocyte → Mature RBC

Sites of erythropoiesis by age:

• Fetal life: Initially in yolk sac, then liver and spleen

• At birth and throughout childhood: In all bones

• In adults: Restricted to axial skeleton (vertebrae, ribs, pelvis, sternum) and proximal femur/humerus

Why the correct answer is right:

• The bone marrow houses the entire process of RBC production from stem cells to reticulocytes in adults.

Why the other options are incorrect:

• Liver:
  Major site of fetal erythropoiesis, but in adults, it no longer produces RBCs under normal conditions.

• Kidney:
  Produces erythropoietin (EPO), which stimulates erythropoiesis, but does not make RBCs itself.

• Spleen:
  Functions in RBC destruction, immune response, and occasionally extramedullary hematopoiesis in disease states—but not the primary site in healthy adults.

• Lymphoid tissues:
  Involved in immune cell development, not erythropoiesis.

Erythroblastosis fetalis, or hemolytic disease of the newborn (HDN), occurs when Rh-negative mothers carry Rh-positive fetuses. During the first pregnancy, fetal red cells may enter the maternal circulation (especially during delivery), sensitizing the mother’s immune system to Rh antigen.

In subsequent Rh+ pregnancies, maternal anti-Rh IgG antibodies cross the placenta, destroying fetal red blood cells, leading to:

• Hemolytic anemia

• Jaundice

• Hydrops fetalis (severe cases)

• Erythroblastosis (release of immature RBCs into circulation)