Nerdspark

MS I. Home: NYC ❤️ \\ city heart, beach soul, nerd mind \\ IG: sharonbopark

[31women]

There is a part of us hidden deep.

It is the portion of us untouched by our difficult circumstances, our cutting-edge need to belong, and the all of the outside forces that morph and mold us.

The sensitive, artistic, generous, whimsical, outlandish parts of us have slowly buried themselves against the steel we have created against the harshness of this world and all of its expectations.

We feel it ache whenever we see a hungry child or a piece of art on the street. An unexpected pang. “Hello? I’m still here. I’m still with you. You haven’t forgotten, have you?“

That is the part, those are the parts, this world yearns for.

All of those soft parts that are so sensitive to the blade of criticism and rejection are what this world craves.

Do me (and you, and your neighbor, and the child you love, and your local grocery store clerk) a favor: do what you’re afraid to do. Turn over to the underbelly of all of those things you’re afraid to show and brave the weight of the world. Yield all of those quirky parts of you against the winds.

Be still. Be vulnerable. Be open. Be funny. Be soft. Be all of those things you never thought you could let yourself be.

Because Jesus made you that way. He crafted you, knitted you, and transformed you to be who you are. And it’s okay to be you.

Because it might save someone. It just might save you.

-31Women (Ansley)

[larstheyeti]

The Awkward Yeti

[medschool-motivation]

Aka my brain on med school

[telep0rt]

Open Letter (to Accompany a Snapshot of a Monday Night) Sent to 16 Year Old Me

Dear 16 year old Katharine, 

Maybe it’s not today, but one of these days, soon, you’re going to wake up and it will be spring outside, warm and fresh – and you’ll feel like giving up. 

You’ll feel like life won’t get better. That it will never make sense. You’ll feel like staying in between the sheets with the curtains drawn for the rest of the day, the week, the year. 

Don’t stay. 

Because one day, you’ll be 26 and you’ll be wrapping dishes in brown paper and bubble wrap. You’ll be closing up the life you had in an apartment so you can move into a house you own. A house you own with a man you love, a man who loves you. 

You’ll have so much living to do that you’ll temporarily live in two places. In this place and in a house pilled up with boxes and the furniture you could move in the back of your car. 

Maybe it’s not today, but one of these days, you and your 16-year-old self will not be able to make sense of where your life is going to go. You’ll have these career plans that you tell adults, but that feel wrong in your mouth and slip through your fingers when you try to write them down on college essays. 

Don’t worry. 

Because one day, you’ll be 26 and you’ll be a doctor and you’ll have done surgeries and pretended to be the PGY2 for the day and made a patient smile and you’ll carry that around with you for the rest of the day and this job will make so much sense you can’t imagine having done anything else. 

And as you’re driving home, on the radio they’re talking about high school and prom and first loves and the pressure of being 16. 

Don’t panic. 

Because one day, you’ll be 26 and there will be a Monday where you stand in the kitchen and wrap dishes and answer the phone to talk about patients at 9 o’clock at night in a slowly emptying apartment… and on that day you’ll be thankful that you chose to get out of bed, to keep fighting through the uncertainty, to survive the “pressure of being 16″ that radio hosts talk about in clipped, practiced voices. Instead of dreading the next 10 years of your life, you’ll be excited for what you’ll look like 10 years from now, the great and incredible and terrifying things ahead.

One day there will be a snapshot of a Monday night: of brown paper and the smell of ink and the sound of old favorite songs from laptop speakers - and a knowledge you realize you didn’t have when you were 16 – that you will be okay. 

Love, 

Me

[nerdspark]

7-13 Oh crap... no crap?

Talking about the colon today, but you all probably figured by the lame (totally me) title. No shame. 

This week we saw the GI system in its entirety in lab. We dissected the anterior musculature to resect and saw the essentially one giant tube from esophagus to anus. Luckily, our cadaver had gas. This is lucky because that meant less feces. Nobody cut the crap though, so what could have been potentially the stinkiest lab ended up being another fascinating one. 

All of the mixing of your meals happens in the colon - it’s the only place where there’s enough time and space for your spread apart meals to come together once again. Thus solidifying my case that food is meant to be taken in for nourishment aka we eat to live not we live to eat. Foodies will vehemently disagree and I might even be a foodie if I had the time and energy to care. Part of the reason I changed to the meal replacement shake was to save the time and energy in deciding and prepping meals. My PT said that’s a little intense -- adjusting my diet to accommodate study time, but hey that’s me. You gotta do what you gotta do. 

Your colon comes after your small intestine (which composed of the duodenum, jejunum and ileum, in that order). After the ileum comes the ascending limb (right side of the body), transverse limb (crossing over), descending limb (left side of body), sigmoid colon connecting to the rectum then the fecal matter moves out through the anus. Your food spends not much time in the ascending colon as it’s continuously being pushed, but it does spend a lot of time in the transverse colon. In both these proximal areas of the large intestine,  H2O and electrolytes are reabsorbed. Then there’s the descending colon where most of the fecal matter is stored. When needed, it is pushed from there, past the sigmoid colon to the rectum to be excreted. The sigmoid colon can be remembered as the “S” shaped portion. S = Sigmoid. This S kink acts as a barrier to the fecal matter so that it delays the movement of the matter straight into the rectum. In the rectum it is stored until excretion. 

I learned in one of our clinical cases classes (we were discussing Crohn’s and IBS) that diarrhea is not really what we think of it as layman’s terms. For example, at the beginning of this school year, I had to use the bathroom urgently and had some watery stool as a nice present during our first MSI exam. Apparently, that’s not diarrhea. Diarrhea is clinically characterized by bowel movements of 3-5x/day for at least 5 days. So really, and thankfully, I’ve never had diarrhea in my life. 

There are 2 types: 1) osmotic diarrhea and 2) secretory diarrhea. The former is due to non-absorbable solutes in the lumen, and the latter is due to excess secretion due to intestinal bacteria. As you can imagine, if fluids are not adequately reabsorbed in the colon which is the final part of the GI, those fluids will be secreted. Cue: Diarrhea. 

The ileocecal sphincter lies between the ileum and the cecum aka the last part of the SI and first part of the LI. This is prominent in the gastroileal reflex: 1. SI peristalsis, 2. relaxation of the ileocecal sphincter, and 3. pushing the matter from ileum to colon. When there is pressure at the cecum (poop fills that late part), there is inhibition of ileal peristalsis (stops trying to move it along) and contraction of the sphincter contraction (so no more crap comes in). This reflex is mediated intrinsically by the myenteric plexus and externally by the ANS. The cecum has a little pouch attached to it that really isn’t there for anything. But if a portion of fecal matter gets stuck in this pouch and calcifies, this can lead to inflammation and infection of that pouch. I’m sure many of you have heard of this pouch: the appendix. So irritation of this = appendicitis.

The motility through the colon is prompted by ICCs - interstitial cells of cajal - which we saw affect the SI as well. The slow segmental propulsion and segmental mixing is caused by the circular muscle contractions as well as the contraction of the SM lining the LI called the taenia coli. These contractions are called haustrations, which solidify the chyme. Then, mass movements, or your body’s way of telling you to “Go Poop!” occurs, during which haustrations stop. Mass movements last for 10-30 minutes and signal your body to GO. 

This is why in cases of ulcerative colitis, where patients have irritation of the colon, patients experience persistent mass movements. On the other side, patients with Hirschsprung’s disease lack the mass movements and suffer the effects of obstruction or megacolon. A big colon = one that is full of crap. 

[foreverhelives-deactivated20170]

Remember: God is using all of your experiences, both good and bad, to develop your character to match your calling.

Lysa TerKeurst  (via littlethingsaboutgod)

[nerdspark]

7-11 Starvation and low carb diets

I’m not ashamed to admit it. I’ve tried many fad diets and may even still be on one right now. If you’ve been paying attention, it’s the low carb, high protein diet that was causing acidosis. Now that we’re no longer on the kidney unit and on the GI unit, I’ll talk about what’s happening physiologically if you happen to be on such a diet. Or if you’re a meal skipper or missed breakfast this morning because really, this applies to you too. 

When you’re body is low in blood glucose levels (as occurs when it doesn’t get the carbs and regular input it needs), it breaks down the glycogen stores in your body to make glucose. This is more difficult than if, say, you’d given it the carbs it needs, because in that case, your body can just digest the carbs taken in and break it down to glucose. When, however, your body is deprived of that necessity, hormones start acting up. One important one is glucagon, which signals your body to increase cAMP, phosphorylation, FBPase-2 and inactivate PFK2. All these abbreviations for enzymes might not mean much to you but the PFK matters because it is a rate limiting step in glycolysis (the breakdown of glucose). Since PFK is inhibited, the opposite reaction will occur - gluconeogenesis. 

Gluco = glucose

neo = new

genesis = make

so essentially, your body is making new glucose. 

At first, your body isn’t used to this, so you feel like crap. I know I did for a couple of weeks. Headaches mostly. Some friends were telling me I had to change my diet because I was going through acidosis and it was really bad but others were saying it’s the norm and to stick with it. Even if it is expected with a low carb diet, some of my close friends had very valid points -- that I’m a medical student and my job right now is to study and do the best that I can. If my headache is preventing me from doing that (I would take loads of naps instead), maybe it wasn’t the best idea. I implemented a little more carbs into the daily intake and adjusted it so the adverse affects wouldn’t be so drastic. Anyways, the reason your body feels like crap is because it needs to readjust, leading to selective activation of the pathway needed. Different routes are required to get around the exergonic, irreversible steps, which is why when you change your diet to a low carb one or if you’re fasting or if you skip breakfast, you might feel dizzy and lightheaded. 

Moral of the story: eat right, be smart, hydrate, and I understand. 

[nerdspark]

7-8 Butterflies in your stomach

It’s a thing. I mean it’s a real thing. Like it isn’t just that you’re nervous and excited and you’re just experiencing this overflow of feelings emotionally. There’s something happening within your body physically that causes you to feel this sensation and it has to do with your GI system. More specifically, your gallbladder. 

Your gallbladder is associated with your GI system and all the organs we’ve touched on so far because it hold the bile that you need to aid in digestion of the food in your small intestine. The bile needs to be released from the gallbladder and secreted into your duodenum (the initial portion of the small intestine), and your body tells it to do so in two ways: hormonally and neurally. When your body senses fatty acids (from fat in your food) in the duodenum, it stimulates the enterocytes to secrete a hormone called cholecystokinin (or CCK). CCK acts by contracting the gallbladder and relaxing the Sphincter of Oddi, which is at the connection of the duodenum and the gallbladder. In doing so, it released the contents of the gallbladder (the bile) and sends it along, past the sphincter of Oddi, into the duodenum. Neurally, what occurs is something called the vagovagal response. This is when the duodenum senses stretch as the food comes in, nerves are activated and the vagal afferent nerves act on the muscarinic receptors of the gallbladder. The receptors sense the activation and this leads to contraction of the gallbladder. 

This is when the fun comes in. These contractions of the gallbladder are essentially what you’re feeling when you have the “butterflies in your stomach” sensation. Strong emotions can circumvent the vagovagal response and activate the vagal afferent nerves leading to the same gallbladder contractions. 

So there you have it. Maybe you don’t actually love them. Maybe your body is just telling you that you’re scared -- to run away. I jest. You’re fine. It’s me with the problem seeing as I’ve never had butterflies for someone in my life...

[medschool-motivation]

[nerdspark]

What we talked about in class today. 

[nerdspark]

7-7 In front of buttholes

Ever wonder what it was called? The portion of skin in front of your anus but behind the vagina/scrotum? Probably not, if you’re a normal human, but I’ll tell you anyway. It’s the perineum, and insignificant though it may seem, it actually ended up there is sort of an amazing fashion. (It’s also the part that is cut during vaginal deliveries if the baby’s head is too big – look up episiotomy).

During development in general, there are often septums that divide tubes so that the body can separate and categorize parts into what they need to become. In GI development, this is especially the case because our GI system is essentially one long tube from mouth to anus. The gut tube is divided into 3 sections: the foregut, midgut and hindgut, which are the superior, middle and end portions, respectively. 

In the foregut, we see this idea of a septum when during development, a septum forms to divide the trachea (your airway) and the esophagus (your food passage-way). This septum is called the transesophageal septum. If this septation is incorrect, the esophagus and the trachea can be connected, which is called a transesophageal fistula, or the esophagus can be blocked, not permitting food to continue down the GI tract. This is called esophageal atresia. 

This septation can also go wrong at the end of our GI tract – the hindgut. Here, the cloaca, is a cavity that separates into the anorectal canal and the urogenital sinus through the urorectal septum. The tip of the septum becomes the future perineum, which brings us back to the beginning of this post – the part that is in front of your anus. Defects in the cloaca or the urorectal septum can lead to a condition called rectourethral or rectovaginal fistula. Here’s an image to help you better understand. Don’t worry, it’s a cartoon version. I’m not subjecting you to real buttholes. There are enough of those in this world… lol.

In another condition, if the cloacal membrane doesn’t break down completely by the end of development, ther eis incomplete perforation of the anus. This condition is called anal stenosis. In other words, these patients would be full of crap. Literally. 

[medschool-motivation]

“The possession of knowledge does not kill the sense of wonder and mystery. There is always more mystery.” - Anais Nin

[nerdspark]

I pray that my love for learning will never falter and the sense of wonder will never diminish.

[gomitablood-blog]

[nerdspark]

7-5 Halitosis aka bad breath

I’m TERRIBLE about smells. Can’t be in a room that’s stuffy or smells weird. Yesterday for lunch, a friend and I went out for sushi and I was a bit put off because the smell was just a little off. Still, the company and conversation kept my mind off it and I managed. 

There are some times, though, when you aren’t in control anId you just need to manage. For example, when you’re speaking with someone who just seems to have really bad breath, and no matter how distant you try to be, it just hits your face like a truck. I remember this one time, I was sitting next to a classmate who was whispering during class, and you guys know how the whispering makes it even worse? I tried to minimize our conversation and hoped he’d think it was just because I was just trying to pay attention to the lecture. I might have come off as a bit cold, haha. 

I talked a little about how even before we start eating, the body prepares itself for the food in ways like secreting saliva, which contains enzymes to break down the molecules in the food when it enters the mouth. The cells that secrete saliva are called acinar cells and they’re located in different locations in our mouths. Most of them (70%) are in the submandibular gland, 25% in the parotid and 5% in the sublingual. These glands are important not only in secreting the saliva because the saliva contains enzymes that help break down the food, but also because saliva can help contribute to the flow of the food and its particles. Imagine if you had some of your last meal sitting in the nooks and crannies of your mouth -- if you’re interacting with someone you’re trying to impress (or not repulse), no bueno. Saliva also contains protective enzymes such as lysozyme and IgA binding proteins which help clear bacteria and reduce bacterial growth. 

If you’re ever interacting with someone whose breath just seems to be knocking your socks off, keep in mind, though, that it may not be entirely their fault. There is an autoimmune disorder called Sjogren syndrome (pronounced Show-grin) that causes the body to destroy the glands that produce saliva. As you might assume, this means that the person can no longer produce saliva (or salivary production is reduced) leading to a decrease or lack of saliva and its many benefits. Similarly, xerostomia is a fancy name for dry mouth, and in this case as well, the person may not have adequate salivary production even if their glands are present. I spoke in one of my previous posts about an anticholinergic drug called atropine, but I’ll remind you just in case. Anticholinergic means that it blocks the cholinergic effects of the parasympathetic nervous system (which secretes ACh, or acetylcholine). The PNS activates secretions of the glands so a drug that blocks this effect would decrease secretions including salivary secretions. Recall that when the PNS is activated, kallikrein is released, which leads to vasodilation d/t bradykinin release, and the vasodilation causes an increased in capillary hydrostatic pressure, leading to increased secretion. Thus, all three of these reasons COULD be why you have to endure stinky breath while communicating with other humans, so show a little grace. Most likely, though, they probably just forgot to brush or decided to thoroughly enjoy their last meal at the expense of your comfort. Maybe just carry a pack of gum with you? 

[nerdspark]

7-4 Cindy Is Kinky So She Fornicates More Often

My way of learning CAC: Citrate Isocitrate alpha-Ketoglutarate SuccinylCoA Succinate Fumarate Malate Oxaloacetate. I suppose you can also use “Citric Acid Is Kreb’s Start For Mitochondrial Oxidation” (Acid = cis-Aconitate) but the dirty ones always stick better, no?

When making succinate from succinyl-CoA, substrate level phosphorylation occurs. This means that the thioester cleavage (breakage of a bond, not boobs) is coupled with the formation of an energy source aka GTP in this case. Also, succinate dehydrogenase facilitates the reaction from succinate to fumarate, but this is the only enzyme that isn’t soluble in the matrix. Thus, it’s bound to the inner mitochondrial membrane (where the ETC is). 

One learning point and I’ll try to make it relevant. Picture mom trying to make chocolate chip cookies. You have a cookie dough with chocolate chips on the kitchen counter, so what is likely to happen? Either someone will eat the chocolate chips as a chocolate snack, or mom will bake the cookie dough. It’s not likely that the cookie dough will last long and stick around for a while on the kitchen counter (provided that there are no other better alternatives because really, what can be better than chocolate? Ya feel me? and also, mom would want to bake the cookie dough and not just leave it lying around). The last product of TCA cycle (or the first, depending on how you look at it) = OAA = oxaloacetate. There’s actually only a SMALL amount of this in the mitochondria. In our analogy, OAA = chocolate chip cookie dough. The reason for this minimal amnt being that the forward reaction of OAA to citrate is SUPER favorable (so mom is like on a baking spree) and the reaction with OAA as the product isn’t. That latter reaction uses malate as the substrate and the thing with malate is that when there is a high concentration, it can be exported and be used in gluconeogensis to make glucose (this would be your sibling eating all the chips before it can be used by mom to make cookies or the chocolate chips having been used to bake something else previously). This means that with malate exported (inside brother’s belly or in the chocolate chip muffins), it’s less likely to make OAA (chocolate chip cookie dough), and even if OAA is made, it’d likely be taken and used as a substrate to make citrate (chocolate chip cookies made by mom) since it’d be when pyruvate is available to bind. 

Point of the story: not a lot of OAA around just like chocolate chip cookie dough. Either the chips got used for muffins or eaten (exported to be used in gluconeogenesis) or if there was some, it is used up to make the final chocolate chips cookies. 

WOW. I wrote an entire story about CHOCOLATE CHIP COOKIE DOUGH. This keto-diet....not fun at all. If you are like me and any other normal being around, you know that carbs = life and chocolate = life and so right now, maybe I’m dying. Jk. Only on the inside. 

[nerdspark]

7-4 PDC and lactic acidosis

Let’s start with the PDC, shall we? This stands for Pyruvate Dehydrogenase Complex. Now, what does that do? Essentially, it’s important because it connects glycolysis (the breaking down of the glucose to pyruvate) and the citric acid cycle (aka Krebs aka TCA cycle, etc) where the pyruvate that was the product of glycolysis is used to be a substrate for the reaction that occurs as a step in Krebs. 

Why is PDC important? PDC takes the pyruvate and converts it into a form that can enter CAC. So when there is a deficiency of PDC, the pyruvate cannot enter into CAC, which leaves a build up of pyruvate. Because of this build up, the body does what it knows how to under these circumstances and converts it into lactate instead. We spoke earlier about how the pyruvate can be converted into CO2+H2O, lactate or ethanol. Because we, as humans, don’t have the ability to ferment (that’s for yeast and making wine), we do the only other method we know how -- using lactate dehydrogenase. This means there’s a build up of lactate leading to lactic acidemia or lactic acidosis (one of the terms they throw around in Grey’s / House). This can present clinically as muscle aches, burning, nausea... The most common reason for this is intense exercise (so something that’s definitely NOT a risk for me...). Other causes can be liver failure, heart failure or chronic alcohol use. I’m totally down for a few drinks but as I learn more and more about our physiology, the more I realize that there are really no physical benefits to alcohol -- it messes with your sleep, it messes with your kidneys, it affects your GI system.. Still, I’m not going to say no to a glass of wine here and there. That would be ridiculous. Especially in this med school environment. If I’ve learned anything this past year, it’s: 

Work hard. Play harder. 

SO back to the alcohol. Sorry for the tangent. Blame it on the a-a-a-a-a-alcohol. Lol, lame. Anyways, the prosthetic group needed for pyruvate dehydrogenase (the PDC we’ve been talking about) is TPP (thiamine pyrophosphate). Anything in there that sounds familiar? Yep, thiamine. Aka, vita B1. Alcoholics can have a deficiency in thiamine which would lead to a deficiency in the pyruvate dehydrogenase required to convert pyruvate to enter the CAC, which means a build up of pyruvate, a conversion of it into lactate, and back to the point of lactic acidosis. And there you go. Now you (sort of) know what they’re talking about whenever that pretty doctor mentions that on House. 

See, this is really cool and all but it’s only the FIRST step. Actually, it’s not even the first step of the CAC. It’s the step that allows the first step of the cycle to happen. Pretty crazy, huh.

[nerdspark]

7-3 Glycolysis & Glycogen

UGH. Biochem. How to make this fun? It’s still amazing though. Even though I don’t really care for the little bonds and details, it amazes me that it’s the little things like that that matter in life. A smile here and a genuine “how are you?” there can go a long way and we might not even know. It might be a stretch, but I’m looking at the little bonds and maneuvers between the molecules during these conversion to be exactly that. They need to rearrange and let go sometimes in order for the reaction to work - for the reaction to move forward so that they can ultimate become and make what the body needs. It’s for the greater good. 

So glucose. This has not only been my enemy in the biochem sense that I don’t want to learn all the mechanisms, pathways and steps, but also in the sense that I wish my body wouldn’t store the extra as glycogen... I started this keto-diet that made my body go through acidosis (clinical presentations of headaches, body injuries, etc but that’s another story for another time about my clinical manifestations that I was going through WHILE we were learning kidney. Fun stuff). 

Glucose is converted into G6P (glucose-6-phosphate) which can be stored as glycogen when we don’t need the energy. When energy is required, however, we go through a 2 stage long ass process which results in pyruvate and some ATP. The first stage requires energy in the form of ATP but the 2nd stage generates it. There are 10 steps in total sot eh first 5 are part of phase 1 and the 6-10 are part of phase 2. In phase one, steos 1 and 3 require ATP. The 1st steo is glucose + ATP --> G6P + ADP by hexokinase, and the 3rd is F6P + ATP --> FBP by phosphofructokinase. Both of these phosphorylation reactions require an ATP, which results in 2 ATPs used during phase I. In step 4, when FBP is broken into 2 products of DHAP and GAP by aldolase, the DHAP is converted into GAP in step 5 in order to prevent waste. If both products become GAP, then there only needs to be one pathway. Thus Triose-P isomerase changes DHAP to GAP even though DHAP is favored 20x more. 

Then comes phase II: the energy yielding phase. How am I going to remember all the enzymes and the reactions of all these steps???? Sigh. It’s literally like that one grueling semester of biochem from undergrad is like a few slides of med school material we’re just expected to know / memorize in a hot sec. But it’s ok. We got this. So, the ATP yielding steps are 

7. 1,3-BPG + ADP --> 3PG + ATP by phosphoglycerate kinase (Which also facilitates step 8 of 3PG --> 2PG)

10. PEP + ADP --> ATP + pyruvate by pyruvate kinase

both these steps are substrate-level phosphorylation which is when the inorganic Phosphate is transferred onto the ADP to result in ATP generation. 

Overview with more deets: 

So then at the end, we have pyruvate. What happens to it? Well, it depends. Most of it can change into CO2 and H2O and help the cycle of oxidative phosphorylation in which NADH is converted back into NAD. It’s not super effecient but the NADH to ATP still works because the energy lost is used as heat to keep the body warm. I’m not complaining about that. If there isn’t enough O2, however, we use good old anaerobic glycolysis and convert pyruvate into lactate aka homolactic fermentation. In yeasts: alchoholic fermentation: pyruvate --> ethanol via oxidative decarboxylation. 

Whew. That was a lot of biochem jargon so here are some clinical pearls. Of course, these are my favourite. The most clinically relevant. There are other hexoses that fit into this metabolism chart. Galactose, mannose and fructose are all hexoses and can be converted in order to somewhat follow this pathway. Galactose enters at step 1 as G6P, mannose and muscle fructose enter at 3 as F6P and liver fructose as GAP in step 4. In the case for fructose, if there is a deficiency in aldolase, this leads to increased F1P which depletes ATP, the inorganic phosphate and leads to liver damage. F1P also inhibits the glycogen breakdown and inhibits gluconeogenesis which results in hypoglycemia. In the case of galactose, G1P can be converted to G6P but if there is a deficiency in galactokinase which converts galactose into G1P, there will be a high galactose concentration, resulting in cataracts. Also, in the case of deficient UMP transferase, there will be an increased galactose-1P which can result in mental retardation and liver failure. The picture below might help with the case of galactose. 

Tl;dr: lots of steps, know them all, understand how build up of something d/t loss of enzyme can lead to clinical findings.

[nerdspark]

7-2 Intro to GI physiology

Today was our first day back from spring break -- we start Unit 7: Gastrointestinal. Shit’s going down... Literally. #punintended 

So here’s a “quick” recap of what we learned today. Basically, your body starts digesting and preparing yourself to absorb and make sense of the nutrients that you intake even before you’re even aware of it. When your brain senses that your body will get food, it preeminently prepares itself by activating the salivary glands to be able to break down the food as soon as it enters your mouth -- pretty cool, huh? There’s this concept called peristalsis that you may have heard of back in middle school science. It’s the way your GI system keeps your food moving in one direction. This is facilitated by the use of sphincters. The 4 we need to know are Upper Esophageal, Lower esophageal, Pyloric, Ileocecal, and Internal & External sphincters. The UES is the only striated, skeletal muscle sphincter, and it prevents backflow into the mouth from the esophagus. the LES is from esophagus to stomach. A defect at this point would result in heart burn or acid indigestion. The pyloric is from the stomach to the duodenum, and any clinical correlations at this point would be gastritis, ulcer formation or perforation. The Ileocecal sphincter separates the ileum and the cecum (look at the name “ileo-cecal”) and this separates the ileum from the colon so prevents the backflow there. If there IS backflow, this could be bad and result in IBS which presents clinically as bloating, pain due to bacterial overgrowth in the small intestine. The internal and external sphincters, of course, control the elimination of the waste products. It takes about 3-5 hrs to move food from the pylorus to the ileocecal valve. The gastroenteric reflex enhances the motility and secretions, the gastroileal reflex triggers passage from Si to LI and the enterogastric reflex decreases motility to inhibit chyme from entering the duodenum. This is so that the chyme stays in the stomach to optimize digestion and absorption. 

All this is pretty amazing as we take in a SHIT TON of fluid per day and excrete a minimal amount in comparison. When you take in fluid, your body also produces it (like in the form of saliva) but you only really excrete about 100mL/day. This means that the rest of it is absorbed back into the blood. We ingest about 2L and our body produces about 8L. 

Histology: 

All of this is made possible by the various structures that line the GI tract. From the mucosal surface to the surface facing the blood is as is: 

1. epithelium - secretory and absorptive

2. lamina propria, 

3. musculrais mucosae - smooth muscle that helps the infolding to promote absorption by enhancing the mixing and contact of chyme with the villi

4. submucosa

5. submucosal plexus - in SI and LI

6. circular muscle

7. myenteric plexus - extends from esophagus to rectum

8. longitudinal muscle

9. serosa

The plexuses are important because they make up the Enteric Nervous System that is essentially the “minibrain” of the GI system. Because the PNS is essentially the “rest and digest” system that we all learned about in high school, it actually increases GI motility and secretions whereas the SNS decreases the GI system activation. The vagus nerve innervates the proximal 2/3 and the pelvic nerve innervates the distal 1/3. ACh acts as the major NT to activate the pre and post ganglionic fibers which lead to the release of substance P and VIP, both of which are inhibitory. This promotes digestion and absorption and results in all the digestive functions we know of - increased salivary, pancreatic, gastric acid secretions, contraction of the smooth muscle wall and relaxation of sphincters. On the other hand, SNS uses norepinephrine as the major NT to produce inhibitory effects on the excitatory cholinergic neurons via presynaptic inhibition. This inhibits digestion and absorption and diverts blood away from the local vasculature. 

in the myenteric plexus, there are these important cells called the ICCs, which stands for the interstitial cells of cajal. These cells are the GI pacemakers. They produce electrical activity in the form of slow waves and spike potentials. Slow waves are seen in the resting membrane potential but spike potentials are during the plateau phase when the electrical threshold of approximately -40mV is reached. Only when there the APs are generated at the peaks of these slow waves do we see contraction. These APs are stimulated by PNS, stretch and ACh and are hyperpolarized by norepi and sympathetics.

The myenteric reflex helps contribute to the idea of peristalsis. When the bolus is pushed along the GI tract, the portion downstream to it relaxes to accept the incoming food whereas the portion upstream contracts to help move the bolus along and towards the cecum. This is called the “law of the gut”. The circular and longitudinal muscles that I aforementioned come into play here. The circular muscle contract upstream (ACh) and relax downstream (NO/VIP) and the opposite occurs in the longitudinal muscles, which relax upstream and contract downstream. Here’s an image that helped me: 

In the physiological state of te ileus, there is an absence of motility in the SI and LI. In pathological ileus, the inhibitory neurons are too active and continually suppress the myogenic activity. This leads to a cramping pain, nausea and vomiting. This is common after surgery, anticholinergic or opiate drug treatment. This ties us back to the PNS and SNS conversation from earlier. Anticholinergics are going to inhibit the ACh that would normally activate the PNS which increases GI activity. Thus, anticholinergics such as atropine will inhibit the PNS and lead to the clinical presentations of cramping pain and nausea. 

[wheresonichedgehogwnt]

You know what bugs me about discussions of physician burnout and resiliency?

They seem to be based on the idea that people who completed four years of medical school and however many years of residency and worked hard and sacrificed and were constantly pushed out of their comfort zone and didn’t see their family or friends as often as they wanted and made new friends and communities wherever they found themselves, and did this their entire young adulthood, aren’t actually resilient and that the issues they’re facing can be fixed by meditating for five minutes a day and taking a walk at lunchtime.

First of all, since when did physicians get lunchtime?

Second of all, since when did becoming a doctor in the first place not take a lot of resiliency, so why do people assume physicians, who have already demonstrated themselves to be resilient, are the ones who need fixing?

[md-admissions]

Couldn’t agree more. Say it louder. Physicians are being blamed for being human in an inhuman system. It’s up to EVERYONE to realize this is a serious issue driving physicians to suicide and abandonment of a passion they once loved. And it’s on all of us to say this is not how we want healthcare delivered.

[telep0rt]

Yes. Yes. Yes.

I get really mad when I sit through those burnout discussions because I feel very blamed.

It is not the fault of someone who works 80-100 hours a week, never sees their family, and puts 100% of their emotional energy into a job that takes and takes from them that they feel burned out. So DON’T tell me to “practice mindfulness” or “do more yoga” or “make time for my family” – like I could somehow fix myself.

I am strong. As physicians and trainees we are incredible to fight through what we do every day. So let’s change the conversation – we’re not burned out. We’re taken advantage of. Our humanity and our love of our jobs is taken advantage of.

Don’t tell me to take a walk. Tell the system to allow me time for one.