1. Insulin suppresses hepatic gluconeogenesis in part by altering the activity of a transcription factor downstream of Akt. Which mechanism mediates this suppression of gluconeogenic gene expression?
A) Akt phosphorylates and activates the gluconeogenic transcription factor, increasing transcription of phosphoenolpyruvate carboxykinase
B) Akt activates the MAPK (mitogen-activated protein kinase) arm, which directly transcribes gluconeogenic genes in the nucleus
C) Akt phosphorylates Foxo1 (forkhead box protein O1), causing its nuclear exclusion and thereby suppressing transcription of gluconeogenic enzymes
D) Akt opens nuclear pores to admit glucose, which allosterically silences gluconeogenic promoters
E) Akt phosphorylates GLUT4 (glucose transporter type 4), which then translocates to the nucleus to repress gluconeogenic genes
ANSWER: C
Rationale:
Insulin-activated Akt phosphorylates Foxo1 (forkhead box protein O1), promoting its nuclear exclusion; because Foxo1 normally drives transcription of gluconeogenic enzymes, removing it from the nucleus suppresses gluconeogenic gene expression and helps lower hepatic glucose output.
Option A: Option A is incorrect because Akt phosphorylation inactivates Foxo1 by excluding it from the nucleus rather than activating a transcription factor to increase gluconeogenesis; the direction is inverted.
Option B: Option B is incorrect because the MAPK arm mediates mitogenic and growth effects and does not transcribe gluconeogenic genes to lower glucose.
Option D: Option D is incorrect because glucose does not enter the nucleus to silence promoters; suppression is achieved through Foxo1 phosphorylation.
Option E: Option E is incorrect because GLUT4 is a plasma-membrane glucose transporter that does not translocate to the nucleus or regulate gene transcription.
2. Beyond increasing glucose uptake, insulin suppresses lipolysis in adipose tissue. Which mechanism best describes how Akt produces this antilipolytic effect?
A) Akt phosphorylates and inhibits HSL (hormone-sensitive lipase) and inactivates PDE3B (phosphodiesterase 3B), lowering the lipolytic drive and suppressing free fatty acid release
B) Akt activates HSL (hormone-sensitive lipase) directly, increasing triglyceride breakdown and free fatty acid release
C) Akt raises intracellular cAMP (cyclic adenosine monophosphate) in adipocytes, stimulating lipolysis
D) Akt promotes GLUT4 (glucose transporter type 4) translocation, which is the mechanism by which insulin suppresses lipolysis
E) Akt phosphorylates Foxo1 (forkhead box protein O1) in adipocytes, and this nuclear exclusion is the direct cause of reduced lipolysis
ANSWER: A
Rationale:
In adipose tissue, Akt phosphorylates and inactivates PDE3B (phosphodiesterase 3B) and directly phosphorylates and inhibits HSL (hormone-sensitive lipase), suppressing lipolysis and reducing free fatty acid release; this is the antilipolytic arm of insulin action, distinct from glucose transport.
Option B: Option B is incorrect because Akt inhibits rather than activates HSL, so it decreases triglyceride breakdown.
Option C: Option C is incorrect because Akt lowers cAMP by activating PDE3B; raising cAMP would promote lipolysis, the opposite effect.
Option D: Option D is incorrect because GLUT4 translocation mediates glucose uptake, not the suppression of lipolysis, so it conflates two separate effects.
Option E: Option E is incorrect because Foxo1 phosphorylation governs hepatic gluconeogenic gene expression rather than serving as the direct mechanism of reduced adipocyte lipolysis.
3. Insulin promotes hepatic glycogen synthesis through an Akt-dependent action on a specific kinase. Which mechanism correctly describes how insulin stimulates glycogen synthesis?
A) Akt activates glycogen synthase kinase 3 (GSK-3), which then directly builds glycogen chains
B) Akt phosphorylates glycogen phosphorylase, stimulating glycogen breakdown into glucose
C) Akt activates the gluconeogenic transcription factor Foxo1 (forkhead box protein O1) to drive glycogen storage
D) Akt phosphorylates and inactivates glycogen synthase kinase 3 (GSK-3), relieving its inhibition of glycogen synthase and thereby promoting glycogen synthesis
E) Akt opens GLUT4 (glucose transporter type 4) channels in the endoplasmic reticulum to deliver glucose directly to glycogen
ANSWER: D
Rationale:
Akt phosphorylates and inactivates glycogen synthase kinase 3 (GSK-3); because GSK-3 normally phosphorylates and inhibits glycogen synthase, inactivating GSK-3 relieves that inhibition and activates glycogen synthase, promoting hepatic glycogen synthesis.
Option A: Option A is incorrect because Akt inactivates GSK-3 rather than activating it, and GSK-3 inhibits glycogen synthase rather than building glycogen itself.
Option B: Option B is incorrect because phosphorylation of glycogen phosphorylase favors glycogen breakdown, the opposite of insulin's synthetic effect.
Option C: Option C is incorrect because Akt inactivates Foxo1 by nuclear exclusion and Foxo1 governs gluconeogenic gene expression, not glycogen storage.
Option E: Option E is incorrect because GLUT4 is a plasma-membrane facilitative transporter, not an endoplasmic reticulum channel delivering glucose to glycogen.
4. A clinician is comparing regular human insulin with rapid-acting analogs for mealtime coverage. Which statement correctly characterizes the time-action profile of regular insulin and its practical dosing requirement?
A) Onset within 10 to 15 minutes, peak at 1 to 2 hours, allowing injection at the start of the meal
B) Onset of 30 to 60 minutes, peak at 2 to 3 hours, and duration of 5 to 8 hours, requiring injection about 30 minutes before the meal to align the peak with the postprandial glucose rise
C) Onset within 2 to 5 minutes, peak at 30 minutes, suitable for post-meal dosing
D) A near-peakless profile lasting more than 24 hours, suitable for once-daily basal coverage
E) A pronounced peak at 4 to 8 hours with duration of 12 to 18 hours, suitable for twice-daily basal dosing
ANSWER: B
Rationale:
Regular human insulin exists predominantly as zinc-stabilized hexamers that must dissociate to monomers before absorption, giving an onset of 30 to 60 minutes, a peak at 2 to 3 hours, and a duration of 5 to 8 hours. This delayed onset requires injection about 30 minutes before a meal so the peak effect aligns with the postprandial glucose excursion.
Option A: Option A describes a rapid-acting analog such as lispro or aspart, not regular insulin.
Option C: Option C describes an ultra-rapid formulation such as faster aspart, which has the fastest onset.
Option D: Option D describes a long-acting basal analog such as glargine or degludec.
Option E: Option E describes NPH (neutral protamine Hagedorn) insulin, an intermediate-acting preparation with a 4- to 8-hour peak.
5. The three rapid-acting insulin analogs each achieve fast absorption through distinct amino acid substitutions. Which substitution pattern correctly identifies insulin glulisine?
A) Reversal of the ProB28-LysB29 sequence to LysB28-ProB29
B) Substitution of ProB28 with aspartic acid
C) Acylation of LysB29 with a C14 (fourteen-carbon) fatty acid chain
D) Substitution of AsnA21 with glycine plus two added B-chain arginine residues
E) Substitution of AsnB3 with lysine and LysB29 with glutamic acid
ANSWER: E
Rationale:
Insulin glulisine is engineered by substituting AsnB3 with lysine and LysB29 with glutamic acid, changes that destabilize self-association and favor the rapidly absorbed monomer state.
Option A: Option A describes insulin lispro, which reverses the ProB28-LysB29 sequence.
Option B: Option B describes insulin aspart, which substitutes ProB28 with aspartic acid.
Option C: Option C describes insulin detemir, a long-acting analog whose C14 acylation promotes albumin binding rather than rapid absorption.
Option D: Option D describes insulin glargine, a long-acting basal analog whose AsnA21-glycine substitution and added arginines shift its isoelectric point.
6. Ultra-rapid insulin formulations achieve even faster absorption than standard rapid-acting analogs not through further amino acid changes but through added excipients. Which statement correctly describes this strategy?
A) Ultra-rapid formulations remove zinc entirely, which is the sole reason for their faster onset
B) Ultra-rapid formulations add protamine to slow dissolution and smooth the peak
C) Ultra-rapid formulations add excipients such as niacinamide (faster aspart) or citrate and treprostinil (ultra-rapid lispro) that accelerate subcutaneous absorption, giving onset within about 2 to 5 minutes
D) Ultra-rapid formulations achieve speed by acylation with a long-chain fatty acid that promotes albumin binding
E) Ultra-rapid formulations are simply more concentrated versions of regular insulin with no excipient changes
ANSWER: C
Rationale:
Ultra-rapid formulations of insulin aspart (faster aspart, Fiasp) and insulin lispro (ultra-rapid lispro, Lyumjev) incorporate added excipients — niacinamide in faster aspart and citrate plus treprostinil in ultra-rapid lispro — that further accelerate subcutaneous absorption, with onset within about 2 to 5 minutes and superior blunting of postprandial glucose excursions compared with standard rapid-acting analogs.
Option A: Option A is incorrect because the faster onset comes from added absorption-accelerating excipients, not from simply removing zinc.
Option B: Option B is incorrect because adding protamine slows absorption, the opposite of the ultra-rapid goal.
Option D: Option D is incorrect because long-chain fatty acid acylation promotes albumin binding and a prolonged basal effect, which is a long-acting strategy.
Option E: Option E is incorrect because ultra-rapid agents are analog formulations with specific excipients, not merely concentrated regular insulin.
7. A highly insulin-resistant patient requires more than 200 units of insulin per day, and large injection volumes are causing erratic absorption. Which statement correctly describes the rationale for U-500 regular insulin in this setting?
A) U-500 regular contains 500 units/mL, a five-fold concentration that reduces injection volume by about 80 percent and, because of depot pharmacokinetics at high local concentration, has a prolonged duration allowing twice- or three-times-daily dosing
B) U-500 regular is a rapid-acting analog that must be injected at the start of each meal
C) U-500 regular is more dilute than U-100, so larger volumes are needed but absorption is more predictable
D) U-500 regular is formulated for intravenous infusion only and cannot be given subcutaneously
E) U-500 regular is a basal analog that precipitates at neutral pH to form a 24-hour depot
ANSWER: A
Rationale:
U-500 regular insulin (Humulin R U-500) contains 500 units/mL, a five-fold concentration relative to U-100, reducing injection volume by roughly 80 percent for patients needing more than 200 units per day; this matters because subcutaneous absorption becomes erratic when volumes exceed about 50 units per injection site. U-500 also has a prolonged duration of action (up to 24 hours at high doses) from depot pharmacokinetics at high local concentration, allowing twice- or three-times-daily dosing as a combined basal-bolus regimen.
Option B: Option B is incorrect because U-500 is concentrated regular insulin, not a rapid-acting analog.
Option C: Option C is incorrect because U-500 is more concentrated, not more dilute, than U-100, so it reduces rather than increases volume.
Option D: Option D is incorrect because U-500 is administered subcutaneously, not exclusively intravenously.
Option E: Option E is incorrect because pH-dependent precipitation describes glargine, not U-500 regular insulin.
8. A patient with variable meal timing who is actively titrating insulin is being considered for a premixed insulin formulation. Which statement best describes the principal trade-off of premixed insulins?
A) Premixed insulins allow fully independent adjustment of basal and bolus doses, making them ideal for active titration
B) Premixed insulins contain only a basal component, so they provide no mealtime coverage
C) Premixed insulins are suitable only for intravenous use because of their fixed ratio
D) Premixed insulins combine a rapid- or short-acting component with an intermediate-acting protamine-complexed component in a fixed ratio, offering injection convenience but sacrificing the ability to independently titrate basal and bolus, which makes them poorly suited to variable meal schedules or active titration
E) Premixed insulins eliminate hypoglycemia risk because the fixed ratio prevents dosing error
ANSWER: D
Rationale:
Premixed insulins combine a rapid- or short-acting component with an intermediate-acting protamine-complexed component in fixed ratios (for example, 70/30 or 75/25). They offer the convenience of fewer injections but sacrifice the ability to independently titrate the basal and bolus components, making them poorly suited to patients with variable meal schedules, active titration needs, or significant hypoglycemia risk; they fit best with stable meal patterns or limited dexterity.
Option A: Option A is incorrect because the fixed ratio specifically prevents independent basal and bolus adjustment.
Option B: Option B is incorrect because premixed insulins include a rapid- or short-acting component that provides mealtime coverage, not basal alone.
Option C: Option C is incorrect because premixed suspensions contain a protamine component and are given subcutaneously, not intravenously.
Option E: Option E is incorrect because premixed insulins do not eliminate hypoglycemia risk; the fixed ratio actually limits the flexibility needed to minimize it.
9. Which statement correctly describes the distribution of absorbed insulin in the body?
A) Insulin has a very large volume of distribution of several liters per kilogram, reflecting extensive tissue sequestration
B) Insulin has a volume of distribution of approximately 0.1 to 0.2 L/kg, consistent with distribution in the extracellular fluid, and it does not cross the blood-brain barrier under normal conditions
C) Insulin distributes freely across the blood-brain barrier, achieving central nervous system concentrations equal to plasma
D) Insulin is almost entirely confined to red blood cells after absorption
E) Insulin is approximately 95 percent protein-bound for all preparations, leaving little free drug in plasma
ANSWER: B
Rationale:
The volume of distribution of insulin is approximately 0.1 to 0.2 L/kg, consistent with distribution in the extracellular fluid; insulin does not cross the blood-brain barrier under normal conditions, and only about 5 percent of circulating insulin is loosely protein-bound while the remainder circulates free.
Option A: Option A is incorrect because the volume of distribution is small and matches the extracellular fluid, not a multi-liter-per-kilogram tissue distribution.
Option C: Option C is incorrect because insulin does not freely cross the blood-brain barrier to equalize with plasma.
Option D: Option D is incorrect because insulin is not confined to red blood cells; it distributes in the extracellular fluid.
Option E: Option E is incorrect because most insulin preparations circulate largely free, with only about 5 percent loosely protein-bound; detemir is the high-binding exception, not the rule for all preparations.
10. Among the insulins, one preparation is distinguished by an unusually high degree of plasma protein binding that lowers its free fraction and its apparent volume of distribution. Which statement correctly identifies this preparation and the basis for its distinct distribution?
A) Regular insulin, because its zinc hexamers bind albumin with high affinity
B) NPH (neutral protamine Hagedorn) insulin, because protamine increases its albumin binding
C) Insulin lispro, because its B28-B29 reversal increases protein binding
D) Insulin glargine, because its acidic formulation drives plasma protein binding
E) Insulin detemir, because its C14 (fourteen-carbon) fatty acid chain produces approximately 98 percent albumin binding, reducing the free fraction and giving a volume of distribution near 0.1 L/kg
ANSWER: E
Rationale:
Insulin detemir is the exception to the low-protein-binding pattern of insulins: its C14 (fourteen-carbon) fatty acid chain produces approximately 98 percent albumin binding, substantially reducing the free fraction and giving a volume of distribution near 0.1 L/kg, with the albumin-bound reservoir buffering absorption fluctuations.
Option A: Option A is incorrect because regular insulin circulates largely free and is not highly albumin-bound.
Option B: Option B is incorrect because protamine slows NPH dissolution but does not confer high albumin binding.
Option C: Option C is incorrect because the lispro B28-B29 reversal accelerates absorption and does not increase protein binding.
Option D: Option D is incorrect because glargine's prolonged action comes from pH-dependent precipitation, not from high plasma protein binding.
11. A trainee is puzzled that subcutaneous insulin acts for hours even though the circulating molecule has a very short half-life. Which statement correctly reconciles the plasma half-life of insulin with its much longer apparent duration of action?
A) The plasma half-life of insulin monomers is several hours, which directly accounts for the prolonged duration of action
B) Insulin has no measurable plasma half-life because it is not cleared from the circulation
C) The plasma half-life of circulating insulin monomers is only about 4 to 6 minutes, but the apparent pharmacodynamic half-life is much longer because of ongoing absorption from the subcutaneous depot
D) The apparent duration of action is short because the subcutaneous depot is absorbed within minutes
E) The long duration reflects irreversible binding of insulin to its receptor, which prevents clearance
ANSWER: C
Rationale:
The half-life of circulating insulin monomers in the peripheral circulation is only about 4 to 6 minutes, but the apparent pharmacodynamic half-life is much longer because insulin continues to be absorbed from the subcutaneous depot over time; the depot, not the plasma half-life, governs the duration of effect.
Option A: Option A is incorrect because the plasma half-life is minutes, not hours, so it cannot directly account for the prolonged action.
Option B: Option B is incorrect because insulin is actively cleared, chiefly by insulin-degrading enzyme in liver and kidney, and does have a measurable short half-life.
Option D: Option D is incorrect because the subcutaneous depot is absorbed gradually over hours, which is precisely why the action outlasts the plasma half-life.
Option E: Option E is incorrect because insulin-receptor binding is reversible and is not the mechanism prolonging the duration of action.
12. A patient with cirrhosis on insulin develops frequent hypoglycemia despite having peripheral insulin resistance. Which statement best explains the effect of cirrhosis on insulin handling?
A) Cirrhosis reduces first-pass hepatic insulin extraction, increasing peripheral insulin exposure and predisposing to hypoglycemia, so cirrhotic patients often require substantially reduced insulin doses
B) Cirrhosis increases first-pass hepatic insulin extraction, lowering peripheral insulin levels and requiring higher doses
C) Cirrhosis has no effect on hepatic insulin extraction because insulin is cleared only by the kidney
D) Cirrhosis accelerates insulin-degrading enzyme activity in the liver, shortening insulin action
E) Cirrhosis eliminates the portal-to-peripheral insulin gradient by increasing hepatic blood flow
ANSWER: A
Rationale:
Cirrhosis reduces first-pass hepatic insulin extraction, increasing peripheral insulin exposure and predisposing to hypoglycemia; as a result, cirrhotic patients often require substantially reduced insulin doses even though they may have peripheral insulin resistance from counter-regulatory hormone excess.
Option B: Option B is incorrect because cirrhosis decreases rather than increases hepatic extraction, so peripheral insulin exposure rises and doses typically fall.
Option C: Option C is incorrect because the liver is a major site of insulin clearance, so impaired hepatic handling does affect insulin exposure.
Option D: Option D is incorrect because cirrhosis does not accelerate insulin-degrading enzyme activity to shorten insulin action; reduced extraction prolongs exposure.
Option E: Option E is incorrect because cirrhosis does not abolish the gradient by raising hepatic blood flow; the relevant change is reduced first-pass extraction.
13. A patient on a basal-bolus regimen has a total daily dose (TDD) of 50 units. Using the 500 Rule to estimate the carbohydrate-to-insulin ratio (CIR), how many grams of carbohydrate are covered by 1 unit of rapid-acting insulin?
A) Approximately 50 grams per unit, because the CIR equals the total daily dose
B) Approximately 10 grams per unit, because 500 divided by the TDD of 50 equals 10, giving the grams of carbohydrate covered per unit
C) Approximately 36 grams per unit, because 1800 divided by the TDD gives the carbohydrate-to-insulin ratio
D) Approximately 500 grams per unit, because the rule sets the CIR equal to the constant 500
E) Approximately 2 grams per unit, because the CIR equals the correction factor divided by the TDD
ANSWER: B
Rationale:
The 500 Rule estimates the carbohydrate-to-insulin ratio (CIR) as 500 divided by the total daily dose (TDD): 500 divided by 50 equals 10, so 1 unit of rapid-acting insulin covers approximately 10 grams of carbohydrate. This is a starting estimate requiring individual titration.
Option A: Option A is incorrect because the CIR is 500 divided by the TDD, not equal to the TDD.
Option C: Option C is incorrect because the 1800 constant is used for the correction factor (CF), not the CIR, so it misapplies the rule.
Option D: Option D is incorrect because the rule divides 500 by the TDD rather than setting the CIR equal to 500.
Option E: Option E is incorrect because the CIR is derived from the 500 Rule, not from the correction factor divided by the TDD.
REFERENCE BOX
500 Rule: carbohydrate-to-insulin ratio (CIR, grams of carbohydrate covered per unit) is approximately 500 divided by the total daily dose (TDD).
1800 Rule: correction factor (CF, mg/dL lowered per unit of rapid-acting insulin) is approximately 1800 divided by the TDD.
Mealtime bolus = (grams of carbohydrate / CIR) + ((current glucose minus target glucose) / CF). These are starting estimates requiring individualized titration.
14. A patient with type 2 diabetes mellitus is starting basal insulin with a treat-to-target titration approach. Which statement correctly describes how this basal titration algorithm is driven?
A) The basal dose is titrated using postprandial glucose readings, since basal insulin chiefly controls after-meal excursions
B) The basal dose is fixed at initiation and never adjusted, since titration applies only to bolus insulin
C) The basal dose is titrated according to the bedtime glucose alone, independent of fasting values
D) The basal dose is adjusted in small stepwise increments (for example, 2 units every 3 days) when the mean fasting glucose of the preceding days exceeds the target, with the dose held or reduced if any fasting glucose falls below the lower threshold
E) The basal dose is doubled each day until the fasting glucose target is reached, regardless of hypoglycemia
ANSWER: D
Rationale:
The treat-to-target basal titration algorithm uses structured self-monitored fasting glucose to drive stepwise adjustment: a common approach raises the basal dose by about 2 units every 3 days when the mean fasting glucose of the preceding days exceeds target (typically 80 to 130 mg/dL), holding or reducing the dose if any fasting glucose falls below the lower threshold. Fasting glucose is the appropriate signal because basal insulin controls hepatic glucose output between meals and overnight.
Option A: Option A is incorrect because postprandial readings guide bolus, not basal, titration.
Option B: Option B is incorrect because the basal dose is actively titrated, not fixed at initiation.
Option C: Option C is incorrect because fasting glucose, not bedtime glucose alone, drives basal titration.
Option E: Option E is incorrect because doubling the dose daily while ignoring hypoglycemia is unsafe and is not the treat-to-target method.
15. A patient with alcohol use disorder presents with severe hypoglycemia and cannot take oral glucose. A caregiver gives intramuscular glucagon, but the response is poor. Which factor best explains why glucagon may fail in this clinical context?
A) Glucagon failed because it stimulates peripheral glucose uptake, which cannot raise a low glucose
B) Glucagon failed because it works only when given intravenously, never intramuscularly
C) Glucagon raises glucose by mobilizing hepatic glycogen, so it is ineffective when hepatic glycogen is depleted, as occurs with prolonged fasting and alcohol intoxication
D) Glucagon failed because alcohol directly destroys the glucagon molecule before it can act
E) Glucagon failed because it lowers rather than raises blood glucose
ANSWER: C
Rationale:
Glucagon raises blood glucose by activating hepatic glucagon receptors, which mobilizes hepatic glycogen through glycogenolysis; it therefore depends on adequate glycogen stores and is ineffective when hepatic glycogen is depleted, as in prolonged fasting, alcohol intoxication, or hepatic failure. Alcohol further impairs glucose recovery by suppressing gluconeogenesis.
Option A: Option A is incorrect because glucagon mobilizes hepatic glycogen rather than stimulating peripheral glucose uptake.
Option B: Option B is incorrect because glucagon is effective intramuscularly or subcutaneously when glycogen is available; the route is not the reason for failure here.
Option D: Option D is incorrect because alcohol does not chemically destroy glucagon; the failure reflects depleted glycogen.
Option E: Option E is incorrect because glucagon raises, not lowers, blood glucose.
16. A pregnant patient with type 1 diabetes mellitus is being managed with insulin. Which statement correctly describes insulin use and insulin requirements in pregnancy?
A) The rapid-acting analogs lispro and aspart have extensive safety data and are recommended, degludec is not recommended owing to insufficient data, and insulin requirements rise substantially in the second and third trimesters before falling abruptly after delivery of the placenta
B) Insulin is contraindicated in pregnancy because it crosses the placenta and causes fetal harm
C) Insulin requirements fall progressively through the second and third trimesters as placental hormones improve insulin sensitivity
D) Degludec is the preferred insulin in pregnancy because of its long duration, while lispro and aspart are contraindicated
E) Insulin requirements remain constant throughout pregnancy and do not change after delivery
ANSWER: A
Rationale:
Insulin is the standard of care in pregnancy and does not cross the placenta in physiologically significant amounts. The rapid-acting analogs lispro and aspart have extensive safety data and are recommended; degludec is not recommended owing to insufficient data. Placental hormones (human placental lactogen, cortisol, progesterone, prolactin) produce progressive insulin resistance, so requirements rise substantially through the second and third trimesters, often markedly above the pre-pregnancy dose, then fall abruptly with delivery of the placenta.
Option B: Option B is incorrect because insulin does not cross the placenta in significant amounts and is the recommended therapy, not a contraindicated one.
Option C: Option C is incorrect because placental hormones increase insulin resistance, raising rather than lowering requirements.
Option D: Option D is incorrect because degludec is not recommended in pregnancy while lispro and aspart are appropriately used.
Option E: Option E is incorrect because requirements change markedly across pregnancy and drop sharply after placental delivery.
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