FMGE 2019 - Internal Medicine Practice Questions

Q: Which of the following is seen in mitral stenosis?

Diastolic murmur. ***Diastolic murmur*** - **Mitral stenosis** is characterized by a narrowing of the mitral valve, impeding blood flow from the left atrium to the left ventricle during **diastole**. - This turbulent flow during ventricular filling produces a characteristic **diastolic murmur**, often described as a low-pitched, rumbling sound [1], [3]. *None of the options* - This option is incorrect because **mitral stenosis** is indeed associated with a specific heart sound abnormality [1]. - The presence of a **diastolic murmur** is a hallmark physical finding in patients with mitral stenosis [1]. *Systolic murmur* - A **systolic murmur** is produced during ventricular contraction (systole), typically associated with **mitral regurgitation** or **aortic stenosis** [2]. - In **mitral stenosis**, the primary pathology is during diastole, making a systolic murmur less characteristic unless there's concomitant mitral regurgitation. *Loud S2* - A **loud S2** (second heart sound) can be heard in conditions like **pulmonary hypertension** or **systemic hypertension**. - While pulmonary hypertension can be a complication of severe **mitral stenosis** due to elevated left atrial pressure, a loud S2 is not the most direct or specific auscultatory finding for mitral stenosis itself; the distinct diastolic murmur is more characteristic [1].

Q: All of the following are the causes for hypercalcemia Except?

Acute pancreatitis. ***Acute pancreatitis*** - **Acute pancreatitis** is most commonly associated with **hypocalcemia**, not hypercalcemia [1]. - The likely mechanism for hypocalcemia in pancreatitis is the **saponification of calcium in necrotic fat** by free fatty acids released from local lipase activity [1]. *Thiazides* - **Thiazide diuretics** can cause a mild increase in calcium levels by **increasing calcium reabsorption in the distal renal tubule** [2]. - This effect is generally not severe enough to cause symptomatic hypercalcemia unless other underlying conditions are present. *Hyperparathyroidism* - **Primary hyperparathyroidism** is a common cause of hypercalcemia, due to the **overproduction of parathyroid hormone (PTH)** [2]. - PTH increases serum calcium by increasing **bone resorption**, renal calcium reabsorption, and intestinal calcium absorption [2]. *Hypervitaminosis of Vitamin D* - Excessive intake or production of **Vitamin D** leads to hypercalcemia by increasing **intestinal absorption of calcium** [2]. - It also enhances **bone resorption**, contributing to elevated serum calcium levels.

Q: Central obesity is seen in;

Cushing's disease. ***Cushing's disease*** - **Cushing's disease** is characterized by **excessive cortisol production**, leading to fat redistribution, including **central obesity** with a 'buffalo hump' and 'moon face' [1]. - **Cortisol's metabolic effects** promote increased visceral fat accumulation and breakdown of peripheral fat [1]. *Crohn's disease* - **Crohn's disease** is an **inflammatory bowel disease** that typically causes **weight loss**, abdominal pain, and diarrhea due to malabsorption and inflammation. - While patients can develop complications like **fistulas** and **abscesses**, central obesity is not a primary feature. *Celiac disease* - **Celiac disease** is an **autoimmune disorder** triggered by gluten, leading to **malabsorption** and usually presenting with **weight loss**, diarrhea, and nutrient deficiencies. - Central obesity is **not a typical presentation** and would be contradictory to the malabsorptive state. *Conn's disease* - **Conn's disease**, or primary aldosteronism, involves **excessive aldosterone** production, primarily causing **hypertension** and hypokalemia. - It **does not directly cause central obesity**; its metabolic effects are unrelated to fat distribution.

Q: Which type of anaemia is seen in vitamin B12 deficiency?

Macrocytic anemia. ***Macrocytic anemia*** - Vitamin B12 is essential for **DNA synthesis**, and its deficiency leads to impaired nuclear maturation and delayed cell division in erythroid precursors, resulting in abnormally large red blood cells called **megaloblasts**. - This impaired maturation process leads to the production of **macrocytic red blood cells** (high MCV) which are also often prematurely destroyed, contributing to the anemia. *Dimorphic anemia* - This term describes the presence of **two distinct red cell populations**, typically microcytic and macrocytic, which can occur with combined deficiencies such as iron and vitamin B12. - While vitamin B12 deficiency primarily causes macrocytic anemia, dimorphic anemia is not its standalone feature unless accompanied by another deficiency. *Microcytic anemia* - Characterized by **abnormally small red blood cells** (low MCV), typically seen in conditions like **iron deficiency anemia** or thalassemia. - Vitamin B12 deficiency causes large red blood cells, thus ruling out microcytic anemia. *Normocytic anemia* - Red blood cells are of **normal size** (normal MCV) but are reduced in number, often seen in conditions like **anemia of chronic disease** or acute blood loss. - Since vitamin B12 deficiency directly impacts red blood cell size by causing megaloblastic changes, normocytic anemia is not the primary presentation.

Q: A 40-year-old male presents with fever and abdominal pain and is diagnosed with HIV and TB. What is the most appropriate sequence of treatment?

ATT followed by ART within 2-8 weeks. ***ATT followed by ART within 2-8 weeks*** - This sequence is crucial for patients with co-infection of **HIV and TB**. Initiating **anti-tuberculous treatment (ATT)** first is vital to control the active TB infection, which can be rapidly fatal [2]. - Subsequently, starting **antiretroviral therapy (ART)** within 2-8 weeks (typically 2-4 weeks after ATT in patients without CNS TB) helps to restore the immune system and prevent other opportunistic infections, but delaying it slightly reduces the risk of **IRIS (Immune Reconstitution Inflammatory Syndrome)** [1]. *First ATT and then ART* - While starting ATT first is correct, this option is too vague regarding the timing of ART initiation. - The specific window of 2-8 weeks (or 2-4 weeks without CNS TB) is important to balance TB treatment efficacy and mitigate **IRIS risk** [1]. *ATT only* - This approach is incorrect as it fails to address the underlying HIV infection, which would lead to continued immune decline and increased morbidity and mortality. - ART is essential for improving prognosis and reducing viral load in HIV-infected individuals. *First ART and then ATT* - Initiating ART before ATT in co-infected patients with active TB can worsen the TB condition due to **IRIS**, which can be severe and life-threatening [1]. - ART can cause a rapid immune reconstitution and paradoxical worsening of symptoms or presentation of subclinical TB [1].

Q: Most common cause of fulminant diabetes is?

Autoimmunity. ***Autoimmunity*** - **Fulminant diabetes** is a distinct subtype of **Type 1 diabetes** with an acute onset and rapid, severe beta-cell destruction [1]. - This rapid destruction is primarily mediated by an **autoimmune process**, leading to profound insulin deficiency during the initial presentation [2]. *Viruses* - While certain **viral infections** (e.g., Coxsackievirus, enteroviruses) are implicated as potential triggers for **Type 1 diabetes**, they are not considered the direct and most common cause of the fulminant form itself [1]. - Viral infections might initiate or accelerate the **autoimmune process**, but autoimmunity is the direct mechanism of beta-cell destruction. *Non-ketotic hyperosmolar coma* - **Non-ketotic hyperosmolar coma (NKHC)** is a severe complication of **Type 2 diabetes**, characterized by extremely high blood glucose levels without significant ketosis [2]. - It is not a cause of fulminant diabetes but rather a distinct acute diabetic emergency. *Diabetic Ketoacidosis* - **Diabetic ketoacidosis (DKA)** is an acute, life-threatening complication of **Type 1 diabetes** (and sometimes Type 2), characterized by hyperglycemia, ketosis, and metabolic acidosis [3]. - DKA is a **result** of severe insulin deficiency, which can be seen in fulminant diabetes, but it is not the underlying cause of the fulminant condition itself.

Q: Raised JVP that does not fall back is a characteristic feature of which condition?

Atrial fibrillation. ***Atrial fibrillation*** - In **atrial fibrillation**, the atria beat chaotically and irregularly, leading to an absence of coordinated atrial contraction [1]. - This results in a lack of measurable 'a' waves in the JVP, and the JVP waveform tends to be **regular without a distinct fall and rise**, reflecting continuous atrial pressure without proper emptying [1]. *Ventricular tachycardia* - While JVP can be elevated due to cardiac decompensation, **ventricular tachycardia** involves rapid, regular ventricular contractions, which would not typically cause a sustained JVP without a clear fall [3]. - The JVP often shows **cannon 'a' waves** in VA dissociation, as the right atrium contracts against a closed tricuspid valve. *Ventricular fibrillation* - **Ventricular fibrillation** is a medical emergency characterized by disorganized ventricular electrical activity, leading to immediate circulatory collapse [3]. - In this state, there is no effective cardiac output, and the patient is typically unconscious, making a JVP assessment less relevant and difficult to interpret in the context of a sustained JVP finding [3]. *Atrial flutter* - **Atrial flutter** typically presents with a regular, characteristic **"sawtooth" pattern** of atrial activity (JVP 'f' waves), and the JVP can show regular, rapid 'a' waves (flutter waves) that are often more prominent than normal [2]. - The JVP usually has a clear, albeit rapid, rise and fall pattern related to the atrial contractions [2].

Q: A long-term diabetic patient with blisters walked barefoot for a few miles on hot sand. He presented with rapidly spreading deep tissue infection with extensive tissue necrosis. What is the most probable diagnosis?

Necrotizing fasciitis. ***Necrotizing fasciitis*** - The rapid spread of deep tissue infection with extensive necrosis, especially in an immunocompromised patient like a diabetic, is highly characteristic of **necrotizing fasciitis**. [1] - **Diabetic peripheral neuropathy** can lead to unnoticed injury (walking barefoot on hot sand) and impaired wound healing, further predisposing to severe infections. [2] *Burn* - While walking on hot sand can cause burns, this patient's presentation of "rapidly spreading deep tissue infection" and "extensive tissue necrosis" goes beyond a typical burn injury, suggesting an overwhelming infection. - Burns primarily involve direct tissue damage from heat, whereas the described pathology is indicative of a **bacterial infection** escalating rapidly. *Cellulitis* - **Cellulitis** is a superficial skin infection that typically presents as localized redness, warmth, and swelling, but it usually does not involve deep tissue necrosis or such rapid, extensive spread. - It lacks the hallmark sign of rapid progression to **necrosis** and involvement of deep fascial planes that necessitate urgent surgical debridement. *Diabetic foot* - **Diabetic foot** is a broad term encompassing various foot complications in diabetes, including ulcers, infections, and Charcot arthropathy. While this patient has a diabetic foot, the specific presentation of **rapidly spreading infection** with **extensive necrosis** points to a particular, severe diagnosis within the diabetic foot spectrum, rather than the general term. [2] - The context describes a specific acute, life-threatening infectious process rather than the chronic complications typically associated with the general term "diabetic foot."

Q: Diagnosis of Gout is confirmed by which test?

Synovial fluid analysis. ***Synovial fluid analysis*** - Diagnosis of gout is definitively confirmed by the presence of **negatively birefringent, needle-shaped urate crystals** within neutrophils in the synovial fluid [1]. - This direct visualization of crystals confirms the diagnosis and differentiates gout from other forms of arthritis [1]. *X-ray changes* - While X-rays can show characteristic changes in chronic gout, such as **punched-out erosions with overhanging edges** (rat-bite erosions), these are not diagnostic of acute gout and may appear late in the disease course. - X-ray findings are less specific and do not confirm the presence of urate crystals. *Urine uric acid levels* - Urine uric acid levels help to distinguish between **overproducers and underexcreters** of uric acid, which can guide long-term management strategies [1]. - However, they do not directly confirm the diagnosis of an acute gouty attack. *Serum Uric acid level* - Elevated serum uric acid (hyperuricemia) is a prerequisite for gout, but many individuals with hyperuricemia never develop gout [1]. - Therefore, a **high serum uric acid level alone is not sufficient** to diagnose gout, especially during an acute attack when levels can sometimes be normal [1].

Question 1

Gynecomastia is seen in all except;

Accepted Answer

Leprosy

Answer

Kidney failure

Answer

Liver failure

Answer

Stilbestrol therapy for prostate cancer

Answer

Teratoma of the testis

Answer

Hormonal

Answer

Idiopathic

Answer

Anorchism and After castration

Answer

Klinefelter's syndrome

Question 2

Which of the following is seen in mitral stenosis?

Accepted Answer

Diastolic murmur

Answer

None of the options

Answer

Systolic murmur

Answer

Loud S2

Question 3

All of the following are the causes for hypercalcemia Except?

Accepted Answer

Acute pancreatitis

Answer

Thiazides

Answer

Hyperparathyroidism

Answer

Hypervitaminosis of Vitamin D

Question 4

Central obesity is seen in;

Accepted Answer

Cushing's disease

Answer

Crohn's disease

Answer

Celiac disease

Answer

Conn's disease

Question 5

Which type of anaemia is seen in vitamin B12 deficiency?

Accepted Answer

Macrocytic anemia

Answer

Dimorphic anemia

Answer

Microcytic anemia

Answer

Normocytic anemia

Question 6

A 40-year-old male presents with fever and abdominal pain and is diagnosed with HIV and TB. What is the most appropriate sequence of treatment?

Accepted Answer

ATT followed by ART within 2-8 weeks

Answer

First ATT and then ART

Answer

ATT only

Answer

First ART and then ATT

Question 7

Most common cause of fulminant diabetes is?

Accepted Answer

Autoimmunity

Answer

Viruses

Answer

Non-ketotic hyperosmolar coma

Answer

Diabetic Ketoacidosis

Question 8

Raised JVP that does not fall back is a characteristic feature of which condition?

Accepted Answer

Atrial fibrillation

Answer

Ventricular tachycardia

Answer

Ventricular fibrillation

Answer

Atrial flutter

Question 9

A long-term diabetic patient with blisters walked barefoot for a few miles on hot sand. He presented with rapidly spreading deep tissue infection with extensive tissue necrosis. What is the most probable diagnosis?

Accepted Answer

Necrotizing fasciitis

Answer

Burn

Answer

Cellulitis

Answer

Diabetic foot

Question 10

Diagnosis of Gout is confirmed by which test?

Accepted Answer

Synovial fluid analysis

Answer

X- ray changes

Answer

Urine uric acid levels

Answer

Serum Uric acid level

FMGE 2019 — Internal Medicine