Biliary Tract Diseases | Clinical Medicine

0:07what's up Ninja nerds in this video

0:08today we're going to be talking about

0:09biliary tract diseases there's a bunch

0:11of things to discuss within this and

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0:47right let's talk a little bit about this

0:49biliary track diseases so biliary tracks

0:53it's the basic anatomy of it is that

0:55you'll have your common bile duct here

0:58right so we have here what we're going

0:59to abbreviate this the the common bile

1:03duct right and then here we'll have the

1:05gallbladder here we'll have What's

1:07called the cystic duct and then here you

1:10have What's called the common hepatic

1:13duct this would be your gallbladder and

1:14these are going to be some of those

1:16smaller hepatic ducks like your right

1:18and left hepatic duck which are break

1:20into smaller

1:21canaliculi when a patient has a disease

1:23of these biliary track system what

1:26happens is it's usually due to one

1:29primary cause by far the most common

1:30cause and that's these dang Stones man

1:33these little gall stones if you will

1:35that kind of can get shot out of the

1:39gallbladder and it can get stuck in the

1:41cystic duct it can get stuck in the

1:42common B duct those are the two most

1:44common areas that these Stones can

1:46really get lodged in and can wreak havoc

1:48on the biliary system so the question is

1:51chasis is really a term for these things

1:55called gallstones it's that AKA gall

1:58stones homie that's really what it is

2:01it's these little stones that are stuck

2:02within the actual particularly in the

2:04gall ladder and then what happens is if

2:07it's small enough it can fling it out

2:09maybe gets stuck in the common bow duct

2:11or it gets stuck in the cystic duct

2:12we'll talk about what those diseases are

2:14in a

2:15second thing I want you to understand is

2:17when a patient comes in with a bilary

2:19tract disease yes by far the most common

2:22com complaint in classic finding is

2:24right upper quadrant abdominal pain and

2:25maybe some jaundice potentially but

2:27right upper quadrant abdominal pain is

2:28the big one to think about for bilary

2:30tract diseases but let's understand real

2:32quick how does cholithiasis actually

2:35form what are these like stones made up

2:37of there's three types of stones so by

2:41far when we talk about these it's going

2:44to be cholesterol Stones man they make

2:46up pretty much most of them they're like

2:4880% of your stones and then it's pretty

2:50much downhill here from here 10% maybe

2:5310% here not too much for these so we

2:56won't go too crazy remembering these but

2:58do think about them if they come up on

3:00the actual exam but cholesterol stone is

3:03by far going to be one of the most

3:04common types of gall stones so you have

3:06to think what are the causes we don't

3:08have like specific causes we have risk

3:11factors that people may exhibit in the

3:14clinical vignette that suggest oh this

3:15is their likely cause of their

3:17cholesterol related

3:19gallstones so we use aonic and I'm not

3:22trying to be mean this is literally how

3:23it's commonly you know remembered is

3:25that these patients are usually female

3:31fat

3:3240 they're

3:35fertile fair

3:38skinned and they have a family

3:41history of some type of biliary tract

3:45disease now all of these things what

3:47they do is in some way shape or form is

3:51they increase the amount of cholesterol

3:54that's present within bile right and you

3:56know that bile is made up of cholesterol

3:58it's made up of bile salt it's made up

4:00of

4:00phospholipids if you increase the amount

4:03of cholesterol within the actual bile

4:06it'll cause it to Super saturate and

4:08make these nasty stones and so that's

4:10one of the reasons we get these Stones

4:13is that there's way too much cholesterol

4:14within the bile and it stimulates Stone

4:17formation right so there's one way

4:20cholesterol Stones female fat 40 fertile

4:22fair skinned family history and again uh

4:26if I miss one here 40 so again that's

4:28going to be the big thing there to

4:29remember for the particular risk factors

4:31associated with cholesterol Stones the

4:33other one is these black pigmented

4:34Stones black pigmented Stones is usually

4:36primarily seen in a disease called

4:39homolysis so homolysis is whenever

4:42you're popping open these red blood

4:45cells you know red blood cells they

4:46contain a molecule called Billy Rubin

4:50and uh Billy Rubin especially the

4:52unconjugated form of Billy ruin we'll

4:55put here we'll put like un conjugated

5:00this is actually G to spill

5:02out of these red blood cells now the

5:06problem is is when you have a ton of

5:08this unconjugated Billy Rubin when it

5:10gets incorporated into the bile it

5:12causes the bile to again become more of

5:15a super saturated solution and increases

5:17the risk of these Stones forming but

5:19they're really pigmented and so that's

5:21why you get these black pigmented stones

5:23but the same concept exists if there's

5:26too much of this Billy Rubin that gets

5:27released because of homolysis then

5:30you'll end up with stone formation and

5:33these are going to be very specific type

5:35of pigmented Stones that'll arise here

5:38and then the last one is brown Stones

5:41these are infected pigmented Stones I

5:44just kind of gave away the answer you'll

5:46see this in patients where they have

5:48infections and if they have an

5:51infection very specifically like you can

5:54see this a lot and what happens is when

5:56you have tons and tons of bacteria when

5:58you have infections you increase the

6:00amount of bacteria that's

6:02present and what happens is if I

6:05increase the amount of bacteria that may

6:08be in some way connected to the biliary

6:10tree these bacteria release a lot of

6:14these bacterial enzymes and so then

6:18there'll be the increased production of

6:20these little guys here which are called

6:23these bacterial prot protolytic enzymes

6:26now these bacterial enzymes what they do

6:28is they chew up some of the bio and make

6:31specific molecules that really help to

6:34increase the super saturation and

6:36precipitation and form these nasty

6:38stones that we can see all right and

6:41that's the same concept is that you're

6:42going to get stones out of these bad

6:44boys so either way what are we able to

6:47surmise from all of this regardless when

6:50a patient has biliary tract disease it

6:54often starts with chasis gall stones

6:57stones that form within the gallbladder

6:59they can flick out into the cystic duct

7:01common bile duct what are they made up

7:03of depends upon the type often time it's

7:06this one remember the 6fs if you can't

7:09remember that one you think about the

7:10actual black ones think about homolysis

7:12if you think about the brown ones think

7:13about infected Stones now when a patient

7:17has gall stones you can have them and

7:20sometimes be completely asymptomatic

7:21never even know that you have them but

7:23every now and then a patient may

7:25experience this thing called biliary

7:26colic super common with kolasis

7:30imagine one of these Stones just so

7:33happens to ball valve back and forth so

7:38it's here free gets stuck in the cystic

7:40duct flips back into the actual Lumen

7:43flips back into the cystic duct flips

7:45back into the Lumen the reason why this

7:48would happen is usually a patient has a

7:50fatty meal so they have some type of

7:53really really fatty

7:55meal and what happens is that increases

7:58the production of an you know hormone

8:00it's called

8:01kisinin kisinin causes

8:05gallbladder

8:07contraction and if the gallbladder

8:10contracts down and pushes one of those

8:13stones on into the cystic duct or clamps

8:17down on it that's going to precipitate a

8:20lot of pain and so often times this will

8:23really precipitate a terrible pain and

8:26so fatty meals increase chinin increase

8:29Gull Bladder contractions and increase

8:31this pain that's usually in some ways

8:34intermittent okay it's because this

8:37thing isn't completely stuck it's just

8:39ball valving in and

8:41out now with that being said when a

8:45patient has

8:47cholithiasis they may present with

8:49bilary colic or be completely

8:51asymptomatic but what happens if this

8:53Stone gets flicked out and gets stuck in

8:55the cystic duct or it goes out here and

9:00gets stuck in the common bow duct and it

9:02doesn't move it doesn't flip back to

9:04where it was originally what's the

9:06problem let's come down and talk about

9:07that so now we got one of these stones

9:10and it got out there and it's about to

9:12wreak havoc so if the stone gets stuck

9:15in the cystic duct so here's our Stone

9:18it gets stuck in the cystic duct doesn't

9:19matter cholesterol uh Black Stone or if

9:22it's some type of uh brown stone doesn't

9:23matter it got stuck here in the cystic

9:26duct if it gets stuck in the cystic duct

9:29what's the underlying problem here well

9:32it's pretty straightforward you're not

9:34able to move bile and other substances

9:37out and so this is going to cause this

9:40back pressure to rise here now as this

9:43occurs what are you going to see you're

9:45going to see a massive increase in back

9:49pressure and that back pressure is going

9:51to cause gallbladder distension and when

9:54that puppy gets nice and big and swollen

9:57you palpate that thing these patients

9:58are going to scream so that's going to

10:00be one big thing so increased back

10:02pressure I done ski a step here back

10:05pressure causes an increase in the

10:07distension so this probably going to be

10:09swollen all right that's one

10:13thing the other thing is that you're

10:15going to have bacteria there this is

10:17just a part of your Flora man it's a

10:19part of your GI Flora in general so

10:21there's going to be bacteria here you

10:23can't avoid that but if I can't move it

10:26along cuz you know where does the

10:28biliary duct eventually dump into it

10:30combines with the pancreatic dump to put

10:31it puts it into the actual um the small

10:34intestine so it can be moved along if it

10:37stays in one place it'll cause infection

10:39and so the other problem here that can

10:41arise potentially is not only increase

10:43back pressure but you can have increased

10:46bacterial

10:47colonization so now we can have an

10:49increased amount of

10:51bacteria that are

10:53colonizing and then these puppies can

10:56cause inflammation

11:00and infection and then you got a recipe

11:04with the combination of these things

11:06dude you're going to end up with a nasty

11:10nasty problem such as

11:13kystis now this thing will start to

11:16become inflamed so it's going to be nice

11:18and red hot it's going to be

11:21distended and it's going to cause so

11:24much pain localized to that particular

11:26area the other thing is that it's going

11:28to become infected this this actual

11:30gallbladder become infected and so we'll

11:32talk about some of the complications

11:33that can arise with that often times

11:34these patients classically have right

11:37quadrant pain and they often times have

11:39a elevated white blood cell count

11:42sometimes but one of the other big

11:43things is that not only they have right

11:44upper quadrant abdominal pain when you

11:46go and you take and you do what's called

11:48um a press down on the actual right

11:51Arbor quadrant and you have them take a

11:52deep breath in they're like they can't

11:54finish their deep breath because it

11:56hurts so bad it's called a Murphy sign

11:59so right a quadrant abdominal pain with

12:01a positive Murphy sign is usually

12:03classic of patient developing

12:05chitis all right so cystic duct chasis

12:10gets boom Lodge there can't go any

12:12further what if it goes

12:15further and it gets lodged here what's

12:18this one this is the

12:20CBD the common bile

12:23duct now if it gets lodged here in the

12:26common bile duct again same thing is

12:28going to happen here you're going to

12:29cause a back pressure this thing is

12:32going to get kind of distended all of

12:34this proximal to the actual

12:37obstruction now here's the thing two

12:39things will happen you'll get some of

12:41this distension if you will of the

12:44actual biliary duct but here's the more

12:46important thing that's really helpful

12:48often

12:50times there's molecules that are present

12:53in the bile that are very specific and

12:55help us to identify that um under lab

12:58values

13:00and so one of the molecules that's

13:01commonly present in the bile is called

13:04alkaline

13:05phosphatase another

13:07one is called and we already should know

13:10this one Billy Ruben Billy

13:13Ruben and here's what's really

13:15interesting about this one the alkaline

13:18phosphatase will be super elevated

13:19because normally again this is supposed

13:21to move downwards you're not moving it

13:24downwards this is being obstructed at

13:26this point here just like it's being

13:28obstructed at this point here here so

13:30this will build up and leak into the

13:31bloodstream so you test it you'll see

13:33that elevated but here's the other

13:35helpful one this one's going to be

13:36elevated you won't see Billy Rubin

13:37generally elevated because it's not

13:39obstructing the flow of bile downwards

13:40here it's obstructing it here so because

13:44of that you know it's one of the common

13:45manifestations that you'll see primarily

13:47in chasis that you won't see in colitis

13:50jaundice you also generally won't

13:53see that massively elevated alkaline

13:57velocitas the other thing is that again

13:59if you distend all of this biliary duct

14:02tree so you are going to get some degree

14:05of um increased back pressure let's say

14:09within the biliary duct and then the

14:12common patic duct and that will cause

14:15distension but in this part yet you

14:19haven't allowed enough bacteria to

14:22colonize so there hasn't been any

14:24bacterial colonization and infection

14:26proximal to that obstruction and that's

14:29really important to remember so there is

14:31no infection or inflammation in the

14:33sense that there's bacteria that are

14:35causing it it's going to be a little

14:36distended because of the actual

14:37obstruction but there is no infection of

14:40that bilary fluid if I tested that fluid

14:41it's not going to be infected if I test

14:43this next one's fluid it will be

14:44infected that's the big difference here

14:46so you're going to have right upper

14:47quadrant pain jaundice and elevated alos

14:49right upper quadrant pain no elevated

14:51alos

14:52jaundice we come to this last one here

14:55this is the scary one this is the one

14:56that will kill people it's called

14:57ascending colitis all right the concept

15:00here is the same thing and sense that

15:03you know how like um

15:05cholithiasis you can have a stone that

15:08gets stuck in a cystic duct like can

15:09ball valve but you don't get an

15:11infection and all that kind of stuff

15:12like that you get the bilary colic

15:14that's one of the big difference between

15:15chasis and Colitis one of the big

15:18differences between kocal lithiasis and

15:20ascending colitis because they're both

15:21stuck in the same place they're both

15:22stuck in the common bile duct the CBD

15:25what's the big

15:26difference well same thing

15:29you're going to get all this back

15:30pressure all that bile is going to

15:32circulate backwards and you're going to

15:35get the

15:36elevation real scary elevation and Al

15:39Foss real significant elevation and

15:42Billy Rubin which will

15:44precipitate jaundice right so these are

15:48going to be

15:49definitely elevated and you're going to

15:52stimulate the formation of jaundice here

15:55so so far

15:57similar big difference is is that all

16:00this

16:01bacteria that is going to be forming

16:05proximal to that obstruction are going

16:07to start colonizing infecting the

16:09biliary fluid and the biliary

16:12tissue now you have infection and

16:14inflammation of the bilary tract and the

16:16thing is is that some of that infected

16:18material can start spreading into the

16:20bloodstream and cause sepsis and so

16:22we'll talk about that a little bit in

16:24the complications but the big kind of

16:26varying differences here is that you'll

16:28get two things

16:29you

16:31get an increase in back

16:34pressure and so you'll get that same

16:36thing you'll get that distension of the

16:38common bow duct and common aaic

16:41duct but one of the delineating kind of

16:44points here is that you'll also have a

16:48lot of bacterial

16:49colonization proximal to that

16:52obstruction and then because of that you

16:56will

16:57develop infection

16:59of the biliary fluid and the bilary

17:01tract and so I think that's one of the

17:03real important differences to delineate

17:06here is that this will trigger this

17:09which is the same in that one but this

17:11one is really the difference here okay

17:14and we'll talk about some of the true

17:16key complication like differences that

17:19are key between these two but again

17:22right quadron abdominal pain right up

17:24quadron abdominal pain jaundice jaundice

17:27infection no infection

17:29both extended this

17:32one stuck in the cystic duct not in the

17:35common bow duct right upper quadrant

17:37pain Murphy sign will have infection

17:40chasis May ball valve between the cystic

17:43duct there will have pain but it's more

17:45of a ky pain in that rer quadrant now

17:48that we've defined that let's now to go

17:50into the complications of each one of

17:51these all right guys so now on to the

17:53complications of billary tract diseases

17:55all right so we talked a lot about the

17:57patho fiz behind develop Ving gallstones

17:59or col lithiasis we talked about the

18:02pathophysiological and definitional

18:05differences of between all the bilary

18:07tract diseases and then we talked about

18:09some subtle differences and we'll repeat

18:11those again in this part of the lecture

18:14but what I want to talk about now is

18:16when you have a patient who comes in

18:17with ROP quadron abdominal pain which is

18:19often times that classic finding they

18:21may or may not have jaice depending upon

18:23which one it is you want to start

18:25thinking about the terrible things that

18:27can go wrong in these diseases

18:29so first one is cois atis what do we say

18:31it's a gallstone stuck wear in the

18:33cystic duct now we said that what

18:36happens is is in the scenario you

18:39develop a lot of back pressure right we

18:41said that that's the classic finding is

18:43that you're going to have lots of back

18:44pressure which causes an intense amount

18:46of

18:47distension so whenever you have this

18:49super high back pressure what do we say

18:53is one potential finding in combination

18:57so you have high back pressure

18:59which is going to trigger that

19:00distension you're also going to have a

19:02lot of we have bacteria we'll use this

19:05kind of color here they kind of colonize

19:07and accumulate here in this particular

19:09area and that's going to cause again

19:12this increase in bacterial colonization

19:15so you're going to have lots of back

19:16pressure and you're going to have lots

19:17of bacteria and this is going to trigger

19:19an infection an inflammation of this

19:22gallbladder so it's going to be super

19:24inflamed and super angry so super

19:27inflamed

19:30gallbladder now when that Gall bag is

19:33all kinds of inflamed the classic things

19:36that you will see in these patients is

19:38we already kind of defined it where is

19:41this kind of located that inflamed

19:42gallbladder it's in the right upper

19:44quadrants often times you'll see this

19:47classic right upper quadrant pain the

19:51other thing is if you go and you try to

19:53palpate on that area when they take a

19:55deep breath in and they stop taking that

19:57deep breath they'll have called a

19:59positive Murphy sign you can do that on

20:01exam you know another way that we do

20:03this a lot of the times is whenever you

20:05grab the ultrasound which is one of the

20:06diagnostic test of choice here and you

20:08push it down oh that hurts also so a

20:11sonographic Murphy sign the other thing

20:14is anytime you have an inflammation an

20:15infection it's going to trigger a cyto

20:17kind storm and so there may potentially

20:19it's not always guaranteed but there

20:22could also just be because of this

20:23intrinsic concept of inflammation an

20:26increase in white blood cell and

20:28increase in the risk of developing a

20:31fever so anytime you have a fever you

20:33have wher PR quadrant abdominal pain and

20:36you have a

21:00then the intraluminal pressure starts

21:04squeezing on the gallbladder wall and I

21:07talked about this a little bit before

21:08imagine here's kind of like some

21:10arteries and these arteries are going to

21:13be supplying the gallbladder there's

21:15also veins and some other Associated

21:17stuff but whenever you compress because

21:19you're causing so much stretching so

21:21there's a let's say a massive

21:24increase in intra luminal pressure right

21:28so that press should be high as a Musta

21:30so high

21:32intra

21:34luminal

21:36pressure when that pressure is crazy

21:39high what it does is it compresses the

21:41vessels and whenever you cause massive

21:44compression of the arterial vessels

21:46you're going to lead to a wall so

21:49gallbladder wall

21:52esea and that is terrifying my friends

21:55is when this actually starts to occur so

21:58if there's an increase in wallisia and

22:00what's the stimulus behind this it's

22:02usually arterial compression but it can

22:04occur with Venus compression lymphatic

22:05compression but I'd say the big one is

22:09arterial compression you compress those

22:12arteries you don't get the oxygen supply

22:15to the actual gallbladder starts to

22:17become super esmic because of the

22:19pressure now when that happens it it's a

22:22terminology that we refer to as

22:25gangrenous CU it's dying it's kind of an

22:27es schic and dying

22:29call Gall bag so we call this K cystitis

22:33so this is an identifying Factor here of

22:36gangrenous colitis now you may not be

22:38able to identify this off of any

22:41particular physical exam findings they

22:43may have an increase in white count they

22:44may have a fever they may have ralas

22:46abdominal pain sounds exactly like

22:48regular chitis how do I identify that

22:52parts of this Gall

22:55bag is becoming a schic and then un

22:58fortunately necrotic it's via the next

23:01set of complications that arise so as

23:04this

23:05occurs you start seeing these patients

23:07convert into these this where you see

23:10some scary stuff so one thing is Imagine

23:14here this Gall black is super es schic

23:16and this tissue is starting to die super

23:19weak and all of a

23:21sudden I get a

23:24perforation that's a terrifying kind of

23:26complication wouldn't you say so this is

23:28definitely one potential complication of

23:30having that gangrenous colitis is that

23:33one thing that can happen is is you can

23:35definitely

23:37trigger perforation so gallbladder

23:40perforation often times this may seem

23:42kind of like odd but I think when I

23:45explain it here in a second it'll make a

23:46lot of sense so usually what happens is

23:49these patients have so much back

23:51pressure and distension it's so painful

23:54when they perf initially they'll have a

23:57mass of relief of their pain so look for

24:02a pain

24:04relief but then you know what will

24:06happen this is going to spill into their

24:08perenium they're going to become per

24:10they're going to develop peritonitis

24:11sepsis and they're going to get sick as

24:12a balls so they're going to get terribly

24:14ill but look for like a temporary or

24:17transient pain relief or if the right

24:19quadrant abdominal pain that could be a

24:21signal this may signal you here I'll

24:24write this down this could

24:26signal the fact that this patient is is

24:28develop a gallbladder perforation

24:31okay so that's one

24:34complication the second one is you can

24:37perf but you don't perforate into the

24:40peritoneum so you'll get pain relief but

24:42then again let's actually make sure we

24:43talk about this it'll be quickly

24:45followed by death I'm not trying to make

24:47that funny but it's it's seriously true

24:49in the sense that these patients will

24:50get terribly sick so they will quickly

24:53follow into peritonitis so I just want

24:56you to understand they'll have a quick

24:57pain relief but then they'll ensue into

24:59peritonitis this next one is they will

25:01not perf they'll actually

25:04falize and so what happen is they'll

25:06create this little tract that occurs

25:10between the gallbladder and the small

25:12intestine and this is really interesting

25:15because now some of these stones that

25:18may be

25:19here can just rock their way out into

25:23the actual small intestine and they may

25:25work their way down the small intestine

25:27these stones

25:29and then what happens if this gall stone

25:31gets stuck and you know where the most

25:33common area for them usually to get

25:34stuck is is in the ilium right at that

25:37Junction and so because they often get

25:39stuck in the ilium they cause features

25:42of small bowle obstruction but it's due

25:45to a gallstone being stuck in the ilum

25:46so we call this wait for it you're never

25:48going to guess it a gallstone

25:52ilas and often times what will happen is

25:56is these patients will develop

25:59features that'll be significantly

26:02identifiable based upon a

26:05small

26:07bowel obstruction so that's one of the

26:10biggest things is that this can trigger

26:12findings of small bowel obstruction

26:14which will be again you know cramping

26:16abdominal pain they'll have vomiting

26:19they'll have difficulty being able to

26:21pass gas or past stool um and they'll

26:24have a lot of abdominal tenderness so

26:26these are usually classic features

26:28associated with a small bowel

26:30obstruction but this is the big things I

26:32think that you should be able to realize

26:34so to again quickly recap kystis right

26:37prau abdominal pain Murphy sign usually

26:40due to an inflamed gallbladder if it

26:42becomes inflamed for a long period of

26:43time and the pressure backs up and it

26:45causes it to become aeic gangrenous

26:46kestis may not identify any particular

26:48findings but when it perfs quick relief

26:52peritonitis we have Gall butter

26:54perforation if it does not per but it

26:56falzes

26:58what's that terminology we should

27:00actually quickly write that down because

27:02you may see this on the

27:03exam it's called a

27:07Ki

27:10cysto

27:12enteric

27:15fistula chicy enteric fistula so uh in

27:19this particular type of problem here

27:21you're having a Fishel that form between

27:23the gallbladder and between the enteric

27:26system in this case the small bow and

27:28then you'll proceed with a small ballop

27:30struction okay we got down the

27:31complications there what about this next

27:33Monster the next Monster here is called

27:35kocal lithiasis we already talked a

27:37little bit about it it's a gallstone

27:38stuck within the common B duct we said

27:43that the problem with here is that

27:44you'll get a lot of back

27:45pressure and we said that that back

27:47pressure will lead to specific molecules

27:49leaking into the bloodstream that we

27:51discussed such as an increase in

27:53alkaline phosphatase an increase in

27:56Billy Rubin they'll have that classic

27:58right upper quadrant abdominal pain that

28:00we talked about here so these are

28:02definitely pretty easy to identify right

28:07now the one thing that we said is that

28:10kocal aasis doesn't have the classic

28:13features of

28:14infection but if if this patient does

28:18allow for bacteria to colonize it can

28:21progress and we'll talk about this this

28:24over time can lead to this disease that

28:28we're going to talk about a little bit

28:30which is ascending colitis okay so I do

28:33want you to understand that it can cause

28:38bacterial uh

28:40infection of the biliary tree and when

28:44that happens we have crossed over from

28:46kolasis to ascending colius and we'll

28:48talk about that in a

28:50second one thing I think going into the

28:53next part here when patients develop

28:55chalasis the stone can get stuck in the

28:57common bile duct

28:59but the common B duct goes all the way

29:01down here to the

29:03pancreas and so here you have two ducts

29:06here is the common bile duct and here is

29:11the pancreatic duct like the main

29:14pancreatic

29:15duct and where they usually join is

29:18called this ampula um called the ampula

29:20VOD or theop pancreatic

29:23ampula sometimes if that stone gets

29:26stuck right there where the common duct

29:28in the pancreatic duct fuse the apop

29:30pancreatic ampula you can get chalasis

29:34so you get all that back flow increase

29:36alos increase Billy ruin potential for

29:38ascending colangitis but you know what

29:40else you can

29:41get all of this pancreatic

29:44fluid can back up and it can cause

29:49obstruction of the pancreatic ducts and

29:51when you obstruct the pancreatic

29:54ducts it'll cause inadvertent activation

29:57of the pancreatic enzymes all these

29:59pancreatic enzymes lipases proteases

30:02amasis will start digesting the

30:04pancreatic tissue

30:06undesirably look at this thing it's

30:08going to get hot it's going to get

30:11inflamed it's going to get angry what

30:12does that call when you inflame the

30:14pancreas it's called pancreatitis right

30:17so another potential complication of

30:19this kind of obstruction here and I'd

30:21say it's by far one of the most common

30:23causes of

30:24pancreatitis is going to be a gall stone

30:26there so watch out for development of

30:29pancreatitis in the setting of Koco

30:32lithiasis I spell it right

30:35pancreatitis now often times

30:37pancreatitis presents with that classic

30:39epigastric abdominal pain elevation in

30:42lipace um that's usually three times the

30:44upper limit of normal we'll talk about

30:45that more in that video But realize that

30:48gallstones particularly at that level

30:50can definitely be a very common cause

30:51along with alcohol as the most common

30:54causes of

30:55pancreatitis okay beautiful with that

30:58being said we've talked about

30:59kystis we've talked about how that one

31:01causes the classic findings gangrenous

31:03chitis gallbladder perforation and

31:05gallstone ilas we talked about this one

31:07with pancreatitis and the risk of

31:09developing ascending colitis let's now

31:12talk about ascending colitis in

31:14ascending colangitis same thing stone

31:16stuck within the common B duct the

31:19differences between kocal lithiasis and

31:22ascending colangitis though is that this

31:23one was just biliary fluid that's not

31:25infected and this one you see these like

31:28kind of maroon Dots here these are going

31:30to be bacteria so here let's actually

31:32recognize that that this is going to be

31:34a biliary fluid so a bacteria Rich bile

31:40we're going to call this infected bile

31:42sounds terrible right but it's because

31:44this obstruction is impeding the flow of

31:47normal bacteria containing bile so what

31:50happens is this biliary

31:53fluid which is rich in this infected

31:56material will move back

31:59backwards and it'll get

32:02into the

32:04bloodstream right so you're going to

32:06have this bacteria it's going to cause

32:08inflammation infection of all of this

32:10bellary duct so you're going to get some

32:11angry inflamed let's actually write that

32:13down you're going to get some inflamed

32:15ducts some

32:19inflamed common B duct and aaic ducts

32:22and that's going to cause that classic

32:23right upper quadrant abdominal pain

32:26right classic

32:29what's associated with this was when the

32:30bacteria get into the bloodstream and

32:33that's what's terrible because sometimes

32:35when the bacteria get into the

32:36bloodstream one of the common things

32:38that usually May Divi actually arise

32:40initially so now we have what's called

32:44bacteria bacteria within the bloodstream

32:46one of the big things is that this may

32:48activate your immune system and so what

32:51will happen is and poor neutrophils are

32:54going to pop off right so you're going

32:56to develop an increase in the white

32:58blood cell count that's one thing right

33:00so this is going to pop off them white

33:03blood cells second thing is it's going

33:06to stimulate cyto kindes which will then

33:09cause your hypothalamus to crank up your

33:11body temperature and so you may have a

33:15fever which is again greater than 38 deg

33:17C or greater than 10.4 degrees

33:20Fahrenheit so you may have a high fever

33:23and white blood cell count you may also

33:25have right upper quadron abdominal pain

33:27but there's one more

33:28thing this bile is rich in bacteria but

33:32I've already said what it's also rich in

33:34it's rich in Billy rubben and so it's

33:36also going to be a

33:38ton of Billy Rubin and what we talked

33:41about before alkaline phosphatases but

33:42this is the pertinent one here it's

33:45going to be in high amounts when this is

33:46in high amounts what do you think it

33:48does deposits into the skin dep posit

33:50into the Scara and causes

33:54jaundice okay with that being said

33:58when a patient

33:59has ROP quadron abdominal

34:03pain when they have

34:05jaundice and when they have features of

34:08infection such as elevat white blood

34:10cell count but more particularly a fever

34:12these are very suggestive of ascending

34:14colitis you know what they call this we

34:16say that this is referred to as um

34:21sharos

34:23Triad so shos Triad is righto precaution

34:26abdominal pain jaundice and a fever and

34:28sometimes if you get a white blood cell

34:29count uh you get a CBC you may develop a

34:32elevated a white blood cell count okay

34:35what if I took this a little bit further

34:37and I had a patient who now had even

34:39worsening bacteremia so going off of

34:43that let's say that we just focus on the

34:46bacteria his bilary fluid is super

34:51scary super rich in

34:53bacteria and now this bacteremia is off

34:56the chain

34:59and when it gets off the

35:01chain it starts wreaking havoc in our

35:03circulatory system so now these patients

35:06get in terrible bacteremia and what

35:09happens is this will then trigger a

35:13massive so now our white blood cells are

35:16going to start trying to fight off this

35:18bacteria and there's going to be a

35:20problem here where not only is there

35:21going to be lots of white blood cells

35:23there's going to be tons and tons of

35:25cyto kindes so you're going to have lots

35:27of white blood

35:29cells lots of cyto so many I'm not going

35:32to go crazy but like interlukin one and

35:33interlan 6 and two microtic Factor all

35:36all these dang things these things are

35:38going to be in massive amounts this is

35:39going to be in massive amounts the whole

35:41problem is they're trying to come and

35:44ward off this

35:46bacteria but unfortunately all of these

35:49cyto kindes wreak havoc on our

35:52circulatory system and what they do is

35:55they make your circulatory system super

35:57dilated and super leaky so here's a

36:00blood

36:01vessel this blood vessel is super leaky

36:05and now fluid will leak

36:07out of these

36:10capillaries and now what happens is I

36:12lose my systemic vascular resistance and

36:15I drop my blood volume and so now what

36:17happens is these patients

36:19usually develop hypotension they develop

36:22low blood

36:25pressure and that low blood pressure

36:28will then lead to the patient having

36:31shock so we call this septic shock when

36:33it's due to bacteria this is a very

36:36specific type so we call this

36:39septic shock if you will here let's

36:42actually write that down so this is

36:43actually specifically what type of shock

36:45as a response to the low blood pressure

36:47this is septic shock so they'll have

36:50terribly low blood pressure they won't

36:52peruse organs and as a result of that

36:56one of the most sens sensitive organs

36:58tends to be the

37:00brain and because of that they'll have

37:02hypo profusion of the brain and they

37:04develop an altered mental

37:09status so now hypo profusion of the

37:12brain due to low blood pressure

37:14stimulates an altered mental

37:18status it's

37:19interesting so now if they have

37:21hypotension shock and alter mental

37:24status you know what we call that we

37:26call that r R

37:28rolds pentad Reynolds pentad all these

37:32like dang weird things but ral's

37:36pentad all that is is a

37:40combination of shos Triad so it's sharos

37:49Triad

37:52plus these two factors here low blood

37:56pressure or shock and altered mental

38:00status so now if a patient has ascending

38:02colangitis this looks like it could be

38:04the worst possible scenario correct

38:06absolutely this is the one that'll kill

38:08you and cause the patient to become

38:10septic I think with that being said we

38:13now have a good idea of De biliary tract

38:14diseases their complications their

38:16pathas now let's hit the Diagnostics so

38:19now you kind of get to the point where

38:20you're like okay I have a patient

38:21they're coming in they have right

38:22quadron abdominal pain maybe or maybe

38:24not they have jaundice I got to start

38:26thinking okay how can I really get to

38:27these diagnostic approaches here well

38:29the first thing is get a CBC I find that

38:31this helps because it helps you to see

38:32is there lucyisanerd

38:57increase in the and the alt here's the

38:59thing that tells me that I have to have

39:01a stone that's somewhere in the common

39:04bile duct so if I have a high white cell

39:06count and I have an high alkaline

39:08phosphatase and Billy Rubin levels I

39:11know that it has to be ascending

39:12colangitis but if I don't have like a

39:14high white blood cell count I don't have

39:16a really high fever but I do have an

39:18increased alos and an increased Billy

39:20Rubin with right upper quadrum pain it's

39:22probably kocal

39:24aasis if I have a high white blood cell

39:26count and I have really no increase in

39:29Billy Rubin or alkaline phosphatase then

39:32I should suggest that it's chitis

39:34especially if I have a fever and right

39:37upper quadron abdominal pain so let's go

39:39to the next step which is let's get a

39:40right upper quadron ultrasound because

39:42this will give me a lot more

39:44information if I do this and I look here

39:47and I say oh here there's a bunch of

39:48gallstones all they have is right upper

39:50quadrant abdominal pain they have no

39:52issues with their lfts no white cell

39:54count well if that's the case it's just

39:57K loiasis maybe they have some biliary

40:00colic that's going on and it's because

40:01of the fat occurring meals all right

40:04that's not a true kystis ascending

40:06colitis or

40:07chalasis cool what if I look at the

40:10right upper quadron ultrasound though

40:12and I say oh shoot here's the biliary

40:15duct the common bile duct and I see a

40:17stone here and the the actual bilary

40:19Duck's pretty

40:20dilated okay well then I know then if

40:22they're presenting with r oradon

40:24abdominal pain increase Al fos increased

40:26Billy Rubin no significant white cell

40:29count or fever it's probably kocal

40:32aasis but if they present with a stone

40:36dilated B duct white cell count high Al

40:39Foss High Billy

40:41rubben then that's probably ascending

40:44colangitis the next thing is if I see oh

40:47man there's definitely a gall stone

40:48that's present in the gallbladder they

40:51have a sonographic Murphy sign so when I

40:52use the Ultras sign I push into that

40:54right upper quadrant it causes an

40:56intense pain and they aren't able to

40:57breathe bre I also see that the

40:59gallbladder wall is really thick it's

41:00distended and it even has some fluid

41:03around this area here that's super

41:05diagnostic of kystis especially if they

41:08have a fever again right Upp quadron

41:10abdominal pain and usually a increase in

41:13white cell count usually no changes in

41:15their alkaline phosphatase or their

41:16Billy Rubin and that's going to help me

41:18out now let's say that I get a patient

41:22who has right uper quadrant Ultras right

41:24uper quadrant pain I give him a

41:26sonographic Murphy sign they have a

41:27fever they have a

41:39lucyisanerd

41:43struction in the gallbladder then it

41:46won't fill the gallbladder and so what

41:48we're looking for is we're looking for

41:49areas where the Tracer is not emptying

41:51into the gallbladder and if we don't see

41:53the Tracer in the gallbladder we know

41:54that there's an obstruction of the

41:55gallbladder and that would tell me oh

41:58they definitely have a stone there it's

42:00likely kystis so again no Tracer filling

42:03the gallbladder it's

42:06kestis so at this point you should have

42:08an idea now of how to go about

42:09diagnosing a patient who has a biliary

42:12tract disorder

42:14cholithiasis kystis kocol lithiasis and

42:18ascending colangitis again look at their

42:21clinical features look for a white count

42:23look at the lfts again only Al fos Billy

42:26Rubin and common bile duct Stones only

42:32lucyisanerd ultrasound if it shows a

42:34stone in the gallbladder but they don't

42:36have any other features of lucacos or

42:39kolasis it's chasis if they have white

42:43cell count no K chasis on their lfts but

42:46they do have a stone in their

42:47gallbladder thickening all of the

42:49findings there it's kystis and if not

42:51get a hi High disc scan to confirm if

42:53they have no white count and they have

42:55again a uh chasis injury and then again

42:59you look at the radon ultrasound and you

43:00see a stone there with ductal dilation

43:02it's chalasis if I see a white count

43:04kolasis and I see a stone with ductal

43:07dilation then I know that it's ascending

43:09colitis all right now we move on to the

43:11treatment how do we treat all of these

43:13well kolis often times we may do nothing

43:17but if you're really trying to reduce

43:18the formation of gallstones you can use

43:20a drug called uro deoxycholic acid this

43:22is preferred for patients who don't want

43:24to go any kind of undergo any surgical

43:26or invasive therapy therapy urod

43:28deoxycholic acid has been shown to

43:29reduce the formation of gallstones so it

43:31can reduce the the rate or recurrence of

43:34gallstone kind of formation and reduce

43:36the events of biliary colic kystis

43:39kolasis

43:41Etc if you completely want to go the

43:44invasive route and prevent a patient

43:45from ever obstructing their biliary tree

43:48because of them having CH lithiasis then

43:51you can just go ahead and ask the

43:52patient if they want to get a cystectomy

43:54and it's more a elective process and

43:55they can do it laparoscopically where

43:57they go in with all of these particular

43:58Scopes and cut out the gallbladder or

44:01they can open the patient up and then

44:03cut out that gallbladder but either way

44:04that'll prevent them from developing

44:06things like chitis kocalis and ascending

44:09colitis what if they have chitis well

44:12it's important you got to get rid of the

44:13infected gallbladder so again you're

44:14either going to do this laparoscopically

44:16or open but it's is important to

44:17emergently get them to the O and cut out

44:20the infected gallbladder and in the

44:22meantime give them some antibiotics to

44:24start cleansing that actual infection so

44:26usually this things like cicin and

44:28metronidazol until you get the patient

44:30to cut that gallbladder out you keep

44:32them on it for a little while and then

44:33eventually they won't need the

44:35antibiotics any

44:36further however some patients may be

44:39super critically ill and not be able to

44:41survive a cystectomy so in that

44:43particular scenario we won't take them

44:45to the O we'll put them on antibiotics

44:47cxis and metronidazol but then we'll

44:49come to the bedside and what we'll do is

44:51we just got to keep getting rid of the

44:53infected biliary material so it doesn't

44:55cause gangrenous chitis they they don't

44:57become have a perforation or a gon ilas

45:00so what we'll do is is we'll take and

45:02we'll provide an alternative path and

45:03we'll take this tube at the bedside run

45:06it right through into the gallbladder

45:08and provide an alternative route for

45:09that area to decompress so it reduces

45:12pain and gets rid of the infected

45:13material this is called a percutaneous

45:16Chic cystostomy we only do this in

45:18patients who are not good candidates for

45:19a emergent laparoscopic or open

45:22cystectomy all

45:24right next one's chalasis it's really

45:27just important to remember if they have

45:28findings of ascending colangitis or if

45:30they have a gallstone

45:32pancreatitis um and there's lots of it

45:34pain that they're not just improving

45:36with medical management you need to

45:38remove that stone and the best way to do

45:40that is what's called an ercp which is

45:42an endoscopic retrograde cangia

45:44pancreatography you take a scope it goes

45:46down through the duodenum you run it and

45:49kind of cut through this little

45:50sphincter of ODI and you run up through

45:52the actual common B duct and you suck

45:55out all of that stone and that's where

45:57you're going to remove these stones but

45:59again it's important to make sure that

46:00you do this in the indication of where

46:01it's necessary such as refractory pain

46:04they have gallstone pancreatitis or

46:06they're developing ascending colangitis

46:08then you'll remove this

46:09stone with that being said if a patient

46:11does have ascending colangitis it is of

46:13utmost importance to get that stone out

46:15of there so you're going to put them on

46:16antibiotics to start to try to clear

46:18some of that uh infected biliary fluid

46:21but then get in there and get that stone

46:22out so that you prevent them from

46:23developing recurrent infections so you

46:25can liberate normal FL flow of bile and

46:28stop that bacterial stasis and

46:30colonization all right the next thing is

46:33what if I have a patient just like a

46:34cystis patient who's super critically

46:37ill well same thing I maybe they're not

46:39a good candidate for me to go to the

46:41endovascular uh the the suite that for

46:43Endo uh endoscopic study in other words

46:47I cannot get them to the endoscopy Suite

46:48to do an ercp they're just not stable

46:50enough and they probably wouldn't do

46:52well with that surgery well I'll

46:54continue the antibiotics to kind of

46:56clear up that infected bilary fluid but

46:59I'll do a percutaneous chol cystostomy

47:01again to keep removing infected fluid

47:04from the gallbladder from the bilary

47:05tree so that it doesn't cause further

47:07distension so that'll remove pain and it

47:09also will clear some of the infected

47:11material so they don't become septic in

47:13developing that Ral pentad and that's

47:15how we would go about treating this all

47:18right my friends that was a lot to talk

47:19about with billary tract diseases I hope

47:21it made sense I hope that you guys did

47:23enjoy it and as always until next time

47:29[Music]