Disorders of lipid metabolism US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Disorders of lipid metabolism. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Disorders of lipid metabolism US Medical PG Question 1: An 8-year-old boy presents to his primary care pediatrician for routine check-up. During the visit, his mom says that she has noticed yellow bumps on his eyelids and was concerned about whether they were a problem. Upon hearing this concern, the physician inquires about parental health history and learns that both parents have high cholesterol despite adhering to a statin regimen. Furthermore, other family members have suffered early myocardial infarctions in their 30s. Physical exam reveals flat yellow patches on the patient's eyelids bilaterally as well as hard yellow bumps around the patient's ankles. Based on clinical suspicion an LDL level is obtained and shows a level of 300 mg/dL. What protein is most likely defective in this patient causing these findings?
- A. Apoprotein B48
- B. Lipoprotein lipase
- C. LDL receptor (Correct Answer)
- D. VLDL receptor
- E. Apoprotein E
Disorders of lipid metabolism Explanation: ***LDL receptor***
- The patient's presentation with **xanthomas** (yellow bumps on eyelids and ankles), a very high **LDL level (300 mg/dL)**, and a strong family history of **early myocardial infarctions** and hypercholesterolemia in both parents is characteristic of **familial hypercholesterolemia**.
- Familial hypercholesterolemia is most commonly caused by a defective or deficient **LDL receptor**, which impairs the uptake of LDL from the blood, leading to significantly elevated LDL levels.
*Apoprotein B48*
- **Apoprotein B48** is primarily found on **chylomicrons** and is essential for their formation and secretion from the intestines.
- A defect in apoB48 would lead to **abetalipoproteinemia**, characterized by very low levels of chylomicrons, VLDL, and LDL, and would present with fat malabsorption and neurological symptoms, which is inconsistent with this patient's findings.
*Lipoprotein lipase*
- **Lipoprotein lipase (LPL)** is an enzyme responsible for hydrolyzing triglycerides in circulating **chylomicrons** and **VLDLs**.
- A deficiency in LPL would cause severe **hypertriglyceridemia** and the accumulation of chylomicrons, leading to eruptive xanthomas and pancreatitis, rather than isolated high LDL and tendinous xanthomas.
*VLDL receptor*
- The **VLDL receptor** is involved in the clearance of VLDL remnants and chylomicrons, especially in peripheral tissues.
- While it plays a role in lipid metabolism, its primary role in familial hypercholesterolemia, which is characterized by profoundly elevated LDL, is less significant than the **LDL receptor**.
*Apoprotein E*
- **Apoprotein E** is crucial for the uptake of **chylomicron remnants** and **VLDL remnants** by the liver.
- Defects in apoE are associated with **Type III hyperlipoproteinemia (familial dysbetalipoproteinemia)**, characterized by elevated levels of chylomicron and VLDL remnants, and typically presents with palmar xanthomas and tuberous xanthomas, which is different from the presentation here.
Disorders of lipid metabolism US Medical PG Question 2: An 18-month-old boy of Ashkenazi-Jewish descent presents with loss of developmental milestones. On ocular exam, a cherry-red macular spot is observed. No hepatomegaly is observed on physical exam. Microscopic exam shows lysosomes with onion-skin appearance.
What is the most likely underlying biochemical abnormality?
- A. Accumulation of ceramide trihexoside
- B. Accumulation of glucocerebroside
- C. Accumulation of galactocerebroside
- D. Accumulation of sphingomyelin
- E. Accumulation of GM2 ganglioside (Correct Answer)
Disorders of lipid metabolism Explanation: ***Accumulation of GM2 ganglioside***
- This constellation of symptoms—**loss of developmental milestones**, **cherry-red macular spot**, absence of hepatomegaly, and **lysosomes with onion-skin appearance** in an individual of **Ashkenazi-Jewish descent**—is classic for **Tay-Sachs disease**.
- **Tay-Sachs disease** is caused by a deficiency of **hexosaminidase A**, leading to the accumulation of **GM2 ganglioside** in neuronal lysosomes.
*Accumulation of ceramide trihexoside*
- This refers to **Fabry disease**, which is an **X-linked disorder** presenting in adolescence or adulthood with acroparesthesias, angiokeratomas, and renal/cardiac complications.
- While it involves a lysosomal storage, its clinical presentation and the absence of a cherry-red spot differentiate it from the case described.
*Accumulation of glucocerebroside*
- This is characteristic of **Gaucher disease**, which is caused by a deficiency in **glucocerebrosidase**.
- Key features include **hepatosplenomegaly**, bone pain, and pancytopenia, which are not consistent with the patient's presentation.
*Accumulation of galactocerebroside*
- This describes **Krabbe disease**, a **globoid cell leukodystrophy** caused by a deficiency in galactocerebrosidase.
- Krabbe disease primarily affects the **myelin sheath** in the nervous system, leading to neurological degeneration but typically does not present with a cherry-red macular spot.
*Accumulation of sphingomyelin*
- This is the hallmark of **Niemann-Pick disease**, caused by **sphingomyelinase deficiency**.
- While Niemann-Pick disease also presents with a **cherry-red macular spot** and neurodegeneration, it is classically associated with **hepatosplenomegaly**, which is explicitly stated to be absent in this patient.
Disorders of lipid metabolism US Medical PG Question 3: A 33-year-old man presents with his recent laboratory results. He has no symptoms currently, but he underwent a medical evaluation as a requirement for taking up a new job. His medical history is not significant. His laboratory reports are as follows:
Blood hemoglobin 13.7 g/dL
Leukocyte count 8,000/mm3
Platelet count 350,000/mm3
Serum creatinine 0.8 mg/dL
Serum alanine aminotransferase 16 U/L
Serum aspartate aminotransferase 14 U/L
Serum cholesterol 450 mg/dL
Serum triglyceride 790 mg/dL
Serum LDL cholesterol 150 mg/dL
Serum HDL cholesterol 55 mg/dL
Which of the following findings is most likely to be present on physical examination of this patient?
- A. Eruptive xanthomas over back
- B. Xanthelasma
- C. Palmar xanthomas in flexor creases (Correct Answer)
- D. Achilles tendon xanthoma
- E. Metacarpophalangeal extensor tendon xanthoma
Disorders of lipid metabolism Explanation: ***Palmar xanthomas in flexor creases***
- This patient presents with significantly elevated **triglycerides (790 mg/dL)** and **total cholesterol (450 mg/dL)** with relatively normal **LDL (150 mg/dL)** and **HDL (55 mg/dL)**.
- This lipid profile pattern—**combined elevation of cholesterol and triglycerides with disproportionately normal/low LDL**—is characteristic of **familial dysbetalipoproteinemia (Type III hyperlipoproteinemia)**.
- **Palmar xanthomas** appearing in the palmar creases are **pathognomonic** for Type III hyperlipoproteinemia, caused by accumulation of chylomicron and VLDL remnants due to defective apolipoprotein E.
- While uncommon even in Type III, palmar xanthomas are the most specific physical finding for this diagnosis.
*Eruptive xanthomas over back*
- **Eruptive xanthomas** typically occur with **very high triglycerides (>1000 mg/dL)**, presenting as sudden crops of small, yellowish-red papules with erythematous halos.
- This patient's triglycerides at 790 mg/dL are elevated but below the threshold that typically produces eruptive xanthomas.
- Eruptive xanthomas are more commonly seen in **Type I or Type V hyperlipoproteinemia** with severe hypertriglyceridemia.
*Xanthelasma*
- **Xanthelasma** are yellowish plaques on the eyelids, the most common type of xanthoma overall.
- Can occur with **any lipid disorder** or even with normal lipid levels in some cases.
- While possible in this patient, xanthelasma lack the diagnostic specificity of palmar xanthomas for Type III hyperlipoproteinemia.
*Achilles tendon xanthoma*
- **Achilles tendon xanthomas** are characteristic of **familial hypercholesterolemia (Type IIa)**, which features markedly elevated **LDL cholesterol (typically >190 mg/dL)** due to defective LDL receptors.
- This patient's LDL is only 150 mg/dL, making familial hypercholesterolemia unlikely.
- The combined cholesterol and triglyceride elevation points away from pure LDL elevation.
*Metacarpophalangeal extensor tendon xanthoma*
- **Tendon xanthomas** on the extensor tendons are also associated with **familial hypercholesterolemia (Type IIa)**.
- Like Achilles tendon xanthomas, these require very high **LDL cholesterol**, which is not the primary abnormality here.
- The patient's lipid profile does not support this diagnosis.
Disorders of lipid metabolism US Medical PG Question 4: A 57-year-old man presents for a regular check-up. He does not have any complaints at the time of presentation. He has a history of several episodes of acute non-necrotizing pancreatitis with the last episode being 2 years ago. Also, he was diagnosed with hypertension 5 years ago. Currently, he takes aspirin, atorvastatin, enalapril, and indapamide. He plays tennis twice a week, does low impact cardio workouts 3 times a week, and follows a low-fat diet. He smokes half a pack of cigarettes per day and refuses to quit smoking. The patient’s blood pressure is 140/85 mm Hg, heart rate is 88/min, respiratory rate is 14/min, and temperature is 36.6°C (97.9°F). His height is 181 cm (5 ft 11 in), weight is 99 kg (218 lb), and BMI is 30.8 kg/m2. Physical examination reveals multiple xanthomas on the patient’s trunk, elbows, and knees. Heart sounds are diminished with fixed splitting of S2 and an increased aortic component. The rest of the examination is unremarkable. The patient’s lipid profile shows the following results:
Total serum cholesterol 235.9 mg/dL
HDL 46.4 mg/dL
LDL 166.3 mg/dL
Triglycerides 600 mg/dL
Glucose 99 mg/dL
Which of the following modifications should be made to the patient’s therapy?
- A. Add aprotinin
- B. Add simvastatin
- C. Add metformin
- D. Add fenofibrate (Correct Answer)
- E. Increase atorvastatin dosage
Disorders of lipid metabolism Explanation: ***Add fenofibrate***
- The patient presents with significantly elevated **triglycerides (600 mg/dL)**, multiple episodes of **acute non-necrotizing pancreatitis**, and **eruptive xanthomas**, which are all indicative of severe hypertriglyceridemia.
- **Fibrates, such as fenofibrate**, are the most effective class of drugs for lowering very high triglyceride levels and reducing the risk of pancreatitis.
*Add aprotinin*
- **Aprotinin** is an antifibrinolytic agent that is no longer used due to safety concerns and is not indicated for the management of hypertriglyceridemia or pancreatitis prevention.
- Its primary use was in reducing blood loss during complex surgeries, specifically cardiac surgery.
*Add simvastatin*
- **Simvastatin** is a statin, and while statins are effective in reducing LDL cholesterol, they have a limited effect on significantly elevated triglycerides.
- The patient is already on atorvastatin, and adding a second statin would not be the primary approach for managing severe hypertriglyceridemia, nor would it provide substantial additional triglyceride-lowering effects compared to a fibrate.
*Add metformin*
- **Metformin** is an oral antihyperglycemic agent used to treat type 2 diabetes by improving insulin sensitivity and reducing hepatic glucose production.
- The patient's **glucose level is normal (99 mg/dL)**, and there is no indication of diabetes or pre-diabetes, making metformin inappropriate.
*Increase atorvastatin dosage*
- While atorvastatin can lower triglycerides to some extent, it is primarily used for LDL-C reduction. Increasing the dosage would not be as effective as a fibrate in addressing the severe **hypertriglyceridemia (600 mg/dL)** and the associated risk of pancreatitis.
- The most significant concern for this patient is the high triglyceride level and the history of pancreatitis, which requires a more targeted therapy beyond increased statin dosage.
Disorders of lipid metabolism US Medical PG Question 5: A 60-year-old patient is at his physician’s office for a routine health maintenance exam. The patient has a past medical history of osteoarthritis in his right knee and GERD that is well-controlled with over the counter medication. On a fasting lipid profile, he is found to have high cholesterol. The patient is started on daily atorvastatin to reduce his risk of cardiovascular disease. What is the major apolipoprotein found on the lipoprotein most directly affected by his statin medication?
- A. Apolipoprotein C-II
- B. Apolipoprotein B-100 (Correct Answer)
- C. Apolipoprotein A-I
- D. Apolipoprotein B-48
- E. Apolipoprotein E
Disorders of lipid metabolism Explanation: ***Apolipoprotein B-100***
- Statins primarily reduce **LDL-C** levels by inhibiting **HMG-CoA reductase**, leading to increased LDL receptor expression and clearance of LDL particles from the blood.
- **Apolipoprotein B-100** is the main apolipoprotein found on **LDL** and is crucial for its binding to the LDL receptor.
*Apolipoprotein C-II*
- This apolipoprotein activates **lipoprotein lipase**, which is involved in the hydrolysis of triglycerides in **chylomicrons** and **VLDL**, not directly targeted by statins.
- While statins can indirectly affect VLDL, ApoC-II is not the major apolipoprotein of the lipoprotein most directly affected by statins.
*Apolipoprotein A-I*
- **Apolipoprotein A-I** is the primary apolipoprotein found on **HDL**, which is involved in **reverse cholesterol transport**.
- While statins can have a modest effect on increasing HDL, their primary action is on reducing LDL.
*Apolipoprotein B-48*
- **Apolipoprotein B-48** is found exclusively on **chylomicrons**, which are responsible for the transport of exogenous dietary fats from the intestines.
- Chylomicrons are not the primary target of statin therapy, which focuses on endogenous cholesterol metabolism.
*Apolipoprotein E*
- **Apolipoprotein E** is found on chylomicrons, VLDL, and HDL and plays a role in receptor binding for their clearance from circulation.
- While important for lipoprotein metabolism, it is not the *major* apolipoprotein of the lipoprotein most *directly* affected by statins (LDL).
Disorders of lipid metabolism US Medical PG Question 6: A 35-year-old man comes to the physician because of fatigue and generalized weakness for the past year. He has noticed he has been having fewer bowel movements. He has had pain with defecation and small amounts of blood when wiping. He has not lost weight despite increased efforts to diet and exercise. He has had no fever, throat pain, or difficulty swallowing. His temperature is 36.5°C (97.7°F), pulse is 50/min, blood pressure is 120/90 mm Hg, and BMI is 35 kg/m2. Physical examination shows dry skin and a distended abdomen. There is 1+ pitting edema in the lower extremities. On neurological examination, deep tendon reflexes are 1+. Further evaluation of this patient is most likely to show which of the following findings?
- A. Hyperglycemia
- B. Decreased serum creatinine
- C. Elevated serum low-density lipoprotein (Correct Answer)
- D. Decreased plasma homocysteine concentrations
- E. Decreased serum creatine kinase
Disorders of lipid metabolism Explanation: ***Elevated serum low-density lipoprotein***
- The patient's symptoms (fatigue, generalized weakness, constipation, weight gain despite efforts, cold intolerance implied by dry skin, bradycardia, and edema) are highly suggestive of **hypothyroidism**.
- **Hypothyroidism** classically leads to **hyperlipidemia**, specifically elevated **LDL cholesterol**, due to decreased catabolism of cholesterol.
*Decreased serum creatine kinase*
- **Hypothyroidism** typically causes **myopathy**, which can manifest as elevated, not decreased, serum **creatine kinase** levels.
- Muscle weakness and fatigue in hypothyroidism are often associated with muscle damage and elevated CK.
*Hyperglycemia*
- While hypothyroidism can impact glucose metabolism, it more commonly leads to **insulin resistance** and can contribute to **hyperglycemia**, but it is not a direct or consistent consequence, and other factors are often more significant.
- However, hypothyroidism is not primarily characterized by hyperglycemia as a direct pathognomonic finding.
*Decreased serum creatinine*
- **Hypothyroidism** is typically associated with **decreased glomerular filtration rate (GFR)**, which can lead to **increased serum creatinine**, not decreased.
- A decreased GFR would imply reduced clearance of creatinine, thus elevating its serum concentration.
*Decreased plasma homocysteine concentrations*
- **Hypothyroidism** is linked to **elevated plasma homocysteine** concentrations, likely due to impaired metabolism (e.g., reduced activity of methionine synthase).
- High homocysteine levels are a risk factor for cardiovascular disease.
Disorders of lipid metabolism US Medical PG Question 7: A 12-year-old boy is brought to the physician because of difficulty in walking for 5 months. His mother reports that he has trouble keeping his balance and walking without support. Over the past year, he has started to have difficulty seeing in the dark and his hearing has been impaired. Examination shows marked scaling of the skin on the face and feet and a shortened 4th toe. Muscle strength is 3/5 in the lower extremities and 4/5 in the upper extremities. Sensation to pinprick is symmetrically decreased over the legs. Fundoscopy shows peripheral pigment deposits and retinal atrophy. His serum phytanic acid concentration is markedly elevated. The patient's condition is most likely caused by a defect in which of the following cellular structures?
- A. Proteasomes
- B. Peroxisomes (Correct Answer)
- C. Smooth endoplasmic reticulum
- D. Mitochondria
- E. Myofilaments
Disorders of lipid metabolism Explanation: ***Peroxisomes***
- The constellation of symptoms including **difficulty walking and maintaining balance**, **impaired night vision and hearing**, **scaling skin**, **distal muscle weakness**, **ataxia**, **peripheral neuropathy**, **pigmentary retinopathy**, and **markedly elevated serum phytanic acid** is characteristic of **Refsum disease**.
- **Refsum disease** is an autosomal recessive disorder caused by a defect in **peroxisomal alpha-oxidation** (specifically phytanoyl-CoA hydroxylase deficiency), leading to the accumulation of phytanic acid in tissues.
- Phytanic acid is a branched-chain fatty acid derived from dietary sources (dairy products, ruminant fats) that cannot undergo beta-oxidation and requires alpha-oxidation in peroxisomes.
*Proteasomes*
- **Proteasomes** are responsible for the degradation of ubiquitinated proteins, important for cellular protein homeostasis.
- Defects in proteasomes are associated with various conditions like **neurodegenerative diseases** (e.g., Parkinson's), but not with the specific symptoms of phytanic acid accumulation.
*Smooth endoplasmic reticulum*
- The **smooth endoplasmic reticulum** is involved in **lipid synthesis**, detoxification, and calcium storage.
- While lipid metabolism is affected in Refsum disease, the primary defect is in the degradation of branched-chain fatty acids like phytanic acid, which occurs in **peroxisomes**, not the smooth ER.
*Mitochondria*
- **Mitochondria** are the primary sites of **ATP production** through oxidative phosphorylation and are involved in fatty acid beta-oxidation.
- While some metabolic disorders affect mitochondria, **phytanic acid accumulation** specifically points to a peroxisomal defect because phytanic acid cannot undergo beta-oxidation due to its 3-methyl branch and requires alpha-oxidation, which is a peroxisomal process.
*Myofilaments*
- **Myofilaments** (actin and myosin) are the contractile proteins within muscle cells.
- While muscle weakness is a symptom, the underlying cause is not a primary defect in myofilaments themselves, but rather the **neurological and systemic effects** of phytanic acid accumulation affecting peripheral nerves and muscle innervation.
Disorders of lipid metabolism US Medical PG Question 8: Steroid hormone synthesis, lipid synthesis, and chemical detoxification are activities of which of the following?
- A. Peroxisomes
- B. Nucleolus
- C. Rough Endoplasmic Reticulum
- D. Smooth Endoplasmic Reticulum (Correct Answer)
- E. Golgi bodies
Disorders of lipid metabolism Explanation: ***Smooth Endoplasmic Reticulum***
- The **smooth endoplasmic reticulum (SER)** is rich in enzymes that catalyze the synthesis of **lipids**, including steroid hormones, and is crucial for the detoxification of drugs and poisons, particularly in liver cells.
- Its tubular structure, devoid of ribosomes, differentiates its functions from the rough ER, focusing on metabolic processes like **calcium ion storage** and carbohydrate metabolism.
*Peroxisomes*
- Peroxisomes are primarily involved in the breakdown of **fatty acids** and amino acids, producing hydrogen peroxide as a byproduct.
- They also play a role in detoxification but are not the primary site for steroid hormone or general lipid synthesis.
*Nucleolus*
- The **nucleolus** is a dense structure within the nucleus responsible for synthesizing **ribosomal RNA (rRNA)** and assembling ribosomes.
- It has no direct role in steroid hormone synthesis, lipid metabolism, or chemical detoxification.
*Rough Endoplasmic Reticulum*
- The **rough endoplasmic reticulum (RER)** is studded with **ribosomes** and is primarily involved in the synthesis and modification of **proteins** destined for secretion or insertion into membranes.
- While it's part of the endomembrane system, it does not directly perform lipid synthesis or chemical detoxification as its main functions.
*Golgi bodies*
- **Golgi bodies (or Golgi apparatus)** are responsible for modifying, sorting, and packaging **proteins and lipids** synthesized in the ER into vesicles for secretion or delivery to other organelles.
- They do not perform the initial synthesis of steroid hormones or lipids, nor are they the primary site for chemical detoxification.
Disorders of lipid metabolism US Medical PG Question 9: A 24-year-old man presents for an annual check-up. He is a bodybuilder and tells you he is on a protein-rich diet that only allows for minimal carbohydrate intake. His friend suggests he try exogenous glucagon to help him lose some excess weight before an upcoming competition. Which of the following effects of glucagon is he attempting to exploit?
- A. Increased glucose utilization by tissues
- B. Decreased blood cholesterol level
- C. Increased hepatic gluconeogenesis
- D. Increased lipolysis in adipose tissues (Correct Answer)
- E. Increased hepatic glycogenolysis
Disorders of lipid metabolism Explanation: ***Increased lipolysis in adipose tissues***
- While **glucagon's primary target is the liver**, it can have **modest lipolytic effects** on adipose tissue by opposing insulin's anti-lipolytic actions.
- Glucagon stimulates cAMP production, which can activate **hormone-sensitive lipase** to break down triglycerides into **fatty acids** and **glycerol**.
- However, **catecholamines (epinephrine/norepinephrine)** are far more potent direct stimulators of adipose tissue lipolysis than glucagon.
- The friend is attempting to exploit this lipolytic effect for fat loss, though **exogenous glucagon is not an evidence-based or safe weight-loss strategy**.
*Increased glucose utilization by tissues*
- This is **opposite** to glucagon's actual effect. **Glucagon raises blood glucose** levels; it does not promote glucose uptake by peripheral tissues.
- **Insulin** is the hormone responsible for promoting glucose uptake and utilization by muscle, adipose, and other tissues.
*Decreased blood cholesterol level*
- Glucagon does not have a direct, clinically significant effect on reducing blood cholesterol levels.
- While glucagon affects overall lipid metabolism through its catabolic actions, it is not used therapeutically for hypercholesterolemia.
*Increased hepatic gluconeogenesis*
- **Glucagon strongly stimulates hepatic gluconeogenesis**, which is the synthesis of glucose from non-carbohydrate precursors (amino acids, lactate, glycerol) in the liver.
- This action **raises blood glucose** levels and would not directly contribute to fat loss or weight reduction.
- In the context of a low-carbohydrate diet, increased gluconeogenesis would maintain blood glucose but not promote the fat loss the bodybuilder seeks.
*Increased hepatic glycogenolysis*
- **Glucagon is a potent stimulator of hepatic glycogenolysis**, the breakdown of stored liver glycogen into glucose.
- This rapidly increases blood glucose levels during fasting or hypoglycemia.
- However, this does not directly target adipose tissue for fat loss; it mobilizes glucose stores rather than fat stores, so it's not the mechanism relevant to weight loss goals.
Disorders of lipid metabolism US Medical PG Question 10: You are a resident on an anesthesiology service and are considering using nitrous oxide to assist in placing a laryngeal mask airway (LMA) in your patient, who is about to undergo a minor surgical procedure. You remember that nitrous oxide has a very high minimal alveolar concentration (MAC) compared to other anesthetics. This means that nitrous oxide has:
- A. no effect on lipid solubility or potency
- B. decreased lipid solubility and decreased potency (Correct Answer)
- C. decreased lipid solubility and increased potency
- D. increased lipid solubility and increased potency
- E. increased lipid solubility and decreased potency
Disorders of lipid metabolism Explanation: ***Decreased lipid solubility and decreased potency***
- A **very high MAC** indicates that a large concentration of the anesthetic agent is required to produce immobility in 50% of patients, signifying **low potency**.
- According to the **Meyer-Overton rule**, anesthetic potency is directly correlated with lipid solubility; therefore, low potency implies **decreased lipid solubility**.
*No effect on lipid solubility or potency*
- This statement is incorrect as MAC is a direct measure of potency, and potency is linked to lipid solubility by the **Meyer-Overton rule**.
- A high MAC unequivocally indicates **low potency**, and indirectly, low lipid solubility.
*Decreased lipid solubility and increased potency*
- This is incorrect because **increased potency** would be associated with a **low MAC**.
- Potency and lipid solubility are positively correlated, so decreased lipid solubility would lead to **decreased potency**.
*Increased lipid solubility and increased potency*
- This is incorrect; while **increased lipid solubility** is associated with **increased potency**, increased potency would manifest as a **low MAC**, not a high one.
- The given information states a **very high MAC**, which signifies low potency.
*Increased lipid solubility and decreased potency*
- This statement contradicts the **Meyer-Overton rule**, which establishes a direct relationship between lipid solubility and anesthetic potency.
- Therefore, **increased lipid solubility** should correspond to **increased potency**, not decreased potency.
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