Complement System — MCQs
Which component is considered the central part of the complement pathway?
What is the classification of intelligence corresponding to an IQ score of 90-109?
PNH is associated with all of the following conditions, except:
Both antibody dependent and independent complement pathways converge on which complement component
Increased susceptibility to N. meningitidis infections is associated with deficiency of which complement component:
Match the following drugs in Column A with their contraindications in Column B. | Column A | Column B | | :-- | :-- | | 1. Morphine | 1. QT prolongation | | 2. Amiodarone | 2. Thromboembolism | | 3. Vigabatrin | 3. Pregnancy | | 4. Estrogen preparations | 4. Head injury |
Hereditary angioneurotic edema is due to?
Which of the following components are involved in non-IgE mediated anaphylactic reactions?
What is the primary effect of superantigens on T-cells?
Which one of the following is a major component in activation of the complement alternative pathway?
Complement System Indian Medical PG Practice Questions and MCQs
Question 1: Which component is considered the central part of the complement pathway?
- A. C1 (complement component 1)
- B. C3 (complement component 3) (Correct Answer)
- C. C2 (complement component 2)
- D. C5 (complement component 5)
Explanation: ***C3*** - **C3** is considered the central component because all three major pathways of complement activation (classical, alternative, and lectin) converge at the point of **C3 activation**. - Its cleavage product, **C3b**, is crucial for opsonization, formation of the C5 convertase, and initiating the assembly of the **membrane attack complex (MAC)**. *C1 (complement component 1)* - **C1** is the initial component of the **classical complement pathway** but does not play a direct role in the alternative or lectin pathways. - Its primary function is to bind to **antibody-antigen complexes** or directly to pathogens to activate C4 and C2. *C2 (complement component 2)* - **C2** is a component of the **classical** and **lectin pathways**, acting as a substrate for C1s and MASP to form the C3 convertase. - It is not involved in the initial activation of the **alternative pathway**. *C5 (complement component 5)* - **C5** is activated downstream of C3 and is a key component in the formation of the **membrane attack complex (MAC)**. - While critical for pathogen lysis, its activation is dependent on the prior cleavage of **C3** into C3b.
Question 2: What is the classification of intelligence corresponding to an IQ score of 90-109?
- A. Below average
- B. Average (Correct Answer)
- C. Slightly below average
- D. Above average
Explanation: ***Average*** - An **IQ score** range of **90-109** is traditionally classified as **Average** intelligence. - This range represents the **mean** and surrounding **standard deviation** of IQ scores in the general population. *Below average* - This classification usually corresponds to IQ scores in the range of **70-79** or **80-89**, depending on the specific scale. - It does not represent the central tendency of the population's intelligence. *Slightly below average* - This category typically corresponds to IQ scores in the range of **80-89**. - It falls just below the average range but is not as low as the "below average" classification. *Above average* - This classification is typically assigned to IQ scores that are in the range of **110-119** or higher. - It signifies cognitive abilities that are greater than the majority of the population.
Question 3: PNH is associated with all of the following conditions, except:
- A. Aplastic anemia
- B. Venous thrombosis
- C. Iron deficiency anemia
- D. Increased LAP scores (Correct Answer)
Explanation: ***Increased LAP scores*** - **Paroxysmal nocturnal hemoglobinuria (PNH)** is characterized by **acquired intrinsic stem cell defect**, leading to a deficiency of **glycosylphosphatidylinositol (GPI)-anchored proteins** on the surface of hematopoietic cells [1]. - PNH typically shows **decreased or low leukocyte alkaline phosphatase (LAP) scores**, similar to chronic myeloid leukemia (CML). **Increased LAP scores are NOT a feature of PNH**, making this the correct answer to the "except" question. - Elevated LAP scores are instead seen in conditions like leukemoid reactions, polycythemia vera, and infections. *Aplastic anemia* - **Aplastic anemia** frequently precedes or coexists with **PNH** due to shared underlying **bone marrow suppression** or immune-mediated injury [2]. - Both conditions involve defects in hematopoietic stem cells, making the development of one a risk factor for the other [3]. *Venous thrombosis* - **PNH** patients have an increased risk of **thrombosis**, particularly in unusual sites such as **hepatic (Budd-Chiari syndrome)** or **mesenteric veins**, due to increased platelet activation and endothelial damage [1]. - This prothrombotic state is a major cause of morbidity and mortality in PNH [1]. *Iron deficiency anemia* - **Chronic intravascular hemolysis** in PNH leads to significant **urinary iron loss** as **hemosiderin**, which can cause **iron deficiency anemia** [1]. - This is a direct consequence of the continuous destruction of **red blood cells** and subsequent **iron excretion** [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 650-651. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 595-596. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, p. 662.
Question 4: Both antibody dependent and independent complement pathways converge on which complement component
- A. C8
- B. C1q
- C. C3 (Correct Answer)
- D. C5
Explanation: ***Correct: C3*** - Both the **classical** (antibody-dependent) and **alternative** (antibody-independent) complement pathways lead to the activation and cleavage of **C3** into C3a and C3b. - This convergence on C3 is critical as **C3b** acts as a central opsonin and initiator of the downstream common pathway (terminal pathway). - The **lectin pathway** also converges at C3, making it the central hub of complement activation. *Incorrect: C8* - **C8** is a component of the **membrane attack complex (MAC)**, which forms much later in the complement cascade and is downstream from C3 activation. - While essential for cell lysis, C8 does not represent the initial point of convergence between the antibody-dependent and independent pathways. *Incorrect: C1q* - **C1q** is specifically involved only in the **classical pathway**, where it binds to antibody-antigen complexes or directly to pathogen surfaces. - It plays no direct role in the **alternative pathway**, thus not a point of convergence for both pathways. *Incorrect: C5* - **C5** is activated downstream of C3 and initiates the formation of the **membrane attack complex (MAC)**, similar to C8. - While central to the lytic phase, its activation occurs after the convergence at C3 and is not the initial point where the classical and alternative pathways meet.
Question 5: Increased susceptibility to N. meningitidis infections is associated with deficiency of which complement component:
- A. C1-C4 deficiency
- B. C3 deficiency
- C. C5-C9 deficiency (Correct Answer)
- D. C2 deficiency
Explanation: ***C5-C9 deficiency*** - Deficiencies in **C5-C9 components** impair the formation of the **Membrane Attack Complex (MAC)**, which is crucial for lysing Gram-negative bacteria like **N. meningitidis**. - Patients with MAC deficiencies are at significantly higher risk for recurrent invasive **N. meningitidis** infections. *C1-C4 deficiency* - Deficiencies in **C1-C4 components** primarily affect the **classical complement pathway** and are associated with increased susceptibility to **bacterial infections** and **immune complex diseases** (e.g., SLE). - While these deficiencies compromise opsonization and inflammation, they are not specifically linked to recurrent **N. meningitidis** infections. *C3 deficiency* - **C3 deficiency** is a severe primary immunodeficiency leading to profound defects in complement activation via all pathways, affecting **opsonization** and the formation of the MAC. - This deficiency causes severe recurrent **pyogenic infections** due to encapsulated bacteria but is not as specifically or commonly linked to **N. meningitidis** as deficiencies in the terminal pathway. *C2 deficiency* - **C2 deficiency** is the most common complement deficiency and primarily impacts the **classical pathway**, leading to impaired opsonization and immune complex clearance. - It is often associated with recurrent infections (especially with encapsulated bacteria) and **lupus-like syndromes**, but not specifically increased susceptibility to **N. meningitidis** infections.
Question 6: Match the following drugs in Column A with their contraindications in Column B. | Column A | Column B | | :-- | :-- | | 1. Morphine | 1. QT prolongation | | 2. Amiodarone | 2. Thromboembolism | | 3. Vigabatrin | 3. Pregnancy | | 4. Estrogen preparations | 4. Head injury |
- A. A-1, B-3, C-2, D-4
- B. A-4, B-1, C-3, D-2 (Correct Answer)
- C. A-3, B-2, C-4, D-1
- D. A-2, B-4, C-1, D-3
Explanation: ***A-4, B-1, C-3, D-2*** - **Morphine** is contraindicated in **head injury** as it can increase intracranial pressure and mask neurological symptoms. - **Amiodarone** is contraindicated in patients with **QT prolongation** due to its risk of inducing more severe arrhythmias like Torsades de Pointes. - **Vigabatrin** is contraindicated during **pregnancy** due to its potential for teratogenicity and adverse effects on fetal development. - **Estrogen preparations** are contraindicated in patients with a history of **thromboembolism** due to their increased risk of blood clot formation. *A-1, B-3, C-2, D-4* - This option incorrectly matches **Morphine** with QT prolongation and **Estrogen preparations** with head injury, which are not their primary contraindications. - It also incorrectly links **Vigabatrin** with thromboembolism and **Amiodarone** with pregnancy. *A-3, B-2, C-4, D-1* - This choice incorrectly associates **Morphine** with pregnancy and **Vigabatrin** with head injury, which are not the most critical or direct contraindications. - It also misaligns **Amiodarone** with thromboembolism and **Estrogen preparations** with QT prolongation. *A-2, B-4, C-1, D-3* - This option incorrectly matches **Morphine** with thromboembolism and **Amiodarone** with head injury, which are not their most significant contraindications. - It also incorrectly links **Vigabatrin** with QT prolongation and **Estrogen preparations** with pregnancy.
Question 7: Hereditary angioneurotic edema is due to?
- A. Deficiency of C1 inhibitor (Correct Answer)
- B. Deficiency of NADPH oxidase
- C. Deficiency of MPO
- D. Deficiency of properdin
Explanation: ***Deficiency of C1 inhibitor*** - **Hereditary angioedema (HAE)** is caused by a genetic deficiency or dysfunction of the **C1 esterase inhibitor (C1-INH)** protein. - C1-INH normally regulates the **complement system**, kinin system (mediating **bradykinin** release), and coagulation pathways, and its deficiency leads to uncontrolled activation and excessive bradykinin production, causing angioedema. *Deficiency of NADPH oxidase* - A deficiency in **NADPH oxidase** is associated with **Chronic Granulomatous Disease (CGD)**, a primary immunodeficiency characterized by recurrent bacterial and fungal infections due to impaired phagocytic oxidative burst. - It does not cause angioedema, which involves fluid extravasation rather than impaired microbial killing. *Deficiency of MPO* - **Myeloperoxidase (MPO) deficiency** typically leads to mild to moderate impairment in the killing of certain microorganisms by phagocytes but is often asymptomatic or causes only recurrent candidal infections. - It is not linked to the pathogenesis of angioedema, which involves dysregulation of vasoactive peptides. *Deficiency of properdin* - A deficiency in **properdin** affects the **alternative pathway of the complement system**, increasing susceptibility to **Neisseria infections**. - While properdin is part of the complement system, its deficiency does not directly lead to the uncontrolled production of bradykinin, which is the primary mediator in angioedema due to C1-INH deficiency.
Question 8: Which of the following components are involved in non-IgE mediated anaphylactic reactions?
- A. Complement
- B. Ig G
- C. Ig M
- D. All of the options (Correct Answer)
Explanation: ***All of the options*** - **Non-IgE mediated anaphylactic reactions** can involve various immune components beyond IgE, including **IgG**, **IgM**, and the **complement system**. - For instance, **IgG antibodies** can bind to mast cells or basophils and trigger degranulation, while **complement activation** can directly release anaphylatoxins, both leading to anaphylactoid symptoms. *Ig G* - While many anaphylactic reactions are **IgE-mediated**, **IgG antibodies** can also contribute to anaphylaxis, particularly in drug reactions or reactions to biologics. - **IgG-mediated anaphylaxis** often involves immune complexes that activate mast cells or basophils through Fcγ receptors. *Ig M* - **IgM antibodies** are less commonly implicated in direct anaphylactic reactions compared to IgE or IgG. - However, **IgM** can play a role in complex formation that activates the complement system, indirectly contributing to **anaphylactoid responses**. *Complement* - The **complement system** can be directly activated by certain drugs, physical stimuli, or immune complexes without the involvement of immunoglobulins. - This activation releases **anaphylatoxins (C3a, C4a, C5a)**, which can directly degranulate mast cells and basophils, leading to symptoms mimicking true anaphylaxis.
Question 9: What is the primary effect of superantigens on T-cells?
- A. Polyclonal activation of T-cells leading to cytokine release (Correct Answer)
- B. Stimulation of B cells and antibody production
- C. Enhancement of phagocytosis by macrophages
- D. Activation of the complement system
Explanation: ***Polyclonal activation of T-cells leading to cytokine release*** - **Superantigens** bypass the normal antigen presentation pathway by binding directly to the **MHC class II molecule** and the **T-cell receptor (TCR) beta chain**, activating a large proportion of T-cells. - This widespread T-cell activation results in a massive release of various **cytokines**, leading to systemic inflammation and conditions like **toxic shock syndrome**. *Stimulation of B cells and antibody production* - While B cells can be activated, the primary and most significant effect of superantigens is on T-cells, leading to **non-specific T-cell activation**. - Superantigen-mediated T-cell activation does not directly lead to **antigen-specific B cell activation** and **antibody production** in the same manner as conventional antigens. *Enhancement of phagocytosis by macrophages* - Superantigens do not primarily enhance **macrophage phagocytosis**. Their main mechanism involves direct interaction with **APC MHC class II** and **TCRs**. - Macrophages themselves can act as **antigen-presenting cells** in the superantigen pathway, but their phagocytic function is not the main target. *Activation of the complement system* - The complement system is primarily activated by **antibody-antigen complexes** or directly by pathogen surfaces, not directly by **superantigens**. - While the inflammatory response from superantigens can indirectly affect other immune components, direct activation of the complement cascade is not their primary mechanism of action.
Question 10: Which one of the following is a major component in activation of the complement alternative pathway?
- A. C2
- B. C3 (Correct Answer)
- C. C4
- D. C1
Explanation: ***C3*** - **C3** is a central component in all complement pathways. In the alternative pathway, spontaneous hydrolysis of **C3** leads to C3(H2O), initiating the formation of the **C3 convertase**. - This **C3 convertase** (C3bBb) further cleaves more **C3** into C3a and C3b, amplifying the pathway and leading to downstream complement activation. *C2* - **C2** is a crucial component of the **classical** and **lectin pathways**, where it is cleaved by C1s or MASP-2, respectively, to form C2b and C2a. - **C2a** then combines with C4b to form the **C3 convertase** (C4b2a) of these pathways; it does not play a direct role in initiating the alternative pathway. *C4* - **C4** is primarily involved in the **classical** and **lectin pathways**, where it is cleaved by C1s or MASP-2 to form C4a and C4b. - **C4b** binds to pathogens or immune complexes and then associates with C2a to form the **C3 convertase** (C4b2a), which is not part of the alternative pathway initiation. *C1* - **C1** is the initiating complex of the **classical complement pathway** and is composed of C1q, C1r, and C1s. - It recognizes and binds to antibody-antigen complexes or pathogen surfaces, but it has no direct role in the **alternative pathway activation**.
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