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2:46

right, greetings, ab-site nerds. By now, you

2:48

are probably sick and tired of studying,

2:50

but fear not, we have a quick

2:53

high-yield review for you today. We got

2:55

Nina, back up. Let's

2:57

talk about the foregut. Please describe

3:00

for me a esophageal anatomy. So

3:04

the esophagus is made up of

3:06

squamous epithelium on the inner layer

3:08

with an inner circular muscle layer

3:10

and an outer longitudinal muscle layer.

3:12

There's no cirrhosa on the esophagus, and

3:15

notably the upper third is made up of

3:18

striated muscle, while the lower two thirds is

3:20

made up of smooth muscle. The

3:23

lower esophageal sphincter is about 40 centimeters

3:25

from the incisors, and

3:27

the avegas nerve is closely affiliated with

3:29

the esophagus. So you think about the

3:31

right and left avegas nerves, the right

3:33

goes posterior to the esophagus, especially distally,

3:35

and the left avegas nerve runs anterior

3:37

to the distal esophagus. There

3:40

are a couple of anatomic areas of

3:42

narrowing where foreign bodies may get stuck

3:44

in an ab-site stem, and those include

3:46

the upper esophageal sphincter, which is also

3:48

the cricopharyngeal death muscle. The left

3:50

main stem raucous or the aortic

3:52

arch cross over the esophagus or

3:55

the diaphragmatic hiatus. Alright,

3:58

so now I'm thinking about surgical access to the esophagus. ophagous

4:00

I want to get access to the neck which side

4:03

am I going on Nina in

4:05

the neck you're gonna go for a left-sided

4:07

incision okay how about in the upper two-thirds of the

4:09

chest heart gets in the way go

4:11

to the right side okay and the lower

4:13

one-third of the chest back to

4:16

normal go back to the left okay

4:18

so I have a false diverticulum

4:20

between the cricopharyngeus and the pharyngeal

4:22

constrictor muscles what is that this

4:25

is anchorastaberticulum so you treat that

4:28

you treat that by doing a

4:30

cricopharyngeal myotomy or a zinc resection

4:32

generally I think about two options

4:34

endoscopic or open repair if it's

4:37

less than three centimeters and the patients or

4:39

the patients unable to extend their neck all

4:41

the way then you do an open surgical

4:43

repair if it's greater than three centimeters they

4:45

can get it repaired endoscopically okay what's the

4:48

most common type of esophageal cancer also

4:51

kind of a tricky question so this in

4:53

the united states this is adenocarcinoma which I

4:55

think about because it's associated with obesity, GERD,

4:57

barot esophagus all those things we see pretty

4:59

frequently in our four debt clinics elsewhere in

5:02

the world squamous cell carcinoma is the most

5:04

common. Anatomy question please

5:06

describe the blood supply to the stomach.

5:09

Yep so the left gastric comes off

5:11

of the celiac trunk and serves the stomach

5:13

the right gastric comes off of the common

5:16

hepatic artery the left gastropic

5:18

phloic and short gastric those shorties come

5:20

right off the splenic artery and

5:22

finally the right gastropic phloic comes off of

5:24

the gta. Okay what

5:26

cells secrete hydrochloric acid? That

5:29

would be the parietal cells. Okay and

5:31

what signals activate the secretion of

5:34

hydrochloric acid from parietal cells?

5:37

That would be acetylcholine, histamine,

5:39

and gasorin. Okay what's the

5:41

medical treatment for a GIST? That's

5:44

going to be in matinib which is a

5:46

pteracic and kinase inhibitor I've seen it asked

5:48

both ways by mechanism and by the name.

5:50

What's the first sign of leak

5:52

following a bypass? Watch

5:54

out for your tachycardic patients you just got

5:56

a bypass. Okay and

5:59

what are the mineral and vitamin D? that can

6:01

occur following the Rheumatoid Bioblast. I

6:03

think Dan already mentioned a few of

6:05

these in the context of the illegal

6:08

resection for Crohn's but you can get

6:10

B12 deficiency because these patients lack intrinsic

6:12

factor and they also might need an

6:14

acidic environment to activate intrinsic factors so

6:16

both of those might be lacking in

6:19

Rheumatoid patients and then the second

6:21

is iron which is absorbed in the duodenum. Alright

6:24

Dan, let's move on to HPV. What are

6:26

the two most common hepatic artery variants? So

6:29

the most common is the right hepatic artery

6:31

coming off the SMA followed

6:33

by the left hepatic artery coming

6:35

off the left gastric. What

6:38

separates the left and right lobes of

6:40

the liver? So

6:43

this is that imaginary line called can't leave

6:45

the line and it's a line between the

6:47

middle of the gallbladder fossa going back to

6:49

the IVC. Right and then so

6:51

what separates the medial lateral subience of the left lobe

6:53

of the liver? That'd be

6:55

the falsiform. The less

6:58

imaginary dividing line. Describe for me

7:00

briefly in your own words coinades

7:02

segments of the liver. Yeah

7:05

so I always think that this is best learned

7:07

by looking at a picture. You can easily Google

7:09

this but another trick is to make a fist

7:11

with your right hand and the finger

7:13

should be wrapped around your flexed thumb and the

7:16

fist should face you and then looking

7:18

at all the segments. The segment one is a

7:20

caudate which is the thumb in the palm of your head,

7:23

segment two is your index

7:25

fingers proximal phalanx, segment

7:27

three is the index fingers middle phalanx,

7:30

segment four a is the middle

7:32

finger proximal phalanx, segment

7:34

four b is the middle finger middle

7:36

phalanx, and five is

7:38

the ring finger middle phalanx, and

7:41

six is the little finger middle phalanx,

7:44

segment seven is the little finger

7:46

proximal phalanx and segment eight is

7:48

the ring finger proximal phalanx. Perfect.

7:53

Which hepatocytes are most sensitive to ischemia? Yes,

7:55

it's going back in the textbook here, but

7:57

these are the hepatocytes in asthner zone three.

8:00

the central lobular. Dr. Justin Marchegiani Alright. I've

8:03

seen a question on Gil Bearers

8:05

and the Crigler-Nahar syndrome

8:07

versus Rotors and Dubin-Johnson syndromes.

8:10

I butchered that but you all would too so.

8:13

Dr. Justin Marchegiani Yeah, so I group the

8:15

Gil Bearers and Crigler-Nahar into the same group

8:18

here and these are problems with conjugation and

8:20

so with these patients, you see a high

8:22

indirect bilirubin compared to Rotors

8:24

and Dubin-Johnson syndrome which are problems

8:27

with excretion. So in these

8:29

patients, you have a high direct bilirubin. Dr.

8:31

Justin Marchegiani I what's the best indicator of synthetic

8:33

function in a patient with cirrhosis? Dr. Justin Marchegiani

8:36

Yeah, so this is looking at the PTINR

8:38

due to factor 7 having the

8:40

shortest half-life. Dr. Justin Marchegiani Okay.

8:43

Normal portal vein pressure. Dr. Justin

8:45

Marchegiani So normal portal vein pressure is

8:47

5 to 10 millimeters of mercury but

8:49

this is not to be confused with

8:52

the hepatic venous pressure gradient which

8:54

is the portal vein pressure minus the

8:56

hepatic venous pressure or RA pressure and

8:59

this has a normal value of 1 to 5

9:01

millimeters of mercury. Above 5

9:04

is considered mild portal hypertension and over

9:06

10 is clinically significant portal hypertension. Dr.

9:08

Justin Marchegiani Excellent. Thanks for bringing that

9:10

up. Everything you need to know about

9:13

hepatic adenomas, let's hear it. Dr.

9:16

Justin Marchegiani Yeah, so most commonly in

9:18

a question stem, you'll see a woman

9:20

of reproductive age taking oral contraceptives. You

9:22

may also see a male taking using

9:25

anabolic steroids. These are mostly benign but

9:27

they are associated with risk of hemorrhage

9:29

and malignant transformation. On

9:31

CT scan, these demonstrate early arterial

9:34

enhancement followed by iso attenuation during

9:36

the portal and delayed phase imaging.

9:39

If a patient is female and the tumor

9:42

is less than 5 centimeters and asymptomatic, you

9:44

can do conservative therapy which is

9:46

just stopping the oral contraceptives or

9:48

anabolic steroid use. If

9:51

it's a male patient, these are

9:53

always resected and if you have

9:55

a female patient with

9:57

an adenoma greater than 5 centimeters, then you

9:59

would do an elective resection. Okay,

10:02

so hepatic anomer in a male it comes

10:04

out, greater than 5 centimeters in

10:06

field, female comes out. If

10:08

it's less than 5 centimeters in a

10:10

female and they're asymptomatic, you can try

10:12

conservative therapy, stop those contraceptives and or

10:14

steroids. What's the most

10:17

common malignant liver tumor? Yeah,

10:19

so this would be metastasis. It's about

10:22

20 to 1 metastasis to primary. Okay.

10:25

What medication contracts the sphincter of

10:27

OD and what relaxes it? Yeah,

10:30

so think of morphine as the

10:32

contractor of the sphincter and then

10:34

glucagon relaxes it. Think

10:37

that we give a 1-biligram dose of IV glucagon

10:39

during cholangiogram if we can push the stone out

10:41

of the duct to help it relax. I

10:44

think of this one as morphine is an

10:46

opiate which like contracts everything and makes people

10:48

super constipated including with all bladder and that's

10:50

how I remember that. The

10:53

old constipated gallbladder, excellent. So

10:55

what's the normal size for a common bile duct? Yeah,

10:57

so patients under 65 years of age, do

10:59

you think less than 0.8 centimeters? Patients

11:04

over 65 years of age can be a little

11:06

bit more dilated so we think of less than 1.1

11:08

centimeters. After

11:11

a cholecystectomy, a patient can have

11:13

normal common bile dilation up to

11:15

about 1 centimeter.

11:17

What factors increase bile excretion and what

11:19

factors decrease it as well? Yeah,

11:22

so to increase it, you think of

11:25

cholecystentynin, secreting and vagal input and

11:27

decreasing, we think of somatostatin,

11:30

VIP and sympathetic input. Okay,

11:32

you have a question stem in which the patient was

11:35

found to have air in the biliary system what could

11:37

cause this? Yeah, so

11:39

we want to make sure that they haven't had some

11:41

sort of instrumentation usually an ERCP,

11:43

maybe cholangitis and maybe they have

11:46

some fistula to the enteric tract

11:48

caused by a gallstone. What

11:51

are the types of choleidocal cysts? Which one

11:53

is the most common and how would you

11:55

treat that? Yeah,

11:57

so type 1, this is your most common.

11:59

This is the... dylation of the

12:01

common bile duct and

12:03

we treat this with resection and

12:05

hepatic coj. Type 2 you have

12:08

a diverticular dilation anywhere along the

12:10

extra hepatic duct. Type

12:12

3 is also called a choleidocasil.

12:15

This is dilation of the

12:17

distal CBD. Type 4a

12:19

you have multiple dilation affecting both

12:21

the intrahepatic and extrahepatic biliary tree.

12:24

Type 4b you have multiple

12:26

dilation of the extrahepatic duct.

12:29

In type 5 this is your corollis disease.

12:31

This is where you have multiple dilation of

12:34

only the intrahepatic ducts. I

12:36

have a patient who has biliary disease

12:39

and they're found to be positive for

12:41

anti mitochondrial antibodies. What's the diagnosis? Yeah

12:44

so this is a primary biliary

12:46

cirrhosis which has no increased cancer

12:48

risk and but you do think

12:50

about transplant. Fantastic

12:53

what's the most common bugs that

12:55

cause cholangitis? So

12:57

most commonly you have E. coli followed by

12:59

I. klepsiella. And

13:01

describe to me Charcot's triad. So

13:04

this is right upper quadrant pain

13:06

fever and jaundice. And Renan's pentat. So

13:09

you have those same three right upper

13:11

quadrant pain fever and jaundice but you

13:13

add in altramental status and shock. Alright

13:16

and how do you treat cholangitis? So

13:19

these patients need urgent biliary decompression

13:21

usually in the form of E.

13:24

rcp sometimes PTC. Okay

13:26

I'm gonna describe some findings on imaging

13:28

you tell me what to think about.

13:30

So a liver mass with peripheral to

13:32

central enhancement on delayed phase CT. So

13:35

this is a hemangioma.

13:37

Okay what if I see a central scar

13:40

on imaging? This is

13:42

your focal nodular hyperplasia or FNH. Okay

13:45

a heterogeneous poorly circumscribed mass with

13:48

early arterial enhancement and quick washout

13:50

with rim enhancement on delayed images.

13:53

This is concerning for a hepatocellular carcinoma. Right

13:56

and can be diagnostic for it as well.

14:00

issues can subtract some cause when it comes to the

14:02

biliary system. So

14:04

this is debatable among some surgeons,

14:06

but we think of gallbladder sludge

14:08

and cholecystatic jaundice. When

14:11

it comes to the endocrine function of the pancreas, what

14:14

do alpha cells do? So

14:16

alpha cells are responsible for glucagon,

14:18

and I just use the A

14:20

in alpha and the A in

14:22

glucagon. We have beta cells, which

14:24

I just remember are always just

14:26

insulin producing cells. And

14:28

then the delta cells, I think of

14:31

soma-dosedatin, so we remember delta

14:33

and soma-dosedatin. How

14:36

are pancreatic enzymes activated? Yeah,

14:39

so here you have enterocyanase from the

14:41

duodenum, which converts the trypsinogen into

14:44

trypsin, which then activates the other pancreatic

14:46

enzymes. All right, what's

14:49

the name of the pancreatic accessory duct? So

14:52

this is the duct of Santorini compared to

14:54

the major duct, which is the duct

14:56

of Warsaw. And what's

14:58

an annular pancreas? This

15:00

is when the second portion of the duodenum is

15:02

surrounded by a pancreatic band. And

15:05

to tribute this, we

15:07

do a duodenojeginostomy or

15:09

a duodenodetodenostomy. All right,

15:11

what is great turner sign and colon sign,

15:13

and what causes them? So

15:16

great turner sign is echomosis,

15:18

and I think of this as you need

15:20

to turn her to see the flanks. And

15:23

colon sign is umbilical echomosis, and

15:25

these are both caused by hemorrhagic

15:28

pancreatitis. All right, let's

15:30

talk gallbladder olives. So what's the number I need

15:32

to know in my head when it comes to

15:34

treatment plans? Yeah, so

15:37

you really want to think of greater

15:39

than 10 millimeters being concerning. Okay,

15:42

and how do I diagnose biliary dyskinesia?

15:47

So the best test for this is a HIDIS

15:49

scan. You're looking at an ejection fraction of less

15:51

than 35%, and this is testing 20 minutes after

15:56

CCK administration. You also want to

15:58

make sure that there's an absence of stone. or

16:00

cholecystitis prior to making the

16:06

help in