Trace minerals (Fe, Zn, Cu, Se, I) US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Trace minerals (Fe, Zn, Cu, Se, I). These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Trace minerals (Fe, Zn, Cu, Se, I) US Medical PG Question 1: A 26-year-old man from India visits the clinic with complaints of feeling tired all the time and experiencing lack of energy for the past couple of weeks. He also complains of weakness and numbness of his lower limbs. He has been strictly vegan since the age of 18, including not consuming eggs and milk. He does not take any vitamin or dietary supplements. Physical examination reveals a smooth, red beefy tongue along with lower extremity sensory and motor deficits. What other finding is most likely to accompany this patient’s condition?
- A. Upper limb weakness
- B. Psychiatric symptoms
- C. Decreased visual acuity
- D. Microcytic anemia
- E. Ataxia (Correct Answer)
Trace minerals (Fe, Zn, Cu, Se, I) Explanation: **Ataxia**
- The patient's history of being a strict vegan, fatigue, weakness, numbness, and neurological deficits (sensory and motor) along with a **smooth, red beefy tongue** are classic signs of **vitamin B12 deficiency**.
- **Vitamin B12 deficiency** often leads to **subacute combined degeneration of the spinal cord**, which can manifest as **ataxia**, spasticity, and paresthesias due to demyelination.
*Upper limb weakness*
- While B12 deficiency can cause generalized weakness, the question specifically highlights **lower extremity sensory and motor deficits**, with **ataxia** being a more characteristic and often earlier neurological sign of spinal cord involvement than upper limb weakness.
- Upper limb weakness might develop in advanced stages, but it is not the **most likely** accompanying finding in the early or moderate stages often described with lower limb involvement and ataxia.
*Psychiatric symptoms*
- **Psychiatric symptoms** such as depression, irritability, and cognitive impairment can occur in **vitamin B12 deficiency**, but **ataxia** is a more direct and common neurological consequence stemming from the demyelination in the spinal cord.
- While possible, the question asks for the **most likely** additional finding given the specific neurological presentation.
*Decreased visual acuity*
- **Optic neuropathy** and **decreased visual acuity** can occur in some cases of **vitamin B12 deficiency**, but it is less common than the spinal cord and peripheral nerve manifestations like ataxia and paresthesias.
- The presented symptoms directly point to spinal cord involvement, making **ataxia** a more prominent associated neurological finding.
*Microcytic anemia*
- **Vitamin B12 deficiency** typically causes **megaloblastic (macrocytic) anemia**, not microcytic anemia.
- **Microcytic anemia** is primarily associated with **iron deficiency**, lead poisoning, or thalassemia.
Trace minerals (Fe, Zn, Cu, Se, I) US Medical PG Question 2: A 43-year-old woman presents to the physician with the complaint of worsening fatigue over the past several months. She has found that she requires nearly double the amount of coffee consumption each day to stay awake at work and that despite maintaining a balanced, healthy diet, she has experienced significant weight gain. A blood test confirms the presence of anti-thyroid peroxidase antibodies. Which of the following additional findings would be most consistent with the underlying pathophysiology of her condition?
- A. Galactorrhea (Correct Answer)
- B. Constipation
- C. Brisk deep tendon reflexes
- D. Diarrhea
- E. Heat intolerance
Trace minerals (Fe, Zn, Cu, Se, I) Explanation: ***Galactorrhea***
- This patient has **Hashimoto's thyroiditis**, an autoimmune hypothyroidism, given the fatigue, weight gain, and positive **anti-thyroid peroxidase antibodies**.
- **Hypothyroidism** can lead to **hyperprolactinemia** due to increased **TRH** (thyrotropin-releasing hormone), which stimulates both TSH and prolactin release from the anterior pituitary.
- Elevated prolactin can manifest as **galactorrhea**, representing a less commonly recognized endocrine consequence of primary hypothyroidism.
*Constipation*
- **Constipation** is a common symptom of **hypothyroidism** due to decreased gastrointestinal motility.
- While consistent with hypothyroidism, it is a direct consequence of reduced metabolic activity rather than a secondary endocrine effect.
- This is a well-known, expected finding rather than an additional pathophysiologic manifestation.
*Brisk deep tendon reflexes*
- **Hypothyroidism** typically causes **delayed relaxation of deep tendon reflexes** (hung-up reflexes), not brisk reflexes.
- **Brisk reflexes** are characteristic of **hyperthyroidism** due to increased neuromuscular excitability.
*Diarrhea*
- **Diarrhea** is typically associated with **hyperthyroidism** due to increased gastrointestinal motility from elevated metabolic rate.
- **Hypothyroidism** more commonly causes **constipation** due to decreased GI motility.
*Heat intolerance*
- **Heat intolerance** is a classic symptom of **hyperthyroidism** due to an elevated metabolic rate and increased thermogenesis.
- Patients with **hypothyroidism** usually experience **cold intolerance** due to decreased metabolic heat production.
Trace minerals (Fe, Zn, Cu, Se, I) US Medical PG Question 3: What is the primary mechanism for iron absorption in the duodenum?
- A. Simple diffusion
- B. Passive paracellular transport
- C. Endocytosis
- D. DMT1 transporter (Correct Answer)
Trace minerals (Fe, Zn, Cu, Se, I) Explanation: ***DMT1 transporter***
- The **divalent metal transporter 1 (DMT1)** is the primary mechanism for absorbing **non-heme iron (ferrous iron, Fe2+)** into duodenal enterocytes.
- This active transport process is pH-dependent and drives iron uptake against a concentration gradient.
*Simple diffusion*
- Applies to the movement of substances down their concentration gradient without the aid of membrane proteins, which is not the main mechanism for iron due to its ionic nature.
- While some highly lipid-soluble substances can cross membranes this way, metal ions like iron require specific transporters.
*Passive paracellular transport*
- Involves substances moving *between* cells, rather than *through* them, often occurring in leaky epithelia.
- While some fluid and electrolytes may use this route, it is not the primary or regulated pathway for iron absorption.
*Endocytosis*
- A process where cells engulf substances by forming vesicles from the plasma membrane.
- While some macromolecules are absorbed via endocytosis, it is not the major mechanism for absorbing dietary iron in the duodenum.
Trace minerals (Fe, Zn, Cu, Se, I) US Medical PG Question 4: A patient with Graves' disease is treated with thiocyanate (a historical antithyroid agent). Thiocyanate helps reduce thyroid hormone production by:
- A. Inhibiting thyroid peroxidase
- B. Inhibiting 5'-deiodinase
- C. Inhibiting iodide follicular uptake (Correct Answer)
- D. Inhibiting beta-adrenergic receptors
- E. Inhibiting thyroid deiodinase
Trace minerals (Fe, Zn, Cu, Se, I) Explanation: ***Inhibiting iodide follicular uptake***
- Thiocyanate is a competitive inhibitor of the **sodium-iodide symporter (NIS)** on thyroid follicular cells, blocking the uptake of iodide into the thyroid gland.
- By preventing iodide entry, thiocyanate reduces the raw material needed for thyroid hormone synthesis, thereby mitigating the **hyperthyroidism** seen in Graves' disease.
*Inhibiting thyroid peroxidase*
- This is the mechanism of action for **thionamide drugs** (e.g., methimazole, propylthiouracil), which block the oxidation of iodide and its organification.
- While effective in Graves' disease, thiocyanate does not directly inhibit thyroid peroxidase activity.
*Inhibiting 5'-deiodinase*
- **Propylthiouracil (PTU)**, but not thiocyanate, inhibits the peripheral conversion of T4 to the more active T3 by blocking 5'-deiodinase enzymes.
- This action helps to reduce the overall effect of thyroid hormones in the body.
*Inhibiting beta-adrenergic receptors*
- **Beta-blockers** (e.g., propranolol) are used to manage the symptomatic effects of hyperthyroidism, such as palpitations, tremor, and anxiety.
- They do not affect thyroid hormone synthesis or release, but rather block the peripheral actions of thyroid hormones on adrenergic receptors.
*Inhibiting thyroid deiodinase*
- This option refers to the enzymes responsible for removing iodine from thyroid hormones, which is part of the normal catabolism of these hormones or for converting T4 to T3.
- Thiocyanate does not primarily act by inhibiting these deiodinase enzymes within the thyroid gland or peripherally; its main action is on iodide uptake.
Trace minerals (Fe, Zn, Cu, Se, I) US Medical PG Question 5: A 37-year-old man is brought to the emergency department because he was found down on a city sidewalk. Upon presentation he is found to be disheveled with multiple poorly healed wounds on his hands and feet. He has had dozens of previous presentations for alcohol intoxication and is currently known to be homeless. Physical examination reveals multiple minor wounds, alopecia, and decreased axillary hair. Upon being aroused, the patient reveals that he has had difficulty with taste and smell and has also had severe diarrhea over the last week. The deficient substance most likely responsible for this patient's symptoms is associated with which of the following proteins?
- A. Tyrosinase
- B. Hemoglobin
- C. Glutathione peroxidase
- D. RNA polymerase (Correct Answer)
- E. Thyroid hormone
Trace minerals (Fe, Zn, Cu, Se, I) Explanation: ***Correct: RNA polymerase***
* The clinical presentation of **poorly healed wounds, alopecia, decreased axillary hair, dysgeusia/anosmia, and diarrhea** in a homeless patient with chronic alcoholism is classic for **zinc deficiency**.
* **Zinc is an essential cofactor for RNA polymerase**, the enzyme responsible for DNA transcription and ultimately protein synthesis. Zinc deficiency impairs cellular proliferation and protein synthesis, which explains the poor wound healing, hair loss, and other manifestations.
* Zinc is also a cofactor for over 300 enzymes including alkaline phosphatase, carbonic anhydrase, superoxide dismutase, and various matrix metalloproteinases critical for wound healing and tissue maintenance.
*Incorrect: Glutathione peroxidase*
* **Glutathione peroxidase requires SELENIUM, not zinc**, as its essential cofactor. This enzyme protects against oxidative damage by reducing hydrogen peroxide.
* Selenium deficiency presents with **cardiomyopathy (Keshan disease), myopathy, and thyroid dysfunction**, not the constellation of symptoms seen in this patient.
*Incorrect: Tyrosinase*
* **Tyrosinase is a copper-dependent enzyme** involved in melanin synthesis. Copper deficiency causes **anemia, neutropenia, and neurological symptoms** (myelopathy), not the dermatologic and sensory changes seen here.
* While copper deficiency can occur in alcoholism, the specific symptoms of taste/smell disturbances and characteristic skin findings point to zinc deficiency.
*Incorrect: Thyroid hormone*
* Thyroid hormone synthesis requires **iodine**, not zinc. Hypothyroidism presents with **fatigue, weight gain, cold intolerance, and bradycardia**.
* The patient's acute presentation with diarrhea, taste/smell disturbances, and poor wound healing does not fit thyroid dysfunction.
*Incorrect: Hemoglobin*
* Hemoglobin requires **iron** for oxygen transport. Iron deficiency causes **microcytic anemia with fatigue, pallor, and koilonychia**.
* While chronic alcoholics may develop anemia (often macrocytic from folate/B12 deficiency), the specific symptoms of dysgeusia, anosmia, and characteristic dermatologic findings indicate zinc deficiency as the primary issue.
Trace minerals (Fe, Zn, Cu, Se, I) US Medical PG Question 6: A homeless woman presents with shortness of breath on exertion and pedal edema. Cardiac workup performed shows evidence of dilated cardiomyopathy and increased cardiac output. She also has decreased sensation over both extremities bilaterally. Which vitamin deficiency most likely caused these symptoms?
- A. Vitamin B6
- B. Vitamin C
- C. Vitamin B1 (Correct Answer)
- D. Vitamin B3
- E. Vitamin A
Trace minerals (Fe, Zn, Cu, Se, I) Explanation: ***Vitamin B1***
- The combination of **dilated cardiomyopathy**, **high-output heart failure** (manifesting as shortness of breath and pedal edema), and **peripheral neuropathy** (decreased sensation) is classic for **wet beriberi**, caused by thiamine (Vitamin B1) deficiency.
- **Homelessness** is a significant risk factor for nutritional deficiencies, including thiamine deficiency, due to inadequate diet.
*Vitamin B6*
- Deficiency can cause **peripheral neuropathy**, but it does not typically lead to **dilated cardiomyopathy** or **high-output heart failure**.
- Other manifestations of B6 deficiency include **sideroblastic anemia** and **seizures**.
*Vitamin C*
- Deficiency causes **scurvy**, characterized by **gingivitis**, **poor wound healing**, **petechiae**, and joint pain.
- It does not present with **cardiomyopathy** or **neuropathy** as described.
*Vitamin B3*
- Deficiency causes **pellagra**, characterized by the "3 Ds": **dermatitis**, **diarrhea**, and **dementia**.
- While it can affect the nervous system (dementia), it does not typically cause **dilated cardiomyopathy** or **peripheral neuropathy**.
*Vitamin A*
- Deficiency primarily affects **vision** (e.g., **night blindness**, **xerophthalmia**) and immune function.
- It is not associated with **cardiac** or **neurological symptoms** like those described in the patient.
Trace minerals (Fe, Zn, Cu, Se, I) US Medical PG Question 7: A 6-month-old boy presents with decreased growth, pigmented retinopathy, hemolytic anemia, and peripheral neuropathy. You suspect that these signs are the result of a vitamin deficiency leading to increased oxidative damage to lipids. Which of the following is most likely responsible for this patient's symptoms?
- A. Excessive boiling of formula
- B. Goat milk ingestion
- C. Abetalipoproteinemia (Correct Answer)
- D. Pernicious anemia
- E. Hartnup disease
Trace minerals (Fe, Zn, Cu, Se, I) Explanation: ***Abetalipoproteinemia***
- This condition is characterized by a defect in **microsomal triglyceride transfer protein (MTP)**, leading to an inability to synthesize ApoB-containing lipoproteins.
- The resulting **malabsorption of fat and fat-soluble vitamins (especially vitamin E)** leads to the neurological symptoms (retinopathy, neuropathy) and hemolytic anemia due to increased oxidative stress on red blood cell membranes.
*Excessive boiling of formula*
- Excessive boiling of formula could potentially degrade some **heat-sensitive vitamins**, such as vitamin C or thiamine (B1).
- However, this is unlikely to cause a severe, combined deficiency leading to the specific constellation of symptoms seen, particularly the ophthalmologic and neurological signs related to **fat-soluble vitamin malabsorption**.
*Goat milk ingestion*
- Goat milk is naturally low in **folate** and **vitamin D** and can cause **folate deficiency anemia** and rickets if it's the sole source of nutrition for an infant.
- However, it does not typically cause the entire spectrum of symptoms described, particularly **pigmented retinopathy** and **peripheral neuropathy**, which are more indicative of **vitamin E deficiency**.
*Pernicious anemia*
- Pernicious anemia is caused by a deficiency in **intrinsic factor**, leading to **vitamin B12 malabsorption**.
- Symptoms primarily include **megaloblastic anemia**, **glossitis**, and **neurological deficits** (subacute combined degeneration of the spinal cord), but not pigmented retinopathy or hemolytic anemia due to increased fatty acid oxidation via vitamin E malabsorption.
*Hartnup disease*
- Hartnup disease is an inherited disorder of **amino acid transport**, specifically affecting the absorption of **neutral amino acids** like tryptophan.
- It leads to **niacin deficiency** (pellagra-like symptoms) and can cause skin rashes, ataxia, and psychiatric symptoms, but not hemolytic anemia or pigmented retinopathy.
Trace minerals (Fe, Zn, Cu, Se, I) US Medical PG Question 8: A 22-year-old man comes to the physician because of a fall associated with a 6-month history of increasing difficulty walking. Over the last year, his friends have also noticed his speech becoming slower. During this period, he also gave up his hobby of playing video games because he has become clumsy with his hands. His father died of esophageal varices at the age of 40 years. The patient does not smoke or drink alcohol. He takes no medications. He appears sad. His temperature is 37°C (98.6°F), pulse is 70/min, and blood pressure is 120/80 mm Hg. He is alert and oriented to person, place, and time. His speech is slurred and monotonous; his gait is unsteady. Examination shows scleral icterus and some drooling. The liver is palpated 2 to 3 cm below the right costal margin, and the spleen is palpated 1 to 2 cm below the left costal margin. Further evaluation of this patient is most likely to show which of the following findings?
- A. Increased number of CAG repeats
- B. Oligoclonal bands on CSF analysis
- C. Low serum ceruloplasmin concentration (Correct Answer)
- D. Ventriculomegaly on CT scan of the brain
- E. Increased transferrin saturation
Trace minerals (Fe, Zn, Cu, Se, I) Explanation: ***Low serum ceruloplasmin concentration***
- This patient presents with a constellation of symptoms including neurological (difficulty walking, clumsy hands, slurred speech, unsteady gait), hepatic (father died of esophageal varices at an early age, hepatosplenomegaly, scleral icterus), and psychiatric (sadness, slurred and monotonous speech) manifestations, all suggestive of **Wilson's disease**.
- **Wilson's disease** is an autosomal recessive disorder of copper metabolism leading to copper accumulation in various organs, predominantly the **liver**, **brain**, and **cornea**. **Low serum ceruloplasmin** is a hallmark biochemical finding, as ceruloplasmin is a copper-carrying protein, and its synthesis or copper incorporation is defective.
*Increased number of CAG repeats*
- An increased number of **CAG trinucleotide repeats** is characteristic of **Huntington's disease**.
- While Huntington's disease causes neurological and psychiatric symptoms, it does not typically involve significant **liver disease** or scleral icterus, which are prominent features in this patient's presentation.
*Oligoclonal bands on CSF analysis*
- **Oligoclonal bands** in the **cerebrospinal fluid (CSF)** are a key diagnostic finding for **multiple sclerosis**.
- Multiple sclerosis presents with neurological deficits, but it does not account for the prominent liver involvement (scleral icterus, hepatosplenomegaly, family history of varices) seen in this case.
*Ventriculomegaly on CT scan of the brain*
- **Ventriculomegaly** on a CT scan of the brain can be seen in various conditions, including **hydrocephalus** or **cerebral atrophy**.
- While some neurological degenerative diseases can lead to cerebral atrophy and resulting ventriculomegaly, it's a non-specific finding and doesn't explain the patient's severe **hepatic involvement** with scleral icterus and hepatosplenomegaly.
*Increased transferrin saturation*
- **Increased transferrin saturation** is a laboratory finding indicative of **hemochromatosis**, a disorder of iron metabolism leading to iron overload.
- While hemochromatosis can cause liver disease and neurological symptoms, the combination of **scleral icterus**, the specific neurological presentation, and the strong family history of early liver disease in this context points much more strongly towards **Wilson's disease** rather than hemochromatosis.
Trace minerals (Fe, Zn, Cu, Se, I) US Medical PG Question 9: A 25-year-old woman comes to the emergency department because of a mild headache, dizziness, fatigue, and nausea over the past several hours. She has no history of serious illness and takes no medications. She lives in a basement apartment and uses a wood stove for heating. Her temperature is 36°C (96.8°F) and pulse is 120/min. Arterial blood gas analysis shows a carboxyhemoglobin level of 11% (N = < 1.5). Which of the following mechanisms is the underlying cause of this patient's symptoms?
- A. Formation of carboxyhemoglobin reducing oxygen transport capacity (Correct Answer)
- B. Inhibition of hemoglobin synthesis in bone marrow
- C. Direct cellular toxicity from carbon monoxide metabolites
- D. Competitive inhibition of oxygen at tissue level
- E. Decreased hemoglobin-oxygen binding affinity
Trace minerals (Fe, Zn, Cu, Se, I) Explanation: ***Formation of carboxyhemoglobin reducing oxygen transport capacity***
- Carbon monoxide binds to hemoglobin with **200-250 times greater affinity** than oxygen, forming **carboxyhemoglobin (COHb)**.
- This patient's **carboxyhemoglobin level of 11%** (normal <1.5%) confirms CO poisoning from the **wood stove** in her basement apartment.
- COHb formation **reduces oxygen-carrying capacity** of blood, leading to **tissue hypoxia** and symptoms of headache, dizziness, fatigue, and nausea.
- CO also **shifts the oxygen-hemoglobin dissociation curve leftward**, impairing oxygen release to tissues.
*Inhibition of hemoglobin synthesis in bone marrow*
- Carbon monoxide does **not** inhibit hemoglobin synthesis.
- This mechanism would be seen in conditions like **iron deficiency anemia**, **anemia of chronic disease**, or exposure to toxins like **lead**.
- CO poisoning is an **acute** problem of oxygen transport, not a chronic problem of hemoglobin production.
*Direct cellular toxicity from carbon monoxide metabolites*
- Carbon monoxide is **not significantly metabolized** in the human body.
- CO is eliminated unchanged through the **lungs** when the patient breathes fresh air or receives oxygen therapy.
- The toxicity is from **CO itself** binding to hemoglobin, myoglobin, and cytochrome enzymes, not from any metabolites.
*Competitive inhibition of oxygen at tissue level*
- While CO does bind to **myoglobin** and **mitochondrial cytochrome oxidase** at the tissue level, this is a **secondary mechanism**.
- The **primary and most significant mechanism** is carboxyhemoglobin formation, which reduces oxygen delivery to tissues.
- Tissue-level effects contribute to toxicity but don't explain the elevated **carboxyhemoglobin level** seen in this patient.
*Decreased hemoglobin-oxygen binding affinity*
- This is **incorrect**; CO actually causes hemoglobin to bind oxygen **more tightly**, not less.
- CO shifts the **oxygen-hemoglobin dissociation curve to the left**, increasing hemoglobin's affinity for oxygen and impairing oxygen release to tissues.
- The primary problem is **reduced oxygen-carrying capacity** from CO occupying hemoglobin binding sites, not decreased affinity.
Trace minerals (Fe, Zn, Cu, Se, I) US Medical PG Question 10: An 82-year-old woman is brought to the emergency room after her neighbor saw her fall in the hallway. She lives alone and remarks that she has been feeling weak lately. Her diet consists of packaged foods and canned meats. Her temperature is 97.6°F (36.4°C), blood pressure is 133/83 mmHg, pulse is 95/min, respirations are 16/min, and oxygen saturation is 98% on room air. Physical exam is notable for a weak, frail, and pale elderly woman. Laboratory studies are ordered as seen below.
Hemoglobin: 9.1 g/dL
Hematocrit: 30%
Leukocyte count: 6,700/mm^3 with normal differential
Platelet count: 199,500/mm^3
MCV: 110 fL
Which of the following is the most likely deficiency?
- A. Zinc
- B. Vitamin B12
- C. Thiamine
- D. Niacin
- E. Folate (Correct Answer)
Trace minerals (Fe, Zn, Cu, Se, I) Explanation: ***Folate***
- The patient's **macrocytic anemia** (MCV 110 fL, hemoglobin 9.1 g/dL) combined with a diet of **packaged foods and canned meats** with **no fresh fruits or vegetables** strongly suggests folate deficiency.
- **Folate is found exclusively in fresh produce** (leafy greens, fruits, legumes), which is completely absent from this patient's diet.
- **Elderly individuals** living alone with inadequate nutrition are at particularly high risk for **folate deficiency**.
*Vitamin B12*
- While vitamin B12 deficiency also causes **macrocytic anemia**, her diet includes **canned meats which retain B12** (heat-stable vitamin).
- B12 deficiency typically requires years to develop due to large hepatic stores, and often presents with **neurological manifestations** (subacute combined degeneration, peripheral neuropathy), which are absent here.
- The dietary pattern makes folate deficiency more likely than B12 deficiency.
*Zinc*
- Zinc deficiency causes impaired immune function, delayed wound healing, skin lesions, and **taste disturbances**, but **not macrocytic anemia**.
- No clinical or laboratory findings suggest zinc deficiency.
*Thiamine*
- Thiamine (vitamin B1) deficiency causes **Wernicke-Korsakoff syndrome** or **beriberi** (wet or dry), presenting with neurological symptoms, heart failure, or peripheral neuropathy.
- Thiamine deficiency does **not cause macrocytic anemia**.
*Niacin*
- Niacin (vitamin B3) deficiency causes **pellagra**, characterized by the \"3 D's\": **dermatitis, diarrhea, and dementia**.
- Niacin deficiency is **not associated with macrocytic anemia**.
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