A 62-year-old male presents with sudden onset of shortness of breath and bilateral pedal edema. He is compliant with antihypertensive medications. Echocardiography reveals ejection fraction of 60 %, concentric left ventricular hypertrophy, left atrial enlargement, and grade 2 diastolic dysfunction. What is the most appropriate next step to improve his condition?
A 58-year-old male presents with burning micturition. Prostatic examination is normal. Urinalysis shows >50 pus cells per high power field, but urine culture shows no growth. What is the most likely diagnosis?
A 20-year-old male presents with fever, severe headache, vomiting, and photophobia. On examination, neck rigidity and Brudzinskis sign are positive. CT scan of the brain shows hydrocephalus. What is the most likely diagnosis?
Which of the following is not a cause of high anion gap metabolic acidosis?
Choose the correct statement(s): 1. Metformin is contraindicated in patients with severe renal impairment (eGFR <30 mL/min/1.73m²) 2. ACE inhibitors should be discontinued immediately if serum creatinine increases by any amount after initiation 3. Beta-blockers are first-line therapy for heart failure with reduced ejection fraction 4. Statins are recommended for primary prevention in patients with diabetes mellitus aged 40-75 years
What is the role of Procalcitonin in pneumonia?
Why does not every Helicobacter pylori infection lead to ulcers?
Which of the following malignancies is unrelated to obesity?
A 32-year-old woman presents with easy bruising and petechiae. Her platelet count is 18,000 / mm³. Hemoglobin and total leukocyte count are normal. She recently recovered from a mild upper respiratory tract infection. Peripheral smear shows no abnormal cells. What is the most appropriate next step in management?
Which gene would you test if the patient has a family history of breast and ovarian cancer?
INI-CET 2025 - Internal Medicine INI-CET Practice Questions and MCQs
Question 21: A 62-year-old male presents with sudden onset of shortness of breath and bilateral pedal edema. He is compliant with antihypertensive medications. Echocardiography reveals ejection fraction of 60 %, concentric left ventricular hypertrophy, left atrial enlargement, and grade 2 diastolic dysfunction. What is the most appropriate next step to improve his condition?
- A. Start digoxin to enhance myocardial contractility
- B. Perform coronary angiography to rule out ischemic cardiomyopathy
- C. Initiate loop diuretics and SGLT2 inhibitors for management of HFpEF (Correct Answer)
- D. Initiate ivabradine to reduce heart rate and improve diastolic filling
Explanation: ***Initiate loop diuretics and SGLT2 inhibitors for management of HFpEF*** - The clinical picture (sudden onset dyspnea, bilateral **pedal edema**) and echocardiography findings (EF $\ge$ 50%, **concentric LVH**, LA enlargement, **diastolic dysfunction**) define **Heart Failure with Preserved Ejection Fraction (HFpEF)** [3]. Echocardiography is essential to determine the aetiology and identify patients who will benefit from targeted therapy [1]. - **Loop diuretics** are essential for symptom relief (edema, congestion) [2], and **SGLT2 inhibitors** (e.g., empagliflozin, dapagliflozin) are recommended as foundational therapy for HFpEF, improving outcomes regardless of diabetes status. ***Perform coronary angiography to rule out ischemic cardiomyopathy*** - While coronary artery disease is a common cause of heart failure [3], the patient's EF is preserved (60%), making **ischemic cardiomyopathy** less likely as the primary cause of his acute presentation. - Coronary angiography is an invasive procedure and is not the immediate, most appropriate step for managing acute HF symptoms related to **volume overload** and diastolic dysfunction [4]. ***Start digoxin to enhance myocardial contractility*** - **Digoxin** is primarily used in **Heart Failure with Reduced Ejection Fraction (HFrEF)** (EF < 40%) to improve contractility and for rate control in atrial fibrillation. - Since the patient has preserved EF (60%), digoxin would offer little benefit and may increase the risk of toxicity without addressing the underlying **diastolic impairment**. ***Initiate ivabradine to reduce heart rate and improve diastolic filling*** - **Ivabradine** is indicated primarily in **HFrEF** (EF $\le$ 35%) for patients who are in sinus rhythm with a resting heart rate $\ge$ 70 bpm and are unable to tolerate or are maximized on beta-blockers. - It is not a standard or appropriate treatment for acutely decompensated HFpEF, where volume management and **SGLT2 inhibition** are key priorities.
Question 22: A 58-year-old male presents with burning micturition. Prostatic examination is normal. Urinalysis shows >50 pus cells per high power field, but urine culture shows no growth. What is the most likely diagnosis?
- A. Granulomatous prostatitis
- B. Chronic bacterial prostatitis
- C. Acute bacterial prostatitis
- D. Sterile pyuria (Correct Answer)
Explanation: ***Sterile pyuria*** - The combination of **pyuria** (>50 pus cells/HPF) and a **negative urine culture (no growth)** is known as sterile pyuria. This can be idiopathic or indicate conditions like **urethritis**, **tuberculosis**, or non-bacterial infections [1]. - The presence of symptoms (burning micturition) combined with pyuria and a normal prostate examination rules out typical bacterial prostatitis scenarios [1]. ***Chronic bacterial prostatitis*** - While chronic bacterial prostatitis involves recurrent symptomatic episodes and may sometimes show pyuria, it is characterized by **recurrent positive urine cultures** (often *E. coli*) and localization of bacteria to prostatic fluid. - The prostatic examination is often normal, but the hallmark is the presence of bacteria in the urine/prostatic fluid, which is absent here. ***Acute bacterial prostatitis*** - This presents with signs of systemic infection (fever, chills) and a very tender, boggy prostate, which is not mentioned, and the exam here is noted as **normal** [1]. - It always involves a **positive urine culture** due to the high bacterial load in the urine. ***Granulomatous prostatitis*** - This is a rare inflammatory condition, often related to fungal infections or **BCG therapy**, and typically manifests as a firm, nodular prostate that mimics prostate cancer. - While it can cause sterile pyuria, the presentation is usually dominated by prostatic enlargement or hardness, which is contradicted by the **normal prostatic examination** given in the prompt.
Question 23: A 20-year-old male presents with fever, severe headache, vomiting, and photophobia. On examination, neck rigidity and Brudzinskis sign are positive. CT scan of the brain shows hydrocephalus. What is the most likely diagnosis?
- A. Viral Encephalitis
- B. Bacterial Meningitis (Correct Answer)
- C. Subarachnoid Hemorrhage
- D. Normal Pressure Hydrocephalus
Explanation: ***Bacterial Meningitis*** - The clinical triad of **fever**, **headache**, and **neck rigidity** (nuchal rigidity) is classic for acute meningitis [1]. - Positive meningeal signs like **Brudzinski's sign** confirm meningeal irritation, and hydrocephalus may occur due to impaired CSF flow or absorption (communicating or non-communicating) [1]. ***Normal Pressure Hydrocephalus*** - Characterized by the triad of gait disturbance, urinary incontinence, and **dementia** (Wacky, Wobbly, Wet). - Does not typically present with acute systemic symptoms like **fever** or acute signs of meningeal irritation (neck rigidity/Brudzinski's). ***Viral Encephalitis*** - While it presents with fever and headache, the hallmark is altered mental status (confusion, seizures) and focal neurological deficits, indicating **parenchymal involvement**. - Severe, rigid **neck stiffness** (a major sign of meningeal irritation) is usually less prominent compared to bacterial meningitis [1]. ***Subarachnoid Hemorrhage*** - Presents with a sudden worst headache of life (**thunderclap headache**) and meningeal signs (neck rigidity, photophobia) [1]. - **Fever** is usually low-grade (if present) and develops later, unlike the often high fever seen in bacterial meningitis.
Question 24: Which of the following is not a cause of high anion gap metabolic acidosis?
- A. Ketoacidosis
- B. Acute kidney injury
- C. Toxins
- D. Diarrhea (Correct Answer)
Explanation: Diarrhea causes non-anion gap metabolic acidosis (NAGMA) because the excessive loss of bicarbonate-rich fluid (HCO3-) from the lower GI tract requires the retention of chloride (Cl-) to maintain electrical neutrality, leading to hyperchloremia (HCO3- loss replaced by Cl-) [2]. The resulting acidosis has a normal anion gap because the lost bicarbonate is effectively replaced by another unmeasured ion (chloride), keeping the calculated gap ([Na+] - ([Cl-] + [HCO3-])) within the normal range [1]. Severe acute kidney injury (AKI) causes high anion gap metabolic acidosis (HAGMA) due to the retention of unmeasured organic acids resulting from decreased glomerular filtration rate (GFR) [2]. Ketoacidosis (Diabetic, Alcoholic, Starvation) is a classic cause of high anion gap metabolic acidosis (HAGMA) [3]. The metabolic acidosis results from the overproduction and accumulation of ketone bodies (beta-hydroxybutyrate and acetoacetate), which are unmeasured organic acids [3]. Many toxins, such as Methanol, Ethylene glycol, and high doses of Salicylates, cause high anion gap metabolic acidosis (HAGMA) [1].
Question 25: Choose the correct statement(s): 1. Metformin is contraindicated in patients with severe renal impairment (eGFR <30 mL/min/1.73m²) 2. ACE inhibitors should be discontinued immediately if serum creatinine increases by any amount after initiation 3. Beta-blockers are first-line therapy for heart failure with reduced ejection fraction 4. Statins are recommended for primary prevention in patients with diabetes mellitus aged 40-75 years
- A. 1, 3, 4 are correct (Correct Answer)
- B. 1, 2, 3 are correct
- C. 1, 2, 3, 4 are correct
- D. 1, 4 are correct
Explanation: ***1, 3, 4 are correct*** - This option cannot be properly evaluated as the question lacks the actual **numbered statements** that need to be assessed for correctness. - Without the specific content of statements 1, 2, 3, and 4, it is impossible to provide meaningful medical reasoning for this selection. *1, 2, 3 are correct* - This combination cannot be validated without access to the **actual statements** referenced in the question stem. - The correctness of this option depends entirely on the medical accuracy of the missing numbered statements. *1, 2, 3, 4 are correct* - This selection suggests that **all statements** would be medically accurate, but verification requires the actual statement content. - Without the numbered statements, no determination can be made about whether this comprehensive selection is appropriate. *1, 4 are correct* - This partial combination cannot be evaluated for medical accuracy without the **specific content** of the referenced statements. - The validity of selecting only statements 1 and 4 depends on the actual medical information contained in those missing statements.
Question 26: What is the role of Procalcitonin in pneumonia?
- A. Requirement of further investigation
- B. Guiding initiation of antibiotic
- C. Early antibiotic discontinuation (Correct Answer)
- D. No role
Explanation: ***Early antibiotic discontinuation*** - Procalcitonin (PCT) is a validated biomarker used to monitor clinical response and guide the safe cessation of antibiotics in patients with **Community-Acquired Pneumonia (CAP)** and other lower respiratory tract infections. - A significant decrease in PCT levels (typically <0.25 ng/mL or a substantial drop from peak) suggests the infection is resolving, facilitating **de-escalation** and reducing unnecessary antibiotic exposure. ***Guiding initiation of antibiotic*** - While elevated PCT levels (e.g., >0.5 ng/mL) strongly suggest a **bacterial etiology** over a viral one, clinical guidelines often mandate immediate empiric antibiotic initiation based on the severity of illness (e.g., **CURB-65** criteria) [1]. - Although useful for differentiating bacterial vs. viral causes, the strongest evidence and clinical application of PCT in pneumonia focus on the timing of **stopping** treatment rather than starting [2]. ***Requirement of further investigation*** - PCT is a specific **biomarker** that helps establish the presence of a **systemic bacterial infection** or sepsis, thus serving as a diagnostic aid itself rather than just indicating the need for additional, generic investigations [2]. - If PCT levels are high, it confirms the likelihood of a bacterial etiology, directing the clinician towards definitive **antibiotic therapy** and close monitoring rather than simply delaying treatment with more tests. ***No role*** - This statement is incorrect; PCT-guided algorithms for antibiotic management are integrated into many international guidelines (like those from the Infectious Diseases Society of America/American Thoracic Society) to reduce the **duration of therapy**. - Its measurable sensitivity and specificity in distinguishing bacterial infections from non-infectious causes or viral infections provide a substantial clinical role in improving **antibiotic stewardship** [2].
Question 27: Why does not every Helicobacter pylori infection lead to ulcers?
- A. H. pylori infects the antrum even in asymptomatic individuals
- B. Disease associated with host factors and environmental influences
- C. Increased risk of peptic ulcer disease when H. pylori is present with NSAIDs
- D. Majority of H. pylori infections are asymptomatic (Correct Answer)
Explanation: The vast majority of H. pylori infections are asymptomatic or cause only mild gastritis, meaning the organism's presence alone is not sufficient to cause pathology [1]. Only a small percentage (around 10-20%) of individuals infected with Helicobacter pylori will develop a peptic ulcer or gastric malignancy [1]. The organism generally colonizes the gastric antrum, leading to chronic gastritis and potentially ulcers through increased gastrin and acid secretion; however, in most people, this subsequent hypergastrinaemia has no clinical consequences [1]. Host factors and environmental influences determine who develops ulcers, but the baseline state is generally non-ulcerative gastritis. While increased risk of peptic ulcer disease occurs when H. pylori is present with NSAIDs, these are cofactors that damage the mucosal barrier and do not explain the high rate of asymptomatic carriage in the general population.
Question 28: Which of the following malignancies is unrelated to obesity?
- A. Pancreas
- B. Stomach
- C. Meningioma
- D. Multiple myeloma (Correct Answer)
Explanation: ***Multiple myeloma*** - While obesity is a risk factor for several cancers, there is limited or conflicting evidence directly linking **multiple myeloma** to high BMI, making it the most unrelated option among the choices provided. - The primary established risk factors for multiple myeloma include age (over 65), African descent, male sex, and a history of monoclonal gammopathy of undetermined significance (**MGUS**). [1] ***Stomach*** - Obesity, particularly abdominal obesity, increases the risk of developing **gastric cardia adenocarcinoma** due to increased prevalence of **gastroesophageal reflux disease (GERD)** and subsequent Barrett's esophagus. - Chronic inflammation and hormonal changes associated with high body fat contribute to the oncogenesis of stomach cancer. ***Pancreas*** - Obesity is a well-established risk factor for **pancreatic cancer**, increasing the risk by approximately 20-50% compared to healthy-weight individuals. [2] - The mechanism involves chronic low-grade inflammation, **insulin resistance**, and altered levels of adipokines (like leptin) and insulin-like growth factors. ***Meningioma*** - **Meningioma**, the most common primary central nervous system tumor, has a clear association with obesity. - High BMI contributes to increased risk, possibly mediated by elevated levels of **leptin** and **estrogen** (especially in postmenopausal women) which can act as growth factors.
Question 29: A 32-year-old woman presents with easy bruising and petechiae. Her platelet count is 18,000 / mm³. Hemoglobin and total leukocyte count are normal. She recently recovered from a mild upper respiratory tract infection. Peripheral smear shows no abnormal cells. What is the most appropriate next step in management?
- A. Platelet transfusion
- B. Splenectomy
- C. Oral corticosteroids (Correct Answer)
- D. Bone marrow biopsy
Explanation: ***Oral corticosteroids*** - This is the **first-line treatment** for newly diagnosed Immune Thrombocytopenic Purpura (ITP), especially when the platelet count is severely low (typically <30,000/mm³) and the patient exhibits bleeding symptoms like **petechiae** and easy bruising [1]. - Corticosteroids reduce the clearance of antibody-coated platelets by the **reticuloendothelial system** (primarily splenic macrophages) and suppress autoantibody production. ***Platelet transfusion*** - Platelet transfusions are generally **contraindicated** in ITP because the transfused platelets are rapidly destroyed by the same autoantibodies that target the patient's native platelets [1]. - They are reserved only for **life-threatening hemorrhage** (e.g., intracranial bleeding) or for pre-operative stabilization, usually given concurrently with high-dose IVIG or corticosteroids. ***Bone marrow biopsy*** - A **bone marrow biopsy** is usually not required for a young patient with classic ITP presentation (isolated thrombocytopenia, normal Hb/TLC, recent infection, and normal peripheral smear). - It is typically mandatory only if the patient is older (e.g., >60), has unexplained cytopenias in other lineages, or is **refractory** to first-line treatment. ***Splenectomy*** - Splenectomy is a **second-line treatment** option, typically reserved for patients with chronic ITP who fail to respond adequately to medical therapy (corticosteroids and IVIG) after 6 to 12 months [2]. - Although the spleen is the primary site of autoantibody production and platelet destruction, it is not the **most appropriate immediate next step** in initial management [2].
Question 30: Which gene would you test if the patient has a family history of breast and ovarian cancer?
- A. P53
- B. CDH1
- C. BRCA1/2 (Correct Answer)
- D. PTEN
Explanation: ***BRCA1/2*** - Mutations in **BRCA1** and **BRCA2** genes are responsible for the majority of hereditary breast and ovarian cancer syndromes (*Hereditary Breast and Ovarian Cancer syndrome*). [1] - Testing these genes is the standard procedure when a patient presents with a strong family history of both breast and ovarian cancers, as they are **tumor suppressor genes** involved in DNA repair. [1] ***P53*** - Mutations in the **TP53** gene are associated with **Li-Fraumeni syndrome**, which increases the risk for a wide spectrum of cancers, including breast cancer, sarcomas, brain tumors, and adrenocortical carcinoma. - While breast cancer is a component, Li-Fraumeni is less specifically linked to the combined presentation of breast and ovarian cancer compared to BRCA mutations. ***PTEN*** - Mutations in the **PTEN** gene cause **Cowden syndrome**, characterized by multiple hamartomas and an increased risk of breast, thyroid, and endometrial cancers. - Ovarian cancer is a less prominent feature of Cowden syndrome, making it a secondary consideration after BRCA testing. ***CDH1*** - Mutations in the **CDH1** gene (which encodes **E-cadherin**) are primarily associated with **Hereditary Diffuse Gastric Cancer (HDGC)**. - These mutations also confer an increased risk for **lobular breast cancer**, but they are not the primary drivers for a syndrome involving both significant breast and ovarian cancer risk.