Chapter 12: Carbohydrate Metabolism

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Welcome to the Deep Dive.

If you're gearing up for a clinical biochemistry exam.

Or just, you know, stepping onto the wards for the first time.

Right.

Pull up a chair.

You are in exactly the right place.

Today we've got a custom tailored mission just for you.

We really do.

We're setting this up as a one -on -one tutoring masterclass.

Instead of just rattling off a list of enzymes and lab values from Chapter 12 for you to memorize.

Which is the worst way to learn it.

Exactly.

We're going to build the architecture of how the body handles glucose.

We'll start with the foundational chemistry, watch what happens when that machinery breaks down, and then, and this is the fun part, equip you with the diagnostic tools to figure out exactly where the breakdown occurred.

The urgency of mastering this stuff.

I mean, it really can't be overstated.

Current projections suggest that in the next decade, we're going to see roughly 250 million people worldwide living with type 2 diabetes.

Yeah, that is a staggering slice of the global population.

It really is.

It means no matter what specialty you end up in, you're going to be managing the downstream effects of abnormal carbohydrate metabolism.

It's the defining metabolic crisis of our era.

So, to tackle this, we really need to start at the chemical level.

Carbohydrates are fundamentally just hydrates of carbon,

but their structure dictates everything.

Right, you've got your simple monosaccharides, which are the single building blocks, glucose, fructose, galactose.

And in the lab, we call these reducing sugars because of their specific chemical properties, and that actually becomes a vital diagnostic clue later on.

But when you bind two sugars together— Like joining glucose and fructose to make everyday table sugar sucrose.

Yeah, exactly.

It actually loses that reducing property.

And structure dictates how we store this energy, too.

Plants store their carbs as starch, which is a mix of straight -chain amylose and branched amylopectin.

But humans need energy fast, especially for muscle contraction and sudden bursts of activity.

So we store our glucose as glycogen.

Which is highly, incredibly brand.

Those numerous branches mean enzymes have multiple endpoints to attack simultaneously.

They can cleave off glucose molecules in a fraction of a second when we need a sudden surge of fuel.

And the primary beneficiary of all this intricate storage and release machinery is the brain.

I mean, the brain is an incredibly demanding organ.

Under normal physiological conditions, it is entirely dependent on the extracellular glucose concentration for its energy.

It simply can't synthesize its own glucose, it doesn't store any meaningful amount of glycogen,

and it can't metabolize stator fats, right?

Because large fatty acids bound to proteins can't easily cross the blood -brain barrier.

Precisely.

Which sets up a very precarious situation.

The brain is burning huge amounts of glucose, but it's entirely at the mercy of whatever is floating by in the blood.

And here's the kicker.

Glucose entry into brain cells is not facilitated by insulin.

The brain cells just act like an open door.

Right, they rely entirely on a concentration gradient to push glucose inside.

And that open door is exactly why blood glucose is so fiercely regulated by the body, usually kept in a tight window between 4 and 10 millimoles per liter.

If the concentration drops too low, that pressure gradient vanishes, the glucose stops flowing into the brain, and the neurons literally begin to starve.

But if it goes too high, the resulting chemical cascade slowly destroys the vascular system.

So keeping the blood glucose in that 4 to 10 millimoles per liter sweet spot requires a maestro.

And that maestro is insulin.

It's the body's ultimate times -of -plenty storage hormone, manufactured in the beta cells of the pancreas.

But it doesn't start as active insulin?

No.

It begins as a larger precursor called pro -insulin.

To make it active, the pancreas has to snip pro -insulin in half, removing this connecting segment in the middle.

And that discarded middle segment is called C -peptide.

Understanding this cleavage gives you one of the most powerful diagnostic tools in clinical biochemistry.

It's the molecular receipt.

It is.

Because insulin and C -peptide are snipped from the exact same precursor, they're released into the blood in a perfect ecomolar one -to -one ratio.

So if your own pancreas made the insulin, it hands you a C -peptide receipt.

Exactly.

And we are going to use that receipt to solve some very tricky clinical mysteries a little later.

Can't wait for that.

So once insulin is released,

usually triggered when blood glucose ticks above 5 millimoles per liter after a meal, it goes to work.

It binds to receptors on muscle and fat cells, unlocking their doors so glucose can flood in.

It stimulates glycogenesis, building up those highly branched glycogen stores in the liver and muscles.

And at the same time, it slams the brakes on the breakdown of fat and protein.

The message is basically, we have plenty of fuel right now, pack it away for winter.

Yeah.

And then you have the opposing forces, the counter -regulatory hormones that step in during fasting or high stress.

Glucagon from the alpha cells, growth hormone, glucocorticoids like cortisol, and adrenaline.

Their entire job is to keep the brain fed when no food is coming in.

They mobilize glucose by breaking apart those glycogen branches, glycogenolysis, and by literally forcing the liver to build new glucose molecules from scratch out of amino acids and other byproducts.

Which is gluconeogenesis.

And watching how different organs respond to these signals reveals this brilliant physiological design.

It's a tale of two enzymes.

I love this part.

Right.

When you eat, the nutrient -rich blood from your gut travels directly to the liver first, the liver gets first dibs, and it uses an enzyme called glucokinase to capture that glucose.

But glucokinase has a surprisingly low affinity for glucose compared to the enzymes used by the rest of the body.

Which sounds totally backwards.

It does, but it's actually a protective mechanism.

Because of that low affinity, the liver only starts grabbing massive amounts of glucose when the concentration is exceptionally high, like the spike immediately following a heavy meal.

So it acts as a buffer.

It prevents a dangerous post -meal surge from hitting the general circulation.

Right.

But when fasting levels are lower, glucokinase just ignores the glucose.

It lets it pass by so the demanding brain can have it.

Meanwhile, skeletal muscle and adipose tissue use a different enzyme called hexokinase.

And hexokinase has a very high affinity.

It's greedy.

So greedy.

It will snatch up glucose even when blood levels are relatively low.

But here is the ultimate betrayal.

The liver is generous, but muscle is entirely selfish.

It really is.

The liver and kidneys possess an enzyme called glucose -6 -phosphatase.

It so it can leave the liver cell and travel through the blood to rescue a starving brain.

But skeletal muscle lacks those specific chemical scissors.

Once glucose enters a muscle cell and gets phosphorylated,

it is trapped there forever.

Muscle tissue absolutely refuses to share its fuel with the rest of the body.

It hoards its glycogen strictly for its own contraction.

So knowing that muscle won't share, what happens during a prolonged fast?

Well, when insulin levels drop to baseline, the body has to find an alternative fuel source.

This initiates ketosis.

Right.

The drop in insulin removes the breaks on adipose tissue.

Fat cells begin breaking down their stored triglycerides, releasing free fatty acids into the bloodstream.

And those travel to the liver where they're converted into ketone bodies, primarily acetoacetate and beta -hydroxybutyrate.

The brain, which normally refuses fat, can actually adapt to use these ketones in an emergency starvation scenario.

It's a fantastic survival mechanism.

It is, but it comes with a severe biochemical cost.

Ketones are acidic.

If the liver produces too many of them, they rapidly overwhelm the body's natural buffering systems.

Causing the blood pH to plummet and creating a dangerous state of metabolic acidosis.

And that brings up another critical form of metabolic acidosis you'll encounter in emergency

medicine—lactic acidosis.

Which isn't driven by a lack of insulin, but by a lack of oxygen—tissue hypoxia.

Exactly.

Imagine a patient in severe shock.

Normally cells generate energy using the tricarboxylic acid cycle, which absolutely requires oxygen.

When the oxygen supply fails, that entire cycle grinds to a halt.

The cells are desperate for ATP, so they fall back on a primitive anaerobic pathway.

Which doesn't need oxygen, but its byproduct is massive amounts of lactic acid.

And to compound the crisis, the liver is supposed to be the clean -up crew.

It's responsible for turning that lactate back into useful glucose.

But the liver needs oxygen to do that work.

So in a hypoxic patient, the factories producing the acid go into overdrive, and the clean -up crew goes on strike.

The lactate accumulates rapidly, dropping the blood pH to life -threatening levels.

Wow.

Okay, so we've established the baseline rules of the metabolic machinery.

Now let's look at what happens when the regulation of blood sugar breaks down entirely.

Diabetes mellitus.

Clinically, it's diagnosed using very specific WHO thresholds.

A patient is considered diabetic if their fasting venous plasma glucose is 7 .0 millimoles per liter or higher.

Or if a random non -fasting glucose check comes back at 11 .1 millimoles per liter or higher.

Right.

And hitting those numbers can happen through several different physiological failures.

Type 1 diabetes is fundamentally an autoimmune disease.

The immune system makes a catastrophic error.

It produces autoantibodies like GAD and IA2 that hunt down and wipe out the beta cells in the pancreas.

So without those beta cells, there is an absolute complete lack of insulin, usually childhood onset.

And because they have zero insulin to hold back fat breakdown, these patients are incredibly susceptible to developing severe ketoacidosis.

Then you have type 2 diabetes, which represents the vast majority of cases globally.

It operates on a different mechanism entirely.

It's a combination of the body's tissues becoming deeply resistant to insulin, paired with the pancreas eventually burning out and failing to secrete enough to overcome that resistance.

Heavy ties to adult onset and central obesity.

But the origins can sometimes be traced back to before the patient was even born.

Yeah, you're referring to the thrifty phenotype hypothesis.

It connects evolutionary biology to modern pathology.

Oh, fascinating.

It really is.

If a fetus experiences poor nutrition or low birth weight in the womb, its developing metabolic system assumes it's going to be born into a world of famine.

So it programs the cells to be incredibly thrifty, hoarding every single calorie for survival.

But then that baby grows up in a modern environment with an abundance of high -calorie food.

That fetal programming clashes with reality, manifesting as profound insulin resistance and eventually type 2 diabetes.

Beyond type 1 and 2, you have to be a detective for the less common variants,

like MEGOD maturity onset diabetes of the young.

MEDIY can easily trick you.

It looks like type 2 because the patients initially don't need insulin injections, but it happens in young, often lean individuals.

It's caused by single genetic mutations, right?

Like a defect in the gene for that glucokinase enzyme we talked about earlier.

If the liver's glucose sensor is broken, the whole regulation system goes offline.

Exactly.

You also have gestational diabetes, which emerges during pregnancy due to placental hormones inducing severe insulin resistance.

It requires careful screening at 24 to 28 weeks to protect the developing fetus.

Not to mention secondary causes like Cushing syndrome or drugs like psiazides and steroids.

But many patients spend years in a warning phase before reaching those diagnostic thresholds.

We call this pre -diabetes.

It encompasses impaired fasting glucose, where the fasting morning sugar sits stubbornly between 6 .1 and 6 .9 millimoles per liter.

Or they might have impaired glucose tolerance, where their body struggles to bring a sugar spike down after a meal.

And this state is frequently a core feature of the metabolic syndrome.

Which is that perfect storm of cardiovascular risk factors.

Central obesity, high triglycerides, dangerously low HDL cholesterol, high blood pressure, and a fasting glucose over 5 .5.

When that blood sugar eventually breaches the diabetic thresholds, the clinical symptoms become glaringly obvious.

Yeah, if a patient comes into your clinic complaining of constant unquenchable thirst and having to pee every hour, the underlying biochemistry explains exactly why.

Under normal conditions, your kidneys are fantastic recyclers.

They reabsorb every single molecule of glucose that gets filtered out of the blood.

But they have a mechanical limit, a renal threshold of roughly 10 millimoles per liter.

The moment the blood glucose concentration pushes past that 10 millimole limit, the kidneys recycling pumps are overwhelmed.

Glucose starts spilling over into the urine.

Glycosuria and glucose is a highly osmotic molecule.

It acts like a sponge.

As it travels down the urinary tract, it drags huge volumes of water along with it.

This creates massive unstoppable urination, polyuria.

The patient is literally peeing away their body's water, leading to profound cellular dehydration.

The brain senses this dehydration and triggers an intense, desperate thirst mechanism, polydipsia.

If that hyperglycemia becomes a chronic long -term state, the sugar literally begins to rot the vascular system.

Macrovascular disease accelerates, leading to early heart attacks and strokes.

But the microvascular damage is where diabetes really shows its devastating specific signature.

Right, the tiny blood vessels in the back of the eye become damaged and leak, causing retinopathy.

The blood vessels feeding the peripheral nerves degrade, leading to neuropathy.

And the microvascular damage to the kidneys is particularly insidious.

Think of the filtering units in the kidneys as delicate microscopic sieves.

When blood sugar remains continuously elevated, the structural proteins in those sieves undergo abnormal chemical changes.

They get sticky, they scar, and they form distinct little nodules.

Pathologists refer to these nodular scars as Kimmel -Steel -Wilson lesions.

It represents the slow, irreversible loss of the kidney's ability to filter waste.

To stop that progression, we track a patient's long -term control.

Using a test called HbA1c.

Rather than just taking a snapshot of the blood sugar at a single moment, HbA1c measures the non -enzymatic glycation of hemoglobin.

Basically, it looks at how much sugar has chemically coated the red blood cells.

And since a red blood cell lives for roughly 120 days, this gives the clinician a beautiful 6 to 8 week historical average of the patient's blood sugar levels.

Target is usually around 53 millimoles per mole, or 7%.

We also actively hunt for the earliest signs of that kidney damage by checking the urine for tiny amounts of protein.

We use the albumin to creatinine ratio, or ACR test.

If we detect microalbuminuria, the protective sieves are just starting to leak.

We respond aggressively.

Typically initiating ACE inhibitors.

Beyond just lowering systemic blood pressure, ACE inhibitors relieve the specific pressure inside the delicate kidney filters, offering vital organ protection.

As for treatments, a type 1 patient needs exogenous insulin to survive.

Full stop.

A type 2 patient starts with lifestyle modifications, but usually progresses to medications.

Metformin is a cornerstone.

It acts directly on the liver, telling it to stop pumping out so much new glucose.

Sulfonylureas act like a chemical whip on the pancreas, forcing the beta cells to squeeze out more insulin.

And newer in creatinine mimetics, like GLP -1 agonists, act as powerful gut hormones that amplify insulin release perfectly timed to a meal.

But even with diligent management, acute crises happen.

And they are terrifying.

Let's examine the diabetic comas, starting with diabetic ketoacidosis or DKA.

Case 2 from the text.

Right.

This is the classic presentation of uncontrolled type 1 diabetes.

Imagine a 24 -year -old woman brought into the emergency department, unconscious.

The lab results are chaotic.

A blood glucose of 35 millimoles per liter.

A severely acidic blood pH of 7 .9 in the row, completely depleted by carbonate.

And urine heavily positive for ketones.

The biochemistry explains every single one of those numbers.

Because she has zero insulin, the brake pedal on her adipose tissue is completely gone.

Massive amounts of fat are mobilized and dumped into the liver.

Which converts them into a tidal wave of acidic ketones.

This drops her blood pH, creating the life -threatening metabolic acidosis.

And in a desperate attempt to fix the acid level, the brain's respiratory center commands deep, heavy, sighing breaths.

Cousmoles respiration.

Exactly.

To literally blow off carbon dioxide, which is an acid, out through the lungs.

Meanwhile, the glucose of 35 is causing that osmotic sponge effect in the kidneys we talked about earlier.

She is experiencing a massive diuresis, leaving her entirely volume depleted.

And this brings us to a trap that catches many young clinicians off guard.

The potassium trap.

Oh, this is a critical tutoring point.

When you look at her initial lab report, her blood potassium will often look deceptively high.

It's a terrifying paradox.

The lack of insulin, combined with the severe acid buildup in the blood, actually forces potassium out of the cells and into the bloodstream.

So the blood test looks high.

But because she is experiencing that massive urinary diuresis, she is literally peeing all that potassium down the drain.

Her total body stores are critically depleted.

The trap springs when you start treating her.

The treatment for DKA is intravenous fluids and continuous IV insulin.

The moment that insulin hits her system, it throws the metabolic machinery into reverse.

It forcefully drives glucose and whatever potassium is left in the blood rapidly back into the cells.

If you do not proactively add potassium to her IV fluid bags, the insulin will drop her blood potassium to zero, triggering a fatal cardiac arrhythmia right there in the resuscitation bay.

You have to anticipate it.

Now, contrast that chaos with the other major hyperglycemic crisis from case 3,

hyperosmolar hyperglycemic state, or HHS.

Sometimes called H -O -N -K.

This typically happens in an older patient with type 2 diabetes who presents severely drowsy or comatose.

Their labs show a jaw drop in glucose, maybe 65 millimoles per liter, and an extremely high blood sodium, like 160.

But surprisingly, their blood is not acidic and there are no ketones.

The mechanism here hinges on the fact that it's type 2 diabetes.

The patient still manufactures a tiny trickle of their own insulin.

That trickle isn't nearly enough to push glucose into the resistant tissues, and it's not enough to stop the liver from making new sugar.

So the glucose climbs to absurd astronomical levels.

However, that tiny trickle of insulin is just enough to keep the fat locked away in the adipose tissue.

Exactly.

No fat breakdown means no ketones, and no ketones means no acidosis.

Instead, the danger is pure, profound dehydration.

With a glucose of 65, the blood becomes incredibly thick, sticky, and hyperosmolar.

It literally acts as a vacuum, sucking water out of the surrounding tissues, including the neurons in the brain, causing them to shrink and shut down.

The clinical imperative here is slow, meticulous correction.

You have to rehydrate them with IV fluids very carefully.

If you give too much insulin too fast and drop the blood sugar rapidly, the vacuum effect reverses.

Water will rush violently back into the dehydrated brain cells, causing massive cerebral swelling and brain death.

So dangerous.

The third coma is entirely different and is by far the most common.

Case one, hypoglycemic coma.

Right.

Imagine a 34 -year -old with type 1 who took her normal dose of morning insulin, but then missed breakfast and lunch.

She's found unconscious at the wheel of her car with a blood glucose of 1 .5 millimoles per liter.

This goes back to the very first physiological rule we established.

The brain has no backup fuel and relies entirely on the concentration of glucose in the blood.

When her level dropped to 1 .5, the gradient vanished.

The doors closed.

Her brain literally began to starve, a state called neuroglycopenia.

The symptoms escalate rapidly from confusion and aggression to memory loss, blackout, and a deep coma.

It is an absolute time -critical emergency.

The treatment is immediate intravenous glucose to restore the gradient.

Or if you're in the field and can't get an IV line, an intramuscular injection of glucagon.

Which forces whatever glycogen is left in her liver to instantly break down and flood the blood with glucose, buying you time.

So we know how the extreme scenarios operate, but as a clinician, you're usually trying to catch this machinery breaking down much earlier.

How do you actually prove someone's glucose regulation is failing if their fasting numbers are just hovering in that borderline pre -diabetic gray zone?

That is when you deploy the oral glucose tolerance test, or OGTT.

The patient comes into the clinic after an overnight fast.

You give them a heavily concentrated drink containing exactly 75 grams of anhydrous glucose.

And then you wait exactly two hours to see how their hormonal machinery handles the load.

If their beta cells and insulin sensitivity are healthy, their two -hour blood glucose should easily be backed down below 7 .8 millimoles per liter.

If the two -hour result lands between 7 .8 and 11 .1, the machinery is struggling.

That confirms impaired glucose tolerance.

And if it breaches 11 .1, their system has failed the stress test, confirming full clinical diabetes.

Diagnosing high blood sugar is routine, but investigating mysterious cases of low blood sugar hypoglycaemia in a non -diabetic patient is some of the most complex, satisfying detective work you will do.

The first step is confirming true hypoglycaemia, defined as a plasma glucose of less than 2 .5 millimoles per liter.

But there is a massive pre -analytical trap here.

Yes.

When you draw the patient's blood, you must put it into a specific tube that contains an inhibitor of glycolysis, usually fluoride oxalate.

Because if you don't, the living red blood cells in that sample tube will continue to eat the glucose in the plasma while it's sitting on the transport cart.

By the time the lab runs the test, the glucose is artificially low.

You have a case of pseudo -hypoglycaemia.

The fluoride oxalate acts as a freeze ray, stopping the red blood cell metabolism in its tracks.

So once you confirm the glucose is genuinely low, figure 12 .9 gives us the algorithm.

You split your investigation down two distinct branches.

Is the body's insulin appropriately low, or is it inappropriately high?

If insulin is appropriately low, meaning the pancreas is correctly sensing the low sugar and shutting off production, you have to look for severe systemic failures.

Like, is the liver entirely destroyed by cirrhosis so it can't make new glucose?

Are the adrenal glands failing to produce the counter -regulatory hormone cortisol, like in Addison's disease?

You also have to consider less obvious culprits.

Massive non -islet cell tumors can occasionally secrete a robe hormone called IGF2, which crashes blood sugar.

You was always asked about alcohol consumption.

The metabolic breakdown of heavy alcohol actively blocks the liver's ability to run glugoneogenesis.

A chronic alcoholic who hasn't eaten in two days can easily present with profoundly low blood sugar and high ketones.

But the real mystery starts when the lab tells you the glucose is dangerously low and the insulin level is inappropriately massively high.

Something is flooding the system with insulin.

And to find the source, we pull out our molecular receipt.

The C -peptide.

Let's run case four.

A 45 -year -old woman is brought to the clinic because she keeps experiencing terrifying, dizzy spells and confusion in the mornings.

Her husband notes that the symptoms miraculously vanish the moment he forces her to drink a sweet drink.

This is the classic Whipple's triad.

Documented low blood glucose, severe neuroglycopenic symptoms, and immediate relief upon glucose administration.

Her fasting labs reveal a blood glucose of 2 .1.

Her insulin is sky high.

But crucially,

her C -peptide level is also sky high.

And a toxicology screen for diabetes drugs is completely negative.

We have to connect the dots.

If she were suffering from fictitious disorder and secretly injecting herself with pharmaceutical insulin, her blood insulin would be massive.

But her C -peptide would be virtually zero.

Because exogenous insulin is manufactured in a lab.

It does not come with a C -peptide receipt.

What if she found someone's type 2 diabetes pills, the sulfonylureas, and took those?

They stimulate the pancreas, so her insulin would be high.

And her C -peptide receipt would be high because it came from her own beta cells.

But her toxicology screen was negative.

Leaving only one biochemical possibility.

High insulin, high C -peptide, negative drug screen.

Her own pancreas is independently autonomously pumping out rogue insulin.

The diagnosis is an insulinoma.

A rare, benign, insulin -secreting tumor hiding inside the islet cells of her pancreas.

The biochemistry pinpoints the exact physical location of the problem.

It is brilliant how the metabolic pathways lead you right to the diagnosis.

It really is.

Now, before we finish, let's touch briefly on the laboratory wrap -up.

Specifically, urinalysis.

Today, if you want to check for sugar in the urine, you dip a standard region strip.

And those modern dipsticks use a specific enzyme called glucose oxidase.

Meaning, they only react to the presence of glucose.

But there is a crucial pediatric scenario where you need to look beyond just glucose.

There's an older chemical test utilizing clanid test tablets.

Clanid test relies on copper reduction.

Meaning, it will change color in the presence of any reducing sugar.

Not just glucose.

Fructose and galactose will trigger it, too.

So why does a clinician need to know that?

Imagine evaluating a sick infant in the neonatal intensive care unit.

Their modern glucose dipstick is totally negative.

But the older clanid test tablet reacts violently positive.

This tells you there is a different dangerous sugar spilling into the baby's urine.

The infant might lack the specific enzymes needed to break down the galactose in breast milk.

The galactose builds up in the blood, acting as a toxin that damages the liver in the brain.

Spying that discrepancy between the two urine tests allows you to immediately suspect an inborn error of metabolism like galactosemia.

Potentially saving the child's life simply by switching their formula.

It perfectly encapsulates our mission today.

Understanding the underlying chemistry isn't just an academic exercise for an exam.

It is the fundamental basis for clinical problem solving and patient safety.

We have traced the journey of a single molecule of glucose from the digestive tract through the greedy muscles and the generous liver all the way to a starving brain shutting down in a hypoglycemic coma.

We really covered it all.

But it leaves me with a fascinating, provocative thought for you to explore.

We've seen how absolutely stubborn the brain is demanding pure glucose and forcing the body into extreme, sometimes fatal cascades like diabetic ketoacidosis when that fuel cannot be delivered.

What if medical science could figure out a way to safely, predictably force the brain to switch its primary fuel preference during an acute metabolic crisis?

If we could engineer a bypass,

a synthetic ketone, or an alternative substrate that temporarily eliminated the brain's absolute reliance on glucose,

we might fundamentally eliminate the lethality of diabetic emergencies entirely.

It's an incredible avenue for research, perhaps one that you listening right now will eventually pioneer.

But for today, mastering these current pathways is your sharpest tool for navigating the wards.

We want to thank you for joining us on this clinical deep dive.

Keep connecting those biochemical dots.

From the Last Minute Lecture Team, we wish you the absolute best of luck.

You are going to be a phenomenal clinician.

You've got this.