Brain Flashcards
(64 cards)
What is one key function of the brain’s circumventricular organs (CVOs)?
A. Let nutrients enter the brain quickly
B. Pump toxins (xenobiotics) from the brain back into the blood
C. Help brain cells grow in response to injury
D. Detect and respond to hormone levels in the blood
D.
Explanation:
Circumventricular organs (CVOs) are special parts of the brain that:
* Lack a blood-brain barrier (or have a very weak one)
* Are located around the third and fourth ventricles
* Can monitor the blood directly because substances can freely pass into them
This makes them perfect for detecting changes in blood chemistry, like hormone levels.
Why is this important?
* Hormones like vasopressin, angiotensin II, or cytokines can influence brain function.
* CVOs help trigger brain responses such as thirst, fever, or blood pressure regulation.
Option-by-option breakdown:
* A. Incorrect. Nutrient entry is controlled tightly by the blood-brain barrier. CVOs are not for general nutrient delivery — their job is sensing, not feeding.
* B. Incorrect. That’s the role of efflux transporters (like P-glycoprotein) at the blood-brain barrier, not the circumventricular organs.
* C. Incorrect. Neuronal hypertrophy or repair may happen after injury, but this isn’t a known function of CVOs.
* D. Correct. This is the main job of CVOs — because they can directly monitor blood content, they help the brain respond to systemic signals.
Key CVOs to remember:
* Area postrema – triggers vomiting when toxins are detected
* Organum vasculosum of the lamina terminalis (OVLT) – involved in thirst and osmoregulation
* Subfornical organ – senses angiotensin II, helps control blood pressure
Memory Tip:
CVOs = Hormone-sensing windows in the brain
Why does brain tissue need so much energy compared to other tissues?
A. Maintenance and reestablishment of ion gradients
B. High levels of protein synthesis and degradation
C. High level of immune surveillance
D. All of the above
A.
Explanation:
The main reason neurons need so much energy is to maintain and reset ion gradients, especially after electrical activity (like action potentials).
Why are ion gradients so important?
* Neurons use Na⁺/K⁺ pumps to keep sodium outside and potassium inside the cell.
* Every time a neuron fires (an action potential), ions move across the membrane.
* Resetting this balance takes a ton of ATP, even at rest.
Option-by-option breakdown:
* A. Correct. This is the primary energy drain in neurons. The Na⁺/K⁺-ATPase pump runs constantly to keep the electrochemical gradient intact.
* B. Partially true, but not the main energy user. Neurons do synthesize proteins (especially at synapses), but this is a smaller energy cost than ion pumping.
* C. Incorrect. The brain has limited immune activity due to the blood-brain barrier. Microglia play a role, but it’s not a major energy sink.
* D. Tempting, but wrong. While B and C may use some energy, they don’t come close to the demands of maintaining ion gradients.
Memory Tip:
“Neurons fire, then reset — and that costs the most energy yet!”
________________________________________
Which drug class is most associated with causing tardive dyskinesia after long-term use?
A. Tricyclic antidepressants
B. Phenothiazines
C. Amphetamines
D. Cocaine
B.
Explanation:
Tardive dyskinesia (TD) is a neurological disorder marked by involuntary, repetitive movements, often of the face, tongue, and limbs.
It is most commonly caused by chronic use of dopamine-blocking drugs, especially typical antipsychotics like phenothiazines.
* These drugs block D2 dopamine receptors, especially in the nigrostriatal pathway, leading to dopamine receptor hypersensitivity over time.
Option-by-option breakdown:
* A. Incorrect. These affect norepinephrine and serotonin, not dopamine. They can have anticholinergic or cardiac side effects but not TD.
* B. Correct. These are dopamine D2 antagonists (e.g., chlorpromazine, fluphenazine), often used for schizophrenia. Long-term use can lead to irreversible TD.
* C. Incorrect. These actually increase dopamine release, and are associated with addiction or psychosis, not TD.
* D. Incorrect. Like amphetamines, it blocks dopamine reuptake, leading to stimulant effects, but not TD.
Memory Tip:
“TD = Too much Dopamine blockade”
Which of the following is an advantage of the developing nervous system over the adult nervous system?
A. Less sensitivity to toxic insult
B. Faster recovery from toxic insult
C. A tighter blood-brain barrier
D. None of the above
B.
Explanation:
Although the developing nervous system is often more vulnerable to certain toxins, it has:
* Higher plasticity (the ability to rewire itself)
* More regenerative potential due to ongoing growth and remodeling
So if damage does happen, the brain has a better chance of functional recovery.
Option-by-option breakdown:
* A. Incorrect. The developing brain is often more sensitive, not less. The BBB isn’t fully formed, and detox systems are immature.
* B. Correct. Due to neuroplasticity and ongoing development, the young brain can reorganize and recover more easily.
* C. Incorrect. In fact, the BBB is less complete early in development, making the brain more vulnerable to toxicants.
* D. Incorrect. Option B is definitely true.
Memory Tip:
“Developing brains are fragile, but flexible.”
- Peripheral Neuropathy Exceptions
Reworded Question:
Which of the following is not commonly associated with causing peripheral neuropathy?
A. Cyanide
B. Organic mercury
C. Doxorubicin
D. Gold
D.
Explanation:
Peripheral neuropathy = damage to nerves outside the brain/spinal cord, often presenting with weakness, numbness, or tingling.
Let’s go option-by-option:
A. Cyanide
Associated with neurotoxicity, though more centrally than peripherally. It disrupts cellular respiration (cytochrome oxidase inhibition), leading to CNS effects like confusion, seizures, and coma.
But it can also contribute to neuronal injury in general toxic contexts.
B. Organic mercury
Strongly associated with neuropathies, especially methylmercury. It causes axonal degeneration, sensory disturbances, and cerebellar symptoms (ataxia, tremors).
C. Doxorubicin
Known for causing neuropathy. While its most famous toxicity is cardiotoxicity, it can also cause peripheral neuropathy, especially at high doses or with prolonged use.
D. Gold
Incorrect. This is the correct answer to the question.
Used historically for rheumatoid arthritis, gold compounds are more likely to cause dermatologic or renal side effects (like proteinuria) rather than neurotoxicity.
Memory Tip:
“Mercury, cyanide, chemo—yes; gold, not so bold.”
Aminoglycoside antibiotics can cause neurotoxic effects. What is a key manifestation of this toxicity?
A. Hearing loss
B. Visual field defects
C. Cognitive dysfunction
D. Peripheral neuropathy
A.
Explanation:
Aminoglycosides (like gentamicin, tobramycin, amikacin) are potent antibiotics, but they come with a well-known side effect: ototoxicity (ear toxicity).
How this happens:
* They damage the hair cells of the cochlea (causing hearing loss) and the vestibular apparatus (causing balance issues).
* The damage is dose-dependent and can be irreversible.
* Some patients may first notice tinnitus or dizziness, progressing to permanent deafness with continued exposure.
Option-by-option breakdown:
* A. Hearing loss – Correct. Classic and most common sign of aminoglycoside-induced neurotoxicity.
* B. Visual field defects – Incorrect. Not a known toxicity of aminoglycosides.
* C. Cognitive dysfunction – Incorrect. These antibiotics don’t cross the blood-brain barrier easily, and they’re not associated with memory or cognitive issues.
* D. Peripheral neuropathy – Incorrect. That’s more associated with drugs like vincristine, taxanes, or heavy metals (e.g., arsenic, mercury).
Memory Tip:
“Aminoglycosides hit the ears — balance and hearing disappear.”
Reworded Question:
Which toxicant is associated with acute encephalopathy and chronic peripheral neuropathy?
A. Methanol
B. Phenytoin
C. Arsenic
D. 6-Aminonicotinamide
C.
Explanation:
Arsenic exposure shows two phases of neurotoxicity:
1. Acute exposure:
o Causes encephalopathy (confusion, delirium, sometimes seizures)
o Often due to ingestion of high doses (e.g., contaminated water or pesticides)
2. Chronic exposure:
o Leads to peripheral neuropathy — usually symmetrical, sensorimotor, and often painful
o Seen with long-term occupational or environmental exposure
Option-by-option breakdown:
A. Methanol
Incorrect. Methanol causes visual system toxicity (optic nerve damage → blindness), not a classic peripheral neuropathy or encephalopathy combo.
B. Phenytoin
Incorrect. Phenytoin (a seizure medication) can cause cerebellar atrophy or nystagmus with chronic use, but not classic acute encephalopathy plus peripheral neuropathy.
C. Arsenic
Correct. Textbook case: acute CNS effects, followed by delayed-onset peripheral neuropathy if exposure is prolonged.
D. 6-Aminonicotinamide
Incorrect. Rare chemical, causes central demyelination, used in research — not a common environmental or medical exposure.
Memory Tip:
“Arsenic attacks the brain fast, then the nerves slowly.”
Reworded Question:
Which of the following is not associated with encephalopathy?
A. Streptomycin
B. Lead
C. Aluminum
D. Carbon monoxide
A.
Explanation:
Encephalopathy refers to global brain dysfunction, often seen as confusion, disorientation, or coma. Many toxicants can cause this, especially those that affect metabolism, oxygen delivery, or accumulate in brain tissue.
Option-by-option breakdown:
A. Streptomycin
Correct answer — it is not associated with encephalopathy.
* Streptomycin is an aminoglycoside antibiotic.
* Its primary neurotoxic effects are vestibular (balance problems), ototoxicity, and rarely neuromuscular blockade — not CNS dysfunction.
B. Lead
Associated with encephalopathy, especially in children.
* High levels cause cerebral edema, seizures, coma.
* Chronic exposure also causes cognitive impairment and behavioral issues.
C. Aluminum
Associated with encephalopathy.
* Notably seen in dialysis patients (dialysis encephalopathy syndrome) due to aluminum accumulation.
* Symptoms: confusion, speech disturbance, seizures.
D. Carbon monoxide
Classic encephalopathy-causing agent.
* Causes hypoxic injury, especially in globus pallidus and white matter.
* Leads to delayed neuropsychiatric symptoms after acute exposure.
Memory Tip:
“Streptomycin hurts your ears, not your brain.
Which of the following pairs of toxicant and associated toxicity is incorrect?
A. Aluminum – Nystagmus
B. Lead – IQ deficits
C. Inorganic mercury – Tremor
D. Manganese – Parkinson’s-like disease
A.
Explanation of Each Pair:
A. Aluminum – Nystagmus
Incorrect pairing (and correct answer for this question).
* Aluminum toxicity is primarily associated with encephalopathy (especially in dialysis patients), speech issues, and memory deficits.
* Nystagmus is not a known or classic symptom of aluminum exposure.
B. Lead – IQ deficits
Correct pairing.
* Chronic lead exposure, especially in children, causes reduced IQ, attention problems, and behavioral changes due to its effects on CNS development.
C. Inorganic mercury – Tremor
Correct pairing.
* Inorganic mercury causes neurobehavioral changes, tremor, and memory deficits. Tremor is a hallmark of mercury exposure (“mad hatter syndrome”).
D. Manganese – Parkinson’s-like disease
Correct pairing.
* Manganese overexposure (e.g., in welders) leads to manganism, a syndrome resembling Parkinson’s disease, affecting basal ganglia and causing motor deficits.
Memory Tip:
“Aluminum clouds your mind, not your eyes.”
What Is Nystagmus?
Definition:
Nystagmus is an involuntary, rhythmic movement of the eyes, often described as a “shaking” or “bouncing” of the eyeballs. It can go:
* Side to side (horizontal)
* Up and down (vertical)
* In circles (rotary)
________________________________________
What Causes Nystagmus?
It results from problems with the balance (vestibular) system, brainstem, or parts of the inner ear or eyes that help coordinate eye movement.
________________________________________
Common causes include:
* Vestibular damage (e.g., inner ear infections, aminoglycosides)
* Brainstem or cerebellar lesions
* Multiple sclerosis
* Alcohol or drug intoxication
* Congenital (present at birth) in some people
________________________________________
Associated symptoms:
* Dizziness or vertigo
* Balance issues
* Blurred vision when moving
* Nausea (if from vestibular causes)
________________________________________
Example in Toxicology:
* Aminoglycoside antibiotics (like gentamicin) may damage the inner ear, causing nystagmus and balance issues.
Memory Tip:
“Nystagmus = Nervous eye shake.”
All of the following are associated with axonopathies (damage to axons) except:
A. n-Hexane
B. Isoniazid
C. Nitrofurantoin
D. Nicotine
D.
Key Definition:
Axonopathy = a type of peripheral neuropathy where the axon (the long projection of a nerve cell that sends signals) is damaged.
* Leads to distal weakness, numbness, and decreased reflexes
* Commonly caused by toxins, metabolic issues, or drugs
________________________________________
Option Breakdown:
A. n-Hexane
Causes axonopathy.
* Found in solvents and industrial exposure
* Causes distal axonal degeneration, especially of motor neurons
* Leads to muscle weakness, numbness, and sensorimotor neuropathy
B. Isoniazid
Causes axonopathy.
* Anti-tuberculosis drug
* Interferes with vitamin B6 (pyridoxine) metabolism, causing sensory neuropathy
* Prevented with vitamin B6 supplementation
C. Nitrofurantoin
Causes axonopathy.
* Antibiotic for UTIs
* Can cause peripheral neuropathy, especially with chronic use
* Symptoms include tingling, numbness, and pain
D. Nicotine
Incorrect pairing (this is the right answer to the question).
* Nicotine acts on nicotinic acetylcholine receptors in the brain and autonomic ganglia
* Not associated with axon damage or peripheral neuropathy
* Chronic use affects cardiovascular and CNS systems, but not axon integrity
________________________________________
Memory Tip:
“Solvents, antibiotics, and TB drugs can wreck axons — but not smokes.”
Which of the following toxicant–toxicity pairs is incorrect?
A. Metronidazole – Seizures
B. Lithium – Ataxia
C. Colchicine – Blindness
D. Dapsone – Peripheral neuropathy
C.
Explanation of Each Option:
A. Metronidazole – Seizures
Correct Pair
* Metronidazole (Flagyl) is associated with neurotoxicity, especially with high doses or long-term use.
* Can cause seizures, ataxia, peripheral neuropathy, and encephalopathy.
* MRI may show symmetric lesions in the cerebellum or brainstem.
B. Lithium – Ataxia
Correct Pair
* Lithium toxicity (especially when levels are high) causes ataxia (loss of coordination), tremors, confusion, and in severe cases, seizures or coma.
* Ataxia is a hallmark sign of cerebellar involvement.
C. Colchicine – Blindness
Incorrect Pair – This is the correct answer to the question.
* Colchicine toxicity can cause GI symptoms, bone marrow suppression, and peripheral neuropathy, but not blindness.
* No established link between colchicine and vision loss.
D. Dapsone – Peripheral neuropathy
Correct Pair
* Dapsone (used for leprosy and dermatitis herpetiformis) can cause dose-related peripheral neuropathy, especially in chronic use or overdose.
* Can also lead to methemoglobinemia.
________________________________________
Definitions for Key Terms:
* Ataxia = impaired coordination and balance (often cerebellar)
* Peripheral neuropathy = damage to nerves outside the brain/spinal cord, causing numbness or weakness
* Blindness = loss of vision (optic nerve or retinal damage)
* Seizures = uncontrolled electrical activity in the brain causing convulsions or altered consciousness
Memory Tip:
“Colchicine crushes nerves, not vision.”
Which of the following is not associated with myelinopathy (damage to the myelin sheath)?
A. Carbon disulfide – Waltzing syndrome
B. Tri-o-cresyl phosphate – OP-induced delayed neurotoxicity
C. Acrylamide – Peripheral neuropathy
D. Pyridinethione – Used in shampoos
A.
Key Definition:
Myelinopathy = damage to the myelin sheath, the protective covering around axons that helps conduct electrical signals efficiently.
Symptoms often include:
* Weakness
* Loss of coordination
* Slowed nerve conduction velocity
________________________________________
Option Breakdown:
A. Carbon disulfide – Waltzing syndrome
Incorrect pair (correct answer to the question).
* Carbon disulfide is a neurotoxic industrial solvent.
* It causes axonopathy, not myelinopathy.
* “Waltzing syndrome” is an observed motor issue in rodents, but the pathology is primarily axonal.
B. Tri-o-cresyl phosphate (TOCP) – OP-induced delayed neurotoxicity
Myelinopathy.
* TOCP is an organophosphate ester that causes delayed myelin degeneration and spinal cord degeneration.
* Classic cause of organophosphate-induced delayed neuropathy (OPIDN) — leads to paralysis and demyelination.
C. Acrylamide – Peripheral neuropathy
Associated with myelinopathy.
* Acrylamide affects long, large-diameter axons and disrupts axon transport.
* It also leads to myelin degeneration over time in chronic exposures.
D. Pyridinethione – Used in shampoos
Myelinotoxic.
* Found in anti-dandruff shampoos (like zinc pyrithione).
* Animal studies show CNS demyelination, especially in developing brains.
________________________________________
Memory Tip:
“Carbon disulfide cuts axons, not myelin.”
The neurotoxicity of cocaine is mediated by…
A. Blockade of cholinergic receptors
B. Stimulation of muscarinic receptors
C. Alterations in striatal dopamine receptors
D. Stimulation of NMDA receptors
Answer: C. Alterations in striatal dopamine receptors
________________________________________
Explanation of Each Option:
A. Blockade of cholinergic receptors
* Cholinergic receptors respond to acetylcholine, which helps with memory, attention, and muscle control.
* Cocaine does not primarily affect these receptors.
* This mechanism is not responsible for cocaine’s neurotoxicity.
B. Stimulation of muscarinic receptors
* Muscarinic receptors are a subtype of cholinergic receptors found in the brain and organs.
* These are also associated with acetylcholine, and cocaine does not stimulate them.
* This is not how cocaine causes nerve damage.
C. Alterations in striatal dopamine receptors
* Cocaine blocks dopamine reuptake, causing it to build up in brain regions like the striatum, which is involved in movement, motivation, and reward.
* This overactivation causes long-term changes or damage to dopamine receptors, contributing to neurotoxicity.
* This is the main mechanism behind cocaine’s toxic effects on the brain.
D. Stimulation of NMDA receptors
* NMDA receptors are linked to glutamate, a different brain chemical.
* While overstimulation of NMDA receptors can cause other types of brain injury, they are not the primary target of cocaine.
* This is not the correct mechanism here.
________________________________________
Quick Summary to Remember:
Cocaine causes nerve damage mainly by changing how dopamine receptors work in the striatum, not by affecting acetylcholine or glutamate systems.
One cause for hepatic encephalopathy is excessive brain levels of…
A. Ammonia
B. Glucose
C. Free fatty acids
D. Glutathione
Answer: A. Ammonia
________________________________________
Explanation of Each Option:
A. Ammonia
* Ammonia is a waste product normally processed by the liver.
* In liver failure or disease, ammonia builds up in the blood and can cross into the brain.
* High levels of ammonia in the brain interfere with neurotransmitter balance, cause brain swelling, and lead to confusion, sleepiness, and even coma—the hallmarks of hepatic encephalopathy.
* This is the main cause of hepatic encephalopathy.
* Correct.
B. Glucose
* Glucose is the brain’s main energy source, and low glucose (hypoglycemia), not high, is more dangerous.
* While abnormal glucose levels can cause brain symptoms, it’s not the primary cause of hepatic encephalopathy.
* Incorrect.
C. Free fatty acids
* These are fats released from fat stores and used for energy when glucose is low.
* They are not directly toxic to the brain and do not cause hepatic encephalopathy.
* Incorrect.
D. Glutathione
* Glutathione is an antioxidant that helps protect cells from damage.
* It actually helps the liver function and is not harmful when increased.
* Incorrect.
________________________________________
Quick Summary to Remember:
In liver disease, the liver can’t clear ammonia, leading to its buildup in the brain. This causes hepatic encephalopathy, a serious condition marked by confusion and altered brain function.
Correct answer: A. Ammonia
A theory for the neurotoxicity of metronidazole is that its metabolites closely resemble…
A. Niacin
B. Biotin
C. Vitamin B12
D. Thiamine
Answer: D. Thiamine
________________________________________
What is Metronidazole?
Metronidazole is an antibiotic and antiprotozoal drug used to treat infections caused by anaerobic bacteria and certain parasites (like Giardia and Trichomonas). It’s used for infections in the gut, vagina, mouth, and skin.
* It works by damaging the DNA of the bacteria or protozoa.
* Usually safe, but long-term or high-dose use can cause neurotoxicity (brain/nerve problems).
* Symptoms include confusion, ataxia (loss of coordination), and seizures.
________________________________________
Explanation of Each Option:
A. Niacin (Vitamin B3)
* Helps turn food into energy and keeps skin and nerves healthy.
* Not related to metronidazole’s neurotoxic effects.
* Incorrect.
B. Biotin (Vitamin B7)
* Important for metabolism and skin/hair health.
* No known connection to metronidazole toxicity.
* Incorrect.
C. Vitamin B12
* Needed for nerve function and making red blood cells.
* Deficiency causes nerve symptoms, but metronidazole’s structure doesn’t mimic B12.
* Incorrect.
D. Thiamine (Vitamin B1)
* Needed for brain and nerve function.
* One theory suggests metronidazole’s breakdown products look like thiamine, interfering with its use in the brain.
* This may explain its neurotoxic side effects.
* Correct.
________________________________________
Quick Summary to Remember:
Metronidazole = antibiotic for anaerobes and parasites.
Neurotoxicity theory = thiamine mimicry → brain symptoms.
Correct answer: D. Thiamine
Exposure to fluoroacetate can occur through use of…
A. Fluoride toothpaste
B. Freon
C. 5-fluorouracil
D. Halothane
Answer: C. 5-fluorouracil
________________________________________
Explanation of Each Option:
A. Fluoride toothpaste
* Contains fluoride, which helps protect teeth from cavities.
* Fluoride is different from fluoroacetate—they are not the same compound.
* Using fluoride toothpaste does not lead to fluoroacetate exposure.
* Incorrect.
B. Freon
* A chlorofluorocarbon (CFC) used as a refrigerant.
* Contains fluorine atoms, but is chemically unrelated to fluoroacetate.
* Freon exposure does not produce fluoroacetate toxicity.
* Incorrect.
C. 5-fluorouracil (5-FU)
* A chemotherapy drug used to treat cancer.
* One of its metabolic byproducts can resemble or be related to fluoroacetate, contributing to toxicity.
* Although rare, this is the most plausible source of fluoroacetate-related exposure among the choices.
* Correct.
D. Halothane
* An older anesthetic gas once used for surgery.
* Not structurally related to fluoroacetate.
* No known risk of fluoroacetate exposure.
* Incorrect.
________________________________________
Quick Summary to Remember:
Fluoroacetate is a toxic compound that can interfere with energy production in cells by blocking the Krebs cycle.
While not common in everyday products, exposure can theoretically occur with 5-fluorouracil metabolism.
Correct answer: C. 5-fluorouracil
Nicotine receptors are located in all of the following areas except…
A. Ganglia
B. Pancreas
C. Neuromuscular junction
D. CNS
Answer: B. Pancreas
________________________________________
Explanation of Each Option:
A. Ganglia
* Ganglia are clusters of nerve cell bodies in the autonomic nervous system (which controls involuntary body functions like heart rate and digestion).
* Nicotinic receptors are present here and help transmit signals between neurons.
* Correct location for nicotine receptors.
B. Pancreas
* The pancreas produces insulin and digestive enzymes—it’s part of the endocrine and digestive systems.
* It does not use nicotinic receptors for neural signaling.
* This is the correct answer—nicotinic receptors are not found here in the way they are in nervous tissue.
C. Neuromuscular junction
* This is where nerve cells meet muscles to control movement.
* Nicotinic receptors are found here and are crucial for muscle contraction.
* Correct location for nicotine receptors.
D. CNS (Central Nervous System)
* Includes the brain and spinal cord.
* Nicotinic receptors are found in many brain regions and influence mood, attention, and addiction.
* Correct location for nicotine receptors.
________________________________________
Quick Summary to Remember:
Nicotinic receptors are found in the CNS, ganglia, and neuromuscular junction, where they help transmit signals.
They are not located in the pancreas, which is why that’s the exception in this question.
Correct answer: B. Pancreas
Question:
Which of the following agents promotes the formation of microtubules instead of their depolarization?
A. Vincristine
B. Colchicine
C. Vinblastine
D. Paclitaxel
Answer: D. Paclitaxel
⸻
Explanation of Each Option:
A. Vincristine
* Vincristine is a vinca alkaloid that inhibits microtubule formation (polymerization).
* It prevents cells from forming the mitotic spindle needed for division.
* Used in cancer treatment, but causes peripheral neuropathy as a side effect.
* Mechanism = inhibits microtubule assembly.
* Incorrect.
B. Colchicine
* Colchicine is used for gout, and it binds tubulin to prevent microtubule assembly.
* It stops white blood cells from moving and causing inflammation.
* Mechanism = inhibits polymerization of microtubules.
* Incorrect.
C. Vinblastine
* Like vincristine, vinblastine is a vinca alkaloid that prevents microtubule formation.
* It’s more bone marrow-toxic than vincristine but works similarly.
* Mechanism = blocks microtubule assembly.
* Incorrect.
D. Paclitaxel
* Paclitaxel (a taxane) is unique—it stabilizes microtubules, making them unable to break down (depolymerize).
* This leads to mitotic arrest because the cell can’t move past metaphase.
* Used in cancers like breast and ovarian.
* Mechanism = promotes microtubule formation & blocks depolymerization.
* Correct.
⸻
Quick Summary to Remember:
* Vinca alkaloids (vincristine, vinblastine) and colchicine = stop tubulin from forming microtubules.
* Paclitaxel (Taxol) = locks microtubules in place, preventing breakdown.
⸻
Memory Tip:
* **“Vin” = “vanish” microtubules (Vincristine/Vinblastine inhibit formation)
* “Colch” = “collapse” prevention (Colchicine stops assembly, like a collapsed tent)
* “Paclitaxel packs the microtubules” so they can’t break down — it freezes them in place.
Peripheral neuropathies from axonopathies are first to involve…
A. Midline area of the body
B. Dorsal surface of arms and legs
C. Cranial nerves
D. Distal parts of hands and feet
Answer: D. Distal parts of hands and feet
⸻
Explanation of Each Option:
A. Midline area of the body
* The midline (like the spine or chest) is not commonly affected first in axonal neuropathies.
* These areas have shorter nerve fibers, which are usually spared early.
* Incorrect.
B. Dorsal surface of arms and legs
* “Dorsal” refers to the back sides of limbs, but axonopathies don’t target specific surfaces.
* Again, this isn’t the typical early pattern of damage.
* Incorrect.
C. Cranial nerves
* Cranial nerves control the face, eyes, and mouth and tend to be spared early in peripheral axonopathies.
* These nerves have shorter axons.
* Incorrect.
D. Distal parts of hands and feet
* These areas are the farthest away from the spinal cord and have the longest axons, making them the most vulnerable to damage.
* This is known as a “length-dependent pattern”, where the longest nerves are affected first.
* This is why symptoms like numbness or tingling usually begin in the toes and fingers.
* Correct.
⸻
Quick Summary to Remember:
Axonopathies (damage to nerve fibers) usually affect the longest nerves first, which are in the distal (far) parts of the hands and feet.
Correct answer: D. Distal parts of hands and feet
MPP⁺ is transported into the CNS by the same system that transports…
A. Glucose
B. Amino acids
C. Dopamine
D. Free fatty acids
Answer: C. Dopamine
⸻
Explanation of Each Option:
A. Glucose
* Glucose uses a glucose transporter (GLUT) to enter the brain.
* MPP⁺ (a toxic compound) does not use this pathway.
* Incorrect.
B. Amino acids
* Amino acids have their own specific amino acid transporters in the blood-brain barrier.
* MPP⁺ is not transported through this system.
* Incorrect.
C. Dopamine
* Dopamine is taken up into neurons via the dopamine transporter (DAT).
* MPP⁺ mimics dopamine and is mistakenly taken up by DAT into dopaminergic neurons.
* Once inside, MPP⁺ causes mitochondrial damage, especially in areas like the substantia nigra, leading to Parkinson-like symptoms.
* Correct.
D. Free fatty acids
* Transported by passive diffusion or fatty acid transport proteins.
* MPP⁺ does not use these routes.
* Incorrect.
⸻
Quick Summary to Remember:
MPP⁺ is a neurotoxin that mimics dopamine and uses the dopamine transporter (DAT) to enter the brain. Once inside, it damages mitochondria in dopamine neurons, causing symptoms like Parkinson’s disease.
Correct answer: C. Dopamine
Question:
Chinese restaurant syndrome is thought to be due to consumption of excessive amounts of…
A. Tyramine
B. Glycine
C. Tyrosine
D. Glutamate
Answer: D. Glutamate
⸻
Explanation of Each Option:
A. Tyramine
* Found in aged and fermented foods (like cheese and wine).
* Can raise blood pressure, especially in people taking MAO inhibitors.
* Not related to Chinese restaurant syndrome.
* Incorrect.
B. Glycine
* An inhibitory neurotransmitter in the central nervous system.
* Not associated with food-related symptoms like those in Chinese restaurant syndrome.
* Incorrect.
C. Tyrosine
* An amino acid used to make neurotransmitters like dopamine.
* Also not linked to the symptoms of Chinese restaurant syndrome.
* Incorrect.
D. Glutamate
* A major excitatory neurotransmitter in the brain.
* The flavor enhancer monosodium glutamate (MSG) contains glutamate.
* High intake has been associated (though not conclusively) with headache, flushing, and chest tightness, often referred to as “Chinese restaurant syndrome.”
* Correct.
⸻
Quick Summary to Remember:
Chinese restaurant syndrome refers to a group of symptoms (like flushing and headache) some people report after eating food with a lot of MSG, which contains glutamate.
Correct answer: D. Glutamate
The mechanism of neurotoxicity for hexachlorophene is…
A. Depletion of CNS dopamine
B. Wallerian degeneration
C. Axonopathy
D. Intramyelinic edema
Answer: D. Intramyelinic edema
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Explanation of Each Option:
A. Depletion of CNS dopamine
* This is seen with toxins like MPP⁺, which damage dopamine-producing neurons.
* Hexachlorophene does not work by depleting dopamine.
* Incorrect.
B. Wallerian degeneration
* A type of nerve injury where the axon distal to the injury site breaks down.
* This occurs with physical trauma or axonal severing, not with hexachlorophene.
* Incorrect.
C. Axonopathy
* General term for damage to the axon, often from toxins like acrylamide or n-hexane.
* Hexachlorophene primarily targets myelin, not the axon.
* Incorrect.
D. Intramyelinic edema
* This is swelling within the layers of the myelin sheath.
* Hexachlorophene disrupts the structure of myelin, causing fluid to accumulate between layers (intramyelinic spaces).
* It leads to spongy degeneration of the brain and is especially harmful to the white matter.
* Correct.
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Quick Summary to Remember:
Hexachlorophene causes neurotoxicity by swelling the myelin sheaths, not by damaging axons or depleting dopamine.
This swelling is called intramyelinic edema.
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Memory Tip:
* Think “Hexachlorophene = Hydraulic swelling” — it puffs up the myelin like a sponge with water.
* “Hexa = Myelin Swell-a” to remember it causes intramyelinic edema.
All of the following are true regarding HIV-associated dementia except…
A. Cocaine causes a synergistic neurotoxicity
B. It can be attenuated by beta-estradiol
C. Amphetamine causes a synergistic neurotoxicity
D. Cigarette use causes a synergistic neurotoxicity
Answer: D. Cigarette use causes a synergistic neurotoxicity
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Explanation of Each Option:
A. Cocaine causes a synergistic neurotoxicity
* True. Cocaine increases oxidative stress and inflammation in the brain, worsening the damage caused by HIV.
* The two together create greater neurotoxicity than either alone (synergistic effect).
* Correct statement.
B. It can be attenuated by beta-estradiol
* True. Estrogen compounds like beta-estradiol have neuroprotective effects.
* They may reduce damage by stabilizing the blood-brain barrier and reducing oxidative stress in HIV-associated dementia.
* Correct statement.
C. Amphetamine causes a synergistic neurotoxicity
* True. Like cocaine, amphetamines amplify neuroinflammation and dopaminergic damage, especially when combined with HIV.
* Leads to greater brain injury and cognitive decline.
* Correct statement.
D. Cigarette use causes a synergistic neurotoxicity
* False. While smoking is harmful overall, there is no clear evidence that it synergistically worsens HIV-associated neurotoxicity in the same way that cocaine or amphetamines do.
* It is not linked directly to worsened HIV-associated dementia in this context.
* Incorrect statement – this is the right answer for “except.”
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Quick Summary to Remember:
* Cocaine + HIV = more brain damage
* Amphetamines + HIV = same
* Estrogen can protect the brain
* Smoking = not shown to worsen HIV dementia directly
Correct answer: D. Cigarette use causes a synergistic neurotoxicity
