Inflammation US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Inflammation. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Inflammation US Medical PG Question 1: A 56-year-old postmenopausal woman comes to the physician because of a 6-month history of worsening pain and swelling in her left knee. She has a history of peptic ulcer disease for which she takes cimetidine. Examination shows palpable crepitus and limited range of motion of the left knee. Which of the following is the most appropriate pharmacotherapy for this patient’s symptoms?
- A. Acetylsalicylic acid
- B. Diclofenac
- C. Meloxicam
- D. Celecoxib (Correct Answer)
- E. Ketorolac
Inflammation Explanation: ***Celecoxib***
- This patient suffers from **osteoarthritis** (evidenced by her age, postmenopausal status, knee pain, crepitus, and limited range of motion) and has a history of **peptic ulcer disease (PUD)**. **Celecoxib** is a **COX-2 selective NSAID**, which reduces the risk of gastrointestinal side effects compared to non-selective NSAIDs.
- Given her history of PUD, a COX-2 selective NSAID is the most appropriate choice to manage her pain while minimizing the risk of a PUD exacerbation or bleed.
*Acetylsalicylic acid*
- **Aspirin** (acetylsalicylic acid) is a non-selective NSAID and would pose a significant risk of **gastrointestinal bleeding** or ulcer exacerbation in a patient with a history of **peptic ulcer disease**.
- While it has anti-inflammatory properties, its adverse effect profile makes it unsuitable for this patient's chronic pain management.
*Diclofenac*
- **Diclofenac** is a **non-selective NSAID**, meaning it inhibits both COX-1 and COX-2 enzymes.
- Due to its inhibition of COX-1, it carries an increased risk of **gastric ulcers** and bleeding, making it less safe for a patient with a history of **peptic ulcer disease**.
*Meloxicam*
- **Meloxicam** is a partially COX-2 selective NSAID, but it still has some affinity for COX-1 at higher doses, conferring a risk for **gastrointestinal adverse effects**.
- Although it may have a slightly better GI safety profile than non-selective NSAIDs, **celecoxib** offers superior GI protection.
*Ketorolac*
- **Ketorolac** is a potent **non-selective NSAID** primarily used for short-term management of moderate to severe acute pain, often administered parenterally.
- Its use is associated with a high risk of **gastrointestinal toxicity** and renal impairment, making it inappropriate for chronic pain management in a patient with **peptic ulcer disease**.
Inflammation US Medical PG Question 2: A 31-year-old female receives a kidney transplant for autosomal dominant polycystic kidney disease (ADPKD). Three weeks later, the patient experiences acute, T-cell mediated rejection of the allograft and is given sirolimus. Which of the following are side effects of this medication?
- A. Nephrotoxicity, hypertension
- B. Hyperlipidemia, thrombocytopenia (Correct Answer)
- C. Nephrotoxicity, gingival hyperplasia
- D. Pancreatitis
- E. Cytokine release syndrome, hypersensitivity reaction
Inflammation Explanation: ***Hyperlipidemia, thrombocytopenia***
- **Sirolimus** (rapamycin) is an **mTOR inhibitor** commonly used in transplant immunology, which frequently causes **hyperlipidemia** (elevated cholesterol and triglycerides) and **thrombocytopenia** (low platelet count).
- Other common side effects include **myelosuppression** (leukopenia, anemia), **mouth ulcers**, and **impaired wound healing**.
*Nephrotoxicity, hypertension*
- **Nephrotoxicity** and **hypertension** are more characteristic side effects of **calcineurin inhibitors** like **tacrolimus** and **cyclosporine**, which are also used in transplant immunosuppression but have a different mechanism of action than sirolimus.
- While sirolimus can indirectly affect kidney function, it is generally considered less nephrotoxic than calcineurin inhibitors.
*Nephrotoxicity, gingival hyperplasia*
- **Gingival hyperplasia** is a hallmark side effect of **cyclosporine**, a calcineurin inhibitor, along with **hirsutism** and **nephrotoxicity**.
- Sirolimus does not typically cause gingival hyperplasia.
*Pancreatitis*
- While some immunosuppressants can rarely cause pancreatitis, it is not a common or characteristic side effect of **sirolimus**.
- **Azathioprine** is more frequently associated with pancreatitis among immunosuppressive agents.
*Cytokine release syndrome, hypersensitivity reaction*
- **Cytokine release syndrome** and acute **hypersensitivity reactions** are more often associated with **monoclonal antibodies** (e.g., **basiliximab**, **daclizumab**) used for induction therapy or treatment of acute rejection, particularly within hours or days of administration.
- Sirolimus is less likely to cause these immediate severe reactions.
Inflammation US Medical PG Question 3: An 18-year-old woman presents to the emergency department with a complaint of severe abdominal pain for the past 6 hours. She is anorexic and nauseous and has vomited twice since last night. She also states that her pain initially began in the epigastric region, then migrated to the right iliac fossa. Her vital signs include a respiratory rate of 14/min, blood pressure of 130/90 mm Hg, pulse of 110/min, and temperature of 38.5°C (101.3°F). On abdominal examination, there is superficial tenderness in her right iliac fossa, rebound tenderness, rigidity, and abdominal guarding. A complete blood count shows neutrophilic leukocytosis and a shift to the left. Laparoscopic surgery is performed and the inflamed appendix, which is partly covered by a yellow exudate, is excised. Microscopic examination of the appendix demonstrates a neutrophil infiltrate of the mucosal and muscular layers with extension into the lumen. Which of the following chemical mediators is responsible for pain in this patient?
- A. IgG and complement C3b
- B. Bradykinin and prostaglandin (Correct Answer)
- C. 5- hydroperoxyeicosatetraenoic acid (5-HPETE) and leukotriene A4
- D. Serotonin and histamine
- E. Tumor necrosis factor and interleukin-1
Inflammation Explanation: ***Bradykinin and prostaglandin***
- **Bradykinin** and **prostaglandins** are key inflammatory mediators that directly stimulate **nociceptors**, leading to the sensation of pain. Prostaglandins are also responsible for inducing fever.
- The patient's symptoms, including **severe abdominal pain**, fever, and local tenderness, are consistent with acute inflammation (appendicitis), where these mediators play a central role.
*IgG and complement C3b*
- **IgG** is an antibody involved in the adaptive immune response, primarily responsible for pathogen neutralization and opsonization.
- **Complement C3b** is a component of the complement system involved in opsonization and forming the membrane attack complex, but neither directly mediates pain.
*5- hydroperoxyeicosatetraenoic acid (5-HPETE) and leukotriene A4*
- **5-HPETE** is an unstable intermediate in the lipoxygenase pathway, leading to the formation of leukotrienes.
- **Leukotriene A4** is a precursor to other leukotrienes (e.g., LTB4, LTC4, LTD4) that are potent **chemotactic agents** and **bronchoconstrictors**, but they are not primary pain mediators.
*Serotonin and histamine*
- **Serotonin** is primarily involved in smooth muscle contraction, vasoconstriction, and neurotransmission; while it can modulate pain, it is not a direct primary mediator in acute appendicitis.
- **Histamine** is released by mast cells and basophils, causing vasodilation and increased vascular permeability (contributing to edema), but its role in direct pain mediation in this context is less significant than bradykinin or prostaglandins.
*Tumor necrosis factor and interleukin-1*
- **Tumor necrosis factor (TNF)** and **interleukin-1 (IL-1)** are **pro-inflammatory cytokines** that are crucial in initiating and amplifying the inflammatory response.
- While they contribute to fever and systemic symptoms of inflammation, their primary role is in cell signaling and immune cell activation rather than direct pain sensation.
Inflammation US Medical PG Question 4: A 55-year-old woman with diabetes presents to the emergency department due to swelling of her left leg, fever, and chills for the past 2 days. The woman’s maximum recorded temperature at home was 38.3°C (101.0°F). Her left leg is red and swollen from her ankle to the calf, with an ill-defined edge. Her vital signs include: blood pressure 120/78 mm Hg, pulse rate 94/min, temperature 38.3°C (101.0°F), and respiratory rate 16/min. On physical examination, her left leg shows marked tenderness and warmth compared with her right leg. The left inguinal lymph node is enlarged to 3 x 3 cm. Which of the following chemical mediators is the most likely cause of the woman’s fever?
- A. Bradykinin
- B. Histamine
- C. PGE2 (Correct Answer)
- D. Arachidonic acid
- E. LTB4
Inflammation Explanation: ***PGE2***
- **Prostaglandin E2 (PGE2)** is a potent **pyrogen** that acts on the **hypothalamus** to reset the body's thermoregulatory set point, leading to fever.
- In infections like **cellulitis**, inflammatory mediators stimulate the production of PGE2, causing the systemic symptom of fever.
*Bradykinin*
- **Bradykinin** primarily mediates **pain** and **vasodilation** at the site of inflammation.
- While it contributes to local signs of inflammation, it is not a direct mediator of systemic fever.
*Histamine*
- **Histamine** is a key mediator in immediate **hypersensitivity reactions** and local inflammation, causing **vasodilation** and increased **vascular permeability**.
- It does not directly induce fever by acting on the thermoregulatory center.
*Arachidonic acid*
- **Arachidonic acid** is a **precursor** molecule derived from membrane phospholipids, which is metabolized to various inflammatory mediators like prostaglandins and leukotrienes.
- It is not a direct chemical mediator of fever itself; rather, its downstream products such as PGE2 are.
*LTB4*
- **Leukotriene B4 (LTB4)** is a potent **chemotactic agent** for neutrophils, playing a role in immune cell recruitment to the site of inflammation.
- While involved in inflammation, LTB4 does not directly cause fever.
Inflammation US Medical PG Question 5: Which of the following patient presentations would be expected in an infant with defective LFA-1 integrin (CD18) protein on phagocytes, in addition to recurrent bacterial infections?
- A. Cardiac defects, hypoparathyroidism, palatal defects, and learning disabilities
- B. Chronic diarrhea, oral candidiasis, severe infections since birth, absent thymic shadow
- C. Progressive neurological impairment and cutaneous telangiectasia
- D. Skin infections with absent pus formation, delayed umbilicus separation (Correct Answer)
- E. Eczema and thrombocytopenia
Inflammation Explanation: ***Skin infections with absent pus formation, delayed umbilicus separation***
- A defect in **LFA-1 integrin (CD18)** prevents phagocytes from adhering to endothelial cells and migrating to sites of infection, leading to **absent pus formation** despite severe infections.
- **Delayed umbilical cord separation** (typically >30 days) is a classic sign due to impaired neutrophil recruitment at the site of cord detachment.
*Cardiac defects, hypoparathyroidism, palatal defects, and learning disabilities*
- This constellation of symptoms is characteristic of **DiGeorge syndrome**, which involves a defect in T-cell development due to thymic aplasia/hypoplasia.
- These specific defects are not directly caused by LFA-1 integrin deficiency.
*Chronic diarrhea, oral candidiasis, severe infections since birth, absent thymic shadow*
- These symptoms are highly suggestive of **Severe Combined Immunodeficiency (SCID)**, which involves a profound defect in both B and T cell immunity.
- SCID presents with a broader spectrum of opportunistic infections and developmental issues not directly related to integrin function.
*Progressive neurological impairment and cutaneous telangiectasia*
- These are hallmark features of **Ataxia-Telangiectasia**, a genetic disorder affecting DNA repair and leading to immune deficiencies and cerebellar degeneration.
- This condition primarily involves T-cell dysfunction and increased cancer risk, not LFA-1 integrin deficiency.
*Eczema and thrombocytopenia*
- The combination of **eczema** (dermatitis) and **thrombocytopenia** (low platelet count), along with recurrent infections, is characteristic of **Wiskott-Aldrich syndrome**.
- This syndrome is caused by a defect in the WASP protein, affecting immune cell function and platelet formation, distinct from LFA-1 integrin deficiency.
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