Complement inhibitors US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Complement inhibitors. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Complement inhibitors US Medical PG Question 1: A 36-year-old woman comes to the emergency department because of an itchy lesion on her skin. The rash developed shortly after she took an antibiotic for a urinary tract infection. Her temperature is 37.5°C (99.3°F), pulse is 99/min, and blood pressure is 100/66 mm Hg. Physical examination shows swelling of the face and raised, erythematous plaques on her trunk and extremities. Which of the following is the most likely cause of this patient's current condition?
- A. Deficiency of C1 inhibitor
- B. Secretion of cytokines by T cells
- C. Deposition of immune complexes
- D. Release of a vasoactive amine (Correct Answer)
- E. Activation of complement cascade
Complement inhibitors Explanation: ***Release of a vasoactive amine***
- The rapid onset of **urticaria (itchy, erythematous plaques)** and **angioedema (facial swelling)** after antibiotic exposure points to a **Type I hypersensitivity (IgE-mediated) reaction**.
- This reaction is characterized by the release of **histamine** and other vasoactive amines from mast cells and basophils, leading to capillary dilation, increased vascular permeability, and the observed symptoms.
*Deficiency of C1 inhibitor*
- A deficiency in **C1 inhibitor** causes **hereditary angioedema**, which typically presents with recurrent episodes of swelling but **without urticaria or itching**, as bradykinin, not histamine, is the primary mediator.
- The episodes are often triggered by trauma or stress and are not typically associated with drug-induced allergic reactions in this manner.
*Secretion of cytokines by T cells*
- Secretion of cytokines by T cells (e.g., in a **Type IV hypersensitivity reaction**) generally causes a **delayed-type hypersensitivity**, manifesting as contact dermatitis or drug rash that appears days after exposure.
- This mechanism would not explain the rapid onset of urticaria and angioedema observed just after antibiotic intake.
*Deposition of immune complexes*
- **Immune complex deposition** (a **Type III hypersensitivity reaction**) can cause conditions like serum sickness or vasculitis, which typically present with fever, arthralgia, and a rash that is often purpuric or palpable, not an itchy, transient urticarial rash.
- The onset of symptoms in Type III reactions is usually hours to days after exposure, not immediately post-ingestion.
*Activation of complement cascade*
- While complement activation can occur in various immune reactions, it is primarily central to **Type II (cytotoxic)** and **Type III (immune complex)** hypersensitivity.
- Although it plays a role in enhancing inflammation, it is not the primary mechanism responsible for the immediate release of vasoactive amines in an **IgE-mediated allergic reaction** leading to urticaria and angioedema.
Complement inhibitors US Medical PG Question 2: A 15-year-old boy is admitted to the emergency department with neck stiffness, maculopapular rash, fever, and a persistent headache. A blood culture shows encapsulated gram-negative diplococci. He has had this same infection before. Which of the following proteins is likely to be deficient in this patient?
- A. C9 (Correct Answer)
- B. C1 esterase inhibitor
- C. CD55 (decay accelerating factor)
- D. Calcineurin
- E. CD4
Complement inhibitors Explanation: **C9**
- A deficiency in C9, or any other terminal complement components (C5-C8), impairs the formation of the **membrane attack complex (MAC)**.
- This significantly increases susceptibility to recurrent, severe infections with **Neisseria meningitidis**, an encapsulated gram-negative diplococcus matching the clinical presentation.
*C1 esterase inhibitor*
- Deficiency of **C1 esterase inhibitor** is associated with **hereditary angioedema**, characterized by recurrent episodes of edema without urticaria.
- It does not primarily predispose to recurrent bacterial infections like meningococcemia.
*CD55 (decay accelerating factor)*
- Deficiency of **CD55 (DAF)**, along with CD59, is pathognomonic for **paroxysmal nocturnal hemoglobinuria** (PNH), a disorder of red blood cell lysis.
- This condition is not typically associated with recurrent meningococcal infections.
*Calcineurin*
- **Calcineurin** is a protein phosphatase involved in T-cell activation; its inhibitors are used as immunosuppressants.
- A defect in calcineurin itself is not a known cause of recurrent bacterial infections, though its inhibition can lead to opportunistic infections.
*CD4*
- **CD4** is a co-receptor on T helper cells essential for immune responses, and its deficiency (e.g., in HIV/AIDS) leads to severe immunodeficiency.
- While it causes increased susceptibility to various infections, it doesn't specifically target encapsulated bacteria like Neisseria in a way that would cause recurrent meningococcal disease with an intact MAC pathway.
Complement inhibitors US Medical PG Question 3: A 25-year-old woman is being evaluated due to complaint of fatigue and voiding pink urine. The laboratory results are as follows:
Hb 6.7
Red blood cell count 3.0 x 1012/L
Leukocyte count 5,000/mm3
Platelets 170 x 109/L
Reticulocyte count 6%
Hematocrit 32%
The physician thinks that the patient is suffering from an acquired mutation in hematopoietic stem cells, which is confirmed by flow cytometry analysis that revealed these cells are CD 55 and CD 59 negative. However, the physician is interested in knowing the corrected reticulocyte count before starting the patient on eculizumab. What value does the physician find after calculating the corrected reticulocyte count?
- A. 3.1%
- B. 0.4%
- C. 0.1%
- D. 0.6%
- E. 4.6% (Correct Answer)
Complement inhibitors Explanation: ***4.6%***
- The corrected reticulocyte count accounts for the degree of anemia by adjusting for the patient's hematocrit compared to normal.
- **Formula: Corrected Retics% = Observed Retics% × (Patient's Hct / Normal Hct)**
- Using normal Hct of 42% for women: 6% × (32/42) = 6% × 0.76 = **4.56% ≈ 4.6%**
- This reflects the actual reticulocyte production capacity adjusted for the anemic state.
*3.1%*
- This value might result from using an incorrect normal hematocrit value in the calculation.
- For example, using 6% × (32/60) would give approximately 3.2%, suggesting use of an inappropriately high reference value.
*0.4%*
- This value likely results from applying the **Reticulocyte Production Index (RPI)** formula, which includes a maturation factor correction: 6% × (32/42) × (1/2.5) = 1.82%, then with further error.
- Such a low value from formula misapplication does not represent the standard corrected reticulocyte count requested.
*0.1%*
- This extremely low value would indicate **severe calculation error** or bone marrow failure, which contradicts the observed 6% reticulocyte count.
- In PNH with hemolysis, reticulocyte production is typically increased, making this value implausible.
*0.6%*
- This incorrect value could result from mathematical errors in applying correction factors or using the wrong hematocrit values in the formula.
- The standard corrected reticulocyte formula would not yield this value with the given parameters.
Complement inhibitors US Medical PG Question 4: A previously healthy 39-year-old man comes to the physician because of a 1-month history of fatigue and red-colored urine. His vital signs are within normal limits. Physical examination shows pallor and jaundice. His platelet count is 90,000/mm3 and creatinine concentration is 1.0 mg/dL. A direct Coombs test is negative. Flow cytometry shows erythrocytes deficient in CD55 and CD59 surface antigens. This patient is at greatest risk for which of the following complications?
- A. Hepatocellular carcinoma
- B. Venous thrombosis (Correct Answer)
- C. Pigmented gallstones
- D. Acrocyanosis
- E. Chronic lymphocytic leukemia
Complement inhibitors Explanation: ***Venous thrombosis***
- The patient's symptoms (fatigue, red urine, pallor, jaundice), lab findings (thrombocytopenia), and especially the immunophenotyping (erythrocytes deficient in **CD55 and CD59**) are highly suggestive of **paroxysmal nocturnal hemoglobinuria (PNH)**.
- Patients with PNH are at significantly increased risk of **venous thrombosis**, particularly in unusual sites such as the **hepatic (Budd-Chiari syndrome)**, mesenteric, or cerebral veins, due to increased red blood cell destruction and release of prothrombotic factors.
- **Venous thromboembolism is the leading cause of morbidity and mortality in PNH**, occurring in 30-40% of patients.
*Hepatocellular carcinoma*
- This condition is typically associated with chronic liver diseases such as **viral hepatitis** (B or C), **cirrhosis**, or **hemochromatosis**.
- While chronic hemolysis in PNH can lead to iron overload, **hepatocellular carcinoma** itself is not a direct or common complication of PNH.
*Pigmented gallstones*
- **Pigmented (bilirubin) gallstones** can develop in conditions with chronic hemolysis (like hereditary spherocytosis or sickle cell anemia) due to increased bilirubin production from red blood cell breakdown.
- These stones are typically **radiopaque** due to calcium bilirubinate content.
- However, the question asks for the *greatest risk*, and **venous thrombosis** is the most life-threatening and common severe complication of PNH.
*Acrocyanosis*
- **Acrocyanosis** is a benign condition characterized by persistent, painless, and symmetrical cyanosis of the hands, feet, and face, often exacerbated by cold.
- It is a peripheral vascular phenomenon and is not a recognized complication of **paroxysmal nocturnal hemoglobinuria (PNH)**.
*Chronic lymphocytic leukemia*
- **Chronic lymphocytic leukemia (CLL)** is a malignancy of B lymphocytes and is characterized by lymphocytosis and often lymphadenopathy or splenomegaly.
- While PNH can be associated with bone marrow failure syndromes (e.g., aplastic anemia, myelodysplastic syndrome), **CLL** is not a direct or typical complication of PNH.
Complement inhibitors US Medical PG Question 5: A 38-year-old woman comes to the physician for a follow-up examination. Two years ago, she was diagnosed with multiple sclerosis. Three weeks ago, she was admitted and treated for right lower leg weakness with high-dose methylprednisone for 5 days. She has had 4 exacerbations over the past 6 months. Current medications include interferon beta and a multivitamin. Her temperature is 37°C (98.6°F), pulse is 90/min, and blood pressure is 116/74 mm Hg. Examination shows pallor of the right optic disk. Neurologic examination shows no focal findings. She is anxious about the number of exacerbations and repeated hospitalizations. She is counseled about the second-line treatment options available to her. She consents to treatment with natalizumab. However, she has read online about its adverse effects and is concerned. This patient is at increased risk for which of the following complications?
- A. Tuberculosis
- B. Syndrome of inappropriate antidiuretic hormone
- C. Parkinsonism
- D. Progressive multifocal leukoencephalopathy (Correct Answer)
- E. Aplastic anemia
Complement inhibitors Explanation: ***Progressive multifocal leukoencephalopathy***
- **Natalizumab** is a monoclonal antibody that blocks the binding of leukocytes to endothelial cells, preventing their entry into the central nervous system. This immunosuppressive effect increases the risk of **progressive multifocal leukoencephalopathy (PML)**, especially in patients who are positive for the **JC virus**.
- PML is a serious and often fatal opportunistic infection of the brain caused by the **JC virus**, which demyelinates axons and leads to severe neurological deficits.
*Tuberculosis*
- While some immunosuppressants can reactivate **latent tuberculosis**, natalizumab is not typically associated with an increased risk of TB compared to other immunomodulatory drugs like TNF-alpha inhibitors.
- The mechanism of action of natalizumab (alpha-4 integrin blocker) does not directly impede the immune response responsible for containing mycobacterial infections to the same extent as other treatments.
*Syndrome of inappropriate antidiuretic hormone*
- **SIADH** is not a known adverse effect of natalizumab.
- SIADH is characterized by excessive secretion of **antidiuretic hormone**, leading to hyponatremia, and is often associated with certain medications (e.g., SSRIs, carbamazepine) or underlying conditions like malignancy or pulmonary disease.
*Parkinsonism*
- Parkinsonism involves symptoms like **bradykinesia**, rigidity, and tremor, and is a neurodegenerative disorder.
- There is **no evidence** suggesting a causal link between natalizumab treatment and the development of Parkinsonism.
*Aplastic anemia*
- **Aplastic anemia** is a rare but severe condition where the bone marrow fails to produce blood cells.
- This adverse effect is not associated with natalizumab; it is more commonly linked to certain **chemotherapeutic agents**, radiation, or specific antimicrobial drugs like chloramphenicol.
Complement inhibitors US Medical PG Question 6: A 28-year-old woman has a follow-up visit with her physician. She was diagnosed with allergic rhinitis and bronchial asthma at 11 years of age. Her regular controller medications include daily high-dose inhaled corticosteroids and montelukast, but she still needs to use a rescue inhaler 3–4 times a week following exercise. She also becomes breathless with moderate exertion. After a thorough evaluation, the physician explains that her medication dosages need to be increased. She declines taking oral corticosteroids daily due to concerns about side effects. The physician prescribes omalizumab, which is administered subcutaneously every 3 weeks. Which of the following best explains the mechanism of action of the new medication that has been added to the controller medications?
- A. Prevention of binding of IgE antibodies to mast cell receptors (Correct Answer)
- B. Inhibition of synthesis of interleukin-4 (IL-4)
- C. Inhibition of synthesis of IgE antibodies
- D. Selective binding to interleukin-3 (IL-3) and inhibition of its actions
- E. Prevention of binding of interleukin-5 (IL-5) to its receptors
Complement inhibitors Explanation: ***Prevention of binding of IgE antibodies to mast cell receptors***
- **Omalizumab** is a **monoclonal antibody** that specifically targets and binds to **free IgE** in the bloodstream, preventing it from attaching to high-affinity IgE receptors on **mast cells** and **basophils**.
- By reducing surface IgE, omalizumab **downregulates IgE receptors** on these cells, thereby reducing the release of inflammatory mediators upon allergen exposure, which is beneficial in **allergic asthma** uncontrolled by standard therapies.
*Inhibition of synthesis of interleukin-4 (IL-4)*
- **IL-4** is a cytokine primarily involved in **Th2 differentiation** and **IgE class switching**, but omalizumab's action is not directly blocking its synthesis.
- While *omalizumab* indirectly reduces IgE levels, its primary mechanism isn't to inhibit the production of IL-4 itself, but rather to prevent the effects of existing IgE.
*Inhibition of synthesis of IgE antibodies*
- **Omalizumab** does not inhibit the *synthesis* of IgE antibodies; instead, it binds to already synthesized **free IgE** circulating in the blood.
- This binding effectively neutralizes IgE, preventing it from contributing to the allergic cascade, but it doesn't stop B cells from producing more IgE.
*Selective binding to interleukin-3 (IL-3) and inhibition of its actions*
- **IL-3** is a cytokine involved in the growth and differentiation of various **hematopoietic cells**, including mast cells and basophils, but it is not the target of omalizumab.
- Omalizumab specifically targets **IgE** and has no known direct action on IL-3 signaling pathways.
*Prevention of binding of interleukin-5 (IL-5) to its receptors*
- **IL-5** is a key cytokine in the **eosinophilic inflammatory pathway** and is targeted by other therapies (e.g., mepolizumab, reslizumab) used for severe eosinophilic asthma.
- Omalizumab's mechanism is distinct, focusing on **IgE-mediated inflammation** rather than direct eosinophil control.
Complement inhibitors US Medical PG Question 7: You are treating a neonate with meningitis using ampicillin and a second antibiotic, X, that is known to cause ototoxicity. What is the mechanism of antibiotic X?
- A. It binds the 50S ribosomal subunit and inhibits formation of the initiation complex
- B. It binds the 30S ribosomal subunit and inhibits formation of the initiation complex (Correct Answer)
- C. It binds the 30S ribosomal subunit and reversibly inhibits translocation
- D. It binds the 50S ribosomal subunit and inhibits peptidyltransferase
- E. It binds the 50S ribosomal subunit and reversibly inhibits translocation
Complement inhibitors Explanation: ***It binds the 30s ribosomal subunit and inhibits formation of the initiation complex***
- The second antibiotic, X, is likely an **aminoglycoside**, such as **gentamicin** or **amikacin**, which are commonly used in combination with ampicillin for neonatal meningitis and are known to cause ototoxicity.
- Aminoglycosides exert their bactericidal effect by **irreversibly binding to the 30S ribosomal subunit**, thereby **inhibiting the formation of the initiation complex** and leading to misreading of mRNA.
*It binds the 50S ribosomal subunit and inhibits formation of the initiation complex*
- This mechanism is characteristic of **linezolid**, which targets the 50S ribosomal subunit to prevent the formation of the initiation complex.
- While linezolid can cause side effects, **ototoxicity** is less commonly associated with it compared to aminoglycosides, and it is not a primary drug for neonatal meningitis alongside ampicillin.
*It binds the 50S ribosomal subunit and inhibits peptidyltransferase*
- This is the mechanism of action for **chloramphenicol**, which inhibits **peptidyltransferase** activity on the 50S ribosomal subunit, preventing peptide bond formation.
- Although chloramphenicol can cause **ototoxicity** and **aplastic anemia**, its use in neonates is limited due to the risk of **Gray Baby Syndrome**.
*It binds the 30s ribosomal subunit and reversibly inhibits translocation*
- This describes the mechanism of action of **tetracyclines**, which reversibly bind to the 30S ribosomal subunit and prevent the attachment of aminoacyl-tRNA, thereby inhibiting protein synthesis.
- Tetracyclines are **contraindicated in neonates** due to their potential to cause **tooth discoloration** and **bone growth inhibition**, and ototoxicity is not their primary adverse effect.
*It binds the 50s ribosomal subunit and reversibly inhibits translocation*
- This mechanism of reversibly inhibiting translocation by binding to the 50S ribosomal subunit is characteristic of **macrolides** (e.g., erythromycin, azithromycin) and **clindamycin**.
- While some macrolides can cause **transient ototoxicity**, they are not typically the second antibiotic of choice for neonatal meningitis in combination with ampicillin, and clindamycin's side effect profile is different.
Complement inhibitors US Medical PG Question 8: A 38-year-old man presents to his physician with recurrent episodes of facial swelling and abdominal pain. He reports that these episodes started when he was approximately 16 years of age. His mother also has similar episodes of swelling accompanied by swelling of her extremities. The vital signs include: blood pressure 140/80 mm Hg, heart rate 74/min, respiratory rate 17/min, and temperature 36.6℃ (97.8℉). His physical examination is unremarkable. The laboratory work-up shows the following findings:
Test Result Normal range
C1 esterase inhibitor 22% > 60%
Complement C4 level 9 mg/dL 14–40 mg/dL
Complement C2 level 0.8 mg/dL 1.1–3.0 mg/dL
Complement component 1q 17 mg/dL 12–22 mg/dL
Which of the following anti-hypertensive medications is contraindicated in this patient?
- A. Amlodipine
- B. Fosinopril (Correct Answer)
- C. Atenolol
- D. Indapamide
- E. Valsartan
Complement inhibitors Explanation: ***Fosinopril***
- This patient presents with symptoms and lab findings consistent with **hereditary angioedema (HAE)**, characterized by recurrent episodes of **facial swelling** and **abdominal pain**, low C1 esterase inhibitor, and low C4/C2 levels. **ACE inhibitors** like fosinopril are absolutely **contraindicated in HAE** because they can trigger life-threatening angioedema attacks by increasing bradykinin levels.
- The family history of similar swelling further supports the diagnosis of HAE, making any medication that exacerbates bradykinin a significant risk.
*Amlodipine*
- **Dihydropyridine calcium channel blockers** such as amlodipine are generally considered safe in patients with angioedema and do not interfere with the bradykinin pathway.
- They are a suitable option for hypertension management in these patients.
*Atenolol*
- **Beta-blockers** like atenolol are generally safe for managing hypertension in patients with a history of angioedema, as they do not affect the complement or bradykinin systems.
- There is no evidence to suggest that atenolol would worsen angioedema symptoms.
*Indapamide*
- **Thiazide diuretics** such as indapamide are safe and effective antihypertensive agents in patients with angioedema.
- They work by increasing sodium and water excretion and do not interact with the pathways involved in angioedema.
*Valsartan*
- **Angiotensin receptor blockers (ARBs)** like valsartan are generally considered safer than ACE inhibitors in patients with angioedema, although a small risk of angioedema still exists due to their weak effect on bradykinin.
- However, the primary family of drugs to avoid in HAE is ACE inhibitors due to their direct and significant impact on bradykinin degradation.
Complement inhibitors US Medical PG Question 9: A 35-year-old woman comes to the physician because of blurred vision for the past 2 months. During this period, she has also had difficulty chewing and swallowing. She reports that her symptoms worsen throughout the day and improve with rest. There is no personal or family history of serious illness. The patient works as a teacher and has had a great deal of stress lately. She does not smoke and drinks a glass of wine occasionally. She takes no medications. Her temperature is 37°C (98.6°F), pulse is 68/min, and blood pressure is 130/80 mm Hg. Physical examination shows bilateral ptosis and mask-like facies. Muscle strength is decreased in both lower extremities. The anti–acetylcholine receptor (AChR) antibody test is positive. Electromyography shows a decremental response following repetitive nerve stimulation. Which of the following is the most appropriate next step in the management of this patient?
- A. Serum ACTH and CRH levels
- B. Plasmapheresis
- C. Anti-VGCC antibody level
- D. Physostigmine therapy
- E. CT scan of the chest (Correct Answer)
Complement inhibitors Explanation: ***CT scan of the chest***
- The patient has symptoms suggestive of **myasthenia gravis**, including **ptosis**, **diplopia** (blurred vision), **dysphagia**, and **fatigue that worsens with activity and improves with rest**. The positive **anti-acetylcholine receptor (AChR) antibody** test and **decremental response on EMG** confirm the diagnosis. A computed tomography (CT) scan of the chest is crucial to evaluate for a **thymoma**, which is present in 10-15% of patients with myasthenia gravis and can be surgically resected, potentially leading to symptom improvement or remission.
- Approximately 85% of myasthenia gravis patients have detectable **AChR antibodies**, making this test highly specific for the condition. The presence of these antibodies, along with the characteristic clinical picture and electromyography findings, establishes the diagnosis of myasthenia gravis. Thymectomy is often considered in patients with generalized myasthenia gravis, even in the absence of a thymoma, due to potential therapeutic benefits.
*Serum ACTH and CRH levels*
- This test is primarily used to investigate conditions related to the **hypothalamic-pituitary-adrenal axis**, such as **Cushing's disease** or **Addison's disease**.
- There are no symptoms presented that would suggest altered ACTH or CRH levels, making this an inappropriate diagnostic step for the current patient's presentation.
*Plasmapheresis*
- **Plasmapheresis** is a treatment for **acute severe myasthenia gravis** or **myasthenic crisis**, involving the removal of plasma to eliminate circulating antibodies.
- While it is a treatment for myasthenia gravis, it is not the *next step* in initial workup after diagnosis for a stable patient as described; the priority is to investigate underlying causes like thymoma.
*Anti-VGCC antibody level*
- **Anti-voltage-gated calcium channel (VGCC) antibodies** are characteristic of **Lambert-Eaton Myasthenic Syndrome (LEMS)**, often associated with **small cell lung cancer**.
- The patient's symptoms (e.g., ptosis, worsening with activity) and the positive **AChR antibodies** are classic for myasthenia gravis, not LEMS, making this test unnecessary.
*Physostigmine therapy*
- **Physostigmine** is an **acetylcholinesterase inhibitor** that reverses anticholinergic effects and can be used in some contexts, but it's not a primary treatment for myasthenia gravis.
- The standard pharmacotherapy for myasthenia gravis includes other anticholinesterase inhibitors like **pyridostigmine**, or immunomodulatory agents. This is a treatment, not a diagnostic step in the workup.
Complement inhibitors US Medical PG Question 10: A 28-year-old female presents to her primary care doctor complaining of new onset blurry vision. She first noticed her vision getting blurry toward the end of the day several days ago. Since then, she reports that her vision has been fine when she wakes up but gets worse throughout the day. She has also noticed that her eyelids have started to droop before she goes to bed. On exam, she has bilateral ptosis that is worse on the right. Administering edrophonium to this patient leads to an immediate improvement in her symptoms. Which of the following is most likely true about this patient’s condition?
- A. It is caused by a type III hypersensitivity reaction
- B. It is associated with a neoplasm of lung neuroendocrine cells
- C. It is caused by antibodies directed against presynaptic P/Q calcium channels
- D. An increasing response will be seen on repeated nerve stimulation
- E. It is associated with a benign proliferation of epithelial cells of the thymus (Correct Answer)
Complement inhibitors Explanation: ***It is associated with a benign proliferation of epithelial cells of the thymus***
- The patient's symptoms of progressive weakness throughout the day, ptosis, and improvement with edrophonium (an acetylcholinesterase inhibitor) are highly suggestive of **myasthenia gravis**.
- Approximately 75% of patients with myasthenia gravis have **thymic abnormalities**, with about 65% having **thymic hyperplasia** (a benign proliferation of epithelial cells) and 10% having a **thymoma**.
*It is caused by a type III hypersensitivity reaction*
- **Type III hypersensitivity reactions** involve immune complex deposition, as seen in diseases like Systemic Lupus Erythematosus or post-streptococcal glomerulonephritis.
- Myasthenia gravis is a **Type II hypersensitivity reaction**, where antibodies directly target specific cell surface antigens, in this case, acetylcholine receptors at the neuromuscular junction.
*It is associated with a neoplasm of lung neuroendocrine cells*
- A neoplasm of **lung neuroendocrine cells**, specifically **small cell lung carcinoma**, is associated with **Lambert-Eaton Myasthenic Syndrome (LEMS)**.
- LEMS presents with proximal muscle weakness that *improves* with activity, unlike the fatiguable weakness seen in myasthenia gravis.
*It is caused by antibodies directed against presynaptic P/Q calcium channels*
- Antibodies directed against **presynaptic P/Q calcium channels** are characteristic of **Lambert-Eaton Myasthenic Syndrome (LEMS)**.
- In LEMS, these antibodies reduce the release of acetylcholine into the synaptic cleft, leading to muscle weakness.
*An increasing response will be seen on repeated nerve stimulation*
- An **increasing (incremental) response** on repeated nerve stimulation is a characteristic finding in **Lambert-Eaton Myasthenic Syndrome (LEMS)**.
- In myasthenia gravis, repeated nerve stimulation typically shows a **decreasing (decremental) response** due to the depletion of functionally available acetylcholine receptors.
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