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Abdomen II > biliary pathology > Flashcards

biliary pathology Flashcards

1
Q

what is choledocholithiasis?

A

stones in the duct

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2
Q

w/ _____ Liver produces too much cholesterol. DM, Pregnancy, Obesity, Genetics can all lead to this

A

Hypercholesteremia

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3
Q

____ is Another mechanism for stone formation is too much bilirubin. Any prolonged hemolytic anemia (breaking down of RBC), sickle cell anemia or thalassemia (An inherited form of anemia occurring chiefly among people of Mediterranean descent, caused by faulty synthesis of part of the hemoglobin molecule).

A

Hyperbilirubinemia:

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4
Q

____ is an –
Inherited autoimmune, lining of the small bowel is damaged from eating gluten and other proteins found in wheat, barley, rye.
–
CF Cystic Fibrosis
–
Pregnancy
–
Various Meds

A

Celiac Dz.

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5
Q

what do these etiologies indicate?

Etiologies
•
Stasis:
If a pt. is not eating regularly, and the GB is not being emptied stones can form. This is termed “Stasis” or “biliary stasis”
IV feedings, 2o to pancreatitis
anorexic
non-functioning GB
•
Inflammation:
Bile makeup is altered. Cholesterol is less soluble, the inflamed mucosa secretes calcium bilirubinates (salts) into the bile. Proteins are secreted into the gallbladder from the from the inflamed gallbladder wall providing a NIDUS or nucleus for stone development.
Abnormalities of Biliary Tree

A

Choledocholithiasis

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6
Q

what are these clinical signs of?

RUQ pain or tenderness
May cause intermittent biliary obstruction, so intermittent pain
May be febrile (fever), chills
N/V
Jaundice if obstructed

A

Choledocholithiasis

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7
Q

what labs might be associated w/ choledocholoithiasis?

A

Can have
•
Increase Alk Phos
•
Increase Direct Bilirubin if obstructed
•
Increase in AST, ALT
•
Increase WBC infection has set in

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8
Q

what is this? descirbe it.

A

Choledocholithiasis
–
Sonographic appearance
Hyperechoic foci within the duct, may or may not have shadowing, depends on size and the operating MHz
May have dilated bile ducts if duct is 100% obstructed.

*look at liver first, not the ducts. checking to see if the biliary tree is

the below:–
Stone stuck in distal duct
Dilated intrahepatic ducts

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9
Q

if a pt had clay colored stool, tea colored pea and jaundice, what might you suspecT?

A

choledocholithiasis

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10
Q

which are choledocholithiasis? why?

A

u know.

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11
Q

___ is inflammation of the bile ducts. it can be intra/extrahepatic

A

cholangitis

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12
Q

what is the etiology of cholangitis?

what will the flow look like thru the PV, HA, Lymphatics throgh the sphincter of oddi?

who is more likely to get this?

A

Associated with stones, inflammation of the GB, Liver, PanC.
•
E-Coli from bowel
•
Bacteria enters the bile ducts via
•
PV, HA, Lymphatics or retrograde through the Sphincter of Oddi
•
2:1 male to female ratio

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13
Q

what do these indicate?

Clinical signs
Fever (90% of pt. present with)
RUQ Pain (70% of pt. present with)
Jaundice (60% of pt. present with)
–
Labs
Leukocytosis (increased WBC)
Usually will have increase in Alk Phos.
Maybe an increase in AST and ALT
If obstructed increased Direct Bili

A

cholangitis

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14
Q

what is this? describe it.

A

cholangitis

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15
Q

what is this?

A

cholangitis

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16
Q

what is cholangiocarcinoma?

wha tis its etiology

where is it usually located?

what type of cancer are these generally?

A

Uncommon primary cancer of the bile ducts.
–
Etiology
Most common risk factor – Primary Sclerosing Cholangitis (PSC)
Occurs equally in females as males
Risk increases with age
Increase risk with multiple recurrences of stone disease or biliary infections

Classified by location of tumors
Intrahepatic aka peripheral (10%)
(** KNOW) Hilar aka Klatskin’s (60%)
Distal (30%)
•
90% are adenocarcinoma
Squamous cell carcinoma being the next most common.

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17
Q

___ is the Tumor which arises at the junction of the Rt. and Lt. hepatic ducts. This has the worst prognosis of all the cholangiocarcinoma’s

A

(**KNOW) –
Klatskin’s tumor

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18
Q

what could be confused for klatskin’s tumor?

A

a node in the porta hepatis

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19
Q

what are teh clinical signs for cholangiocarcinoma?

which type is this?

A

klatskin’s tumor

Clinical Signs
Insidious - notoriously hard to see
RUQ pain
Jaundice
Weight loss
Non specific GI disturbances

20
Q

what is this? how can you tell?

A

cholangiocarcinoma

Dilated Ducts, may not see tumor
Markedly dilated ducts in a patient with no Panc head lesion
Focal duct stricture or abrupt termination
Intraluminal hypoechoic echoes – soft-tissue like
Stent within duct, if known disease is present. Stent keeps the lumen open and prevents complications of biliary obstruction

21
Q

what labs are associated w/ cholangiocarcinoma?

what is the ddx

A

Labs:
Markedly increased D. Bili, Alk Phos
May have normal or mildly elevated AST, ALT

DDX: almost anything which causes ductal dilation
Liver tumors
Stones
Panc tumors
Duodenal tumors

22
Q

describe what you see

A

cholangiocarcinoma

A. Dilated Rt. and Lt ducts, no communication in the middle B. Dilated Rt. and Lt ducts, no communication in the middle C. Abrupt ending ducts D. Tumor encasing PV

23
Q

what is a ddx for this image?

A

tumor (cholangiocarcinoma) or sludge/bile,

Distal Duct Cholangio CA
Polypoid tumor, well defined intraductal mass, Often no visible vascularity

24
Q

___ is a slow, chronic liver disease which can cause progressive destruction of the bile ducts.

A

Primary Biliary Cirrhosis (PBC)

25
Q

do ppl w/ PBC usually develop cirrhosis?

what is secondary biliary cirrhosis from?

A

many who have PBC may never develop cirrhosis. Cirrhosis is often assumed to mean damage to the liver caused by excessive alcohol consumption. This is not the case - cirrhosis simply means an advanced form of scarring, which changes the structure of the liver cells, and can be associated with a whole range of liver and biliary diseases (autoimmune due to biliary cells)
•
Secondary Biliary Cirrhosis is from Chronic Ductal Obstruction

26
Q

what is this etiology

The cause is at present unknown.
•
is thought to be an autoimmune disease whereby the body’s immune system malfunctions and turns on itself. (i.e., not related to alcohol or drug abuse)
•
The body attacks the cells lining the bile ducts within the liver as if they are foreign to the body itself. This damage causes poor drainage of bile acids, which leak outwards and damage the normal liver cells. This causes inflammation and scarring which may, after many years become extensive. This widespread damage and scarring is commonly called cirrhosis.
•
it predominantly affects females at a ratio of approximately nine women to every one man.
•
it can sometimes become apparent during or just after pregnancy. The trigger could be an infection, a toxin, stress, or some hereditary factor It cannot be spread by sexual intercourse and there is no evidence of infection. Generally, it presents in women aged between thirty and fifty-five although, at present, the peak incidence is fifty to seventy years.

A

PBC

27
Q

name a few clinical signs associated w/ biliary cirrhoses

A

Chronic fatigue and lethargy - mild or severe
Intense itching of the skin (pruritus) which can affect any part of the body
Frequent indigestion or nausea, poor appetite
Sore joints/bone pain
Easy bruising or bleeding WHY? NOT MAKING CLOTTING FACTOR
Persistent ache or discomfort in the upper right hand side of the abdome
Weakness in wrists and/or hands
Dark urine and/or pale stools WHY? Bile in urine, kidney filter it out of the blood
Diarrhea
Jaundice - yellowing of the skin or eyes - is a sign of progression
1/3 of patients have portal HTN
Can control symptoms with meds, however when liver finally goes into failure Liver Transplant is indicated

28
Q

what labs are associated w/ biliary cirrhosis?

what might it look like?

A

Labs
Increased Alk. Phos
May have AST, ALT
Eventually bilirubin levels elevate

normal cirrhosis

You will see these patient come through down in Radiology.
Non specific
Check to R/O dilated intrahepatic ducts, On the other hand, in PBC, the ducts that are being destroyed are so small that any dilation of upstream ducts cannot be seen with any of the imaging techniques.
May have course texture

29
Q

___ is air/gas w/i the biliary tree

A

pneumobilia

30
Q

what ist he etiology of pneumobilia?

clinical signs?

labs?

A

Post procedure, ERCP, Post Sphincterotomy, SOD disorder, Post biliary stent placement, Gas producing bacteria within the biliary tree
•
DDX is gas within the portal vein. Usually Biliary gas is more centrally located, whereas PV air is more peripherally located

Clinical Signs -None specific, unless etiology from infectious source
–
Labs – None specific

31
Q

what might you see w/ pneumobilia in 2D

what is different about this as opposed to portal vein air?

A

the air may move or “undulate” with vascular pulsations

stays centered. portal spreads out

32
Q

___ is a a clinical syndrome. “Jaundice with pain and fever”. Jaundice is secondary to a specific obstruction of the proximal CHD. As a result of this obstruction the prox. CHD and Intrahepatic biliary ducts are dilated. The CBD and distal CBD are normal diameter.
–

A

mirizzi’s syndrome

33
Q

what etiology is associated w/ mirizzi’s?

clinical signs?

labs?

A

Uncommon
Extrinsic compression of the biliary tree, resulting from the obstruction of the CHD by a stone impacted in the cystic duct
This is more than just a stone obstructing the cystic duct.

•
clinical: Jaundice, Pain, Fever
–
Labs: Increased in WBC, Direct bili, Alk Phos., May have increase in AST, ALT

34
Q

what lab is highly associated w/ biliary dx?

A

alkaline phosphate followed by AST and ALT

35
Q

which image is mirizzi’s syndrome? describe it.

A

3rd. Dilated above the obstruction and normal below

36
Q

what can you say about this?

This pt. has pain, fever and is jaundiced. Shown is a dilated CHD. It can easily be mistaken for a CBD stone

A

it is mirizzi’s syndrom.

Difficult to show in one ultrasound image
Arrow showing thickened wall of the cystic duct

Real time or multiple is necessary to diagnosis this condition. You will not be able to diagnosis this syndrome with only one image.

37
Q

what studies are designed to

To evaluate the function of the GB and biliary tree.
1. Evaluate the Ejection fraction of the GB. How well does the GB contract post meal.
2. Another ? May be does a bile duct become enlarged? – Pt.s often have continuation of symptoms post cholecystectomy. The GB wasn’t the problem it was the SOD. This exam can evaluate the SOD, pre or post chole.
Does this exam reproduce the pt. symptoms?
•Protocol
–NPO 8-12 hrs.
–Measured dose based on pt’s weight.

A

Fat stimulation (Microlipid) / CCK (Kinevac)

38
Q

____ is the fatty substance which we give the pt. Made up of mostly corn oil. It is taken orally. Simulates 1050 calories. it is used is a fat stimulation/CCK study

A

Microlipid 2 cc of Microlipid / Lb. With a MAX dose of 300cc.
After pt. drinks the microlipid, 100 cc of H20 is given to pt. to help wash down Microlipid.

39
Q

____ is an injectable form of Cholecystokinin, a hormone secreted naturally by the duodenum. Stimulates delivery into the small intestine of digestive enzymes from the pancreas and bile from the gallbladder. Functions the same as fatty meal, however it works faster and can be used if the pt. is unable to drink the microlipid, or keep it down. what is it used for?

A

Kinevac

CCK part of fat stimulation study

40
Q

what is this?

A

–
Fat stimulation
Fat Stim. Protocol timing
Notice 30 and 60 min post drink.
–
Measurements obtained in
CHD
Prox CBD
Dist CBD
Panc Duct
GB Volume

41
Q

what is this?

A

CCK
CCK protocol timing
Faster image acquisition, done in 30 minutes

Measurments obtained in
CHD
Prox CBD
Dist CBD
Panc Duct
GB Volume

42
Q

what are significant findings associated w/ fat stimulation/CCK?

A

Significant findings
Increase of > 1mm in a duct diameter
Reproduction of pt. symptoms
Diminished GB ejection fraction of < 30%
Globular configuration of GB: It is contracting, and just balling up because it is unable to empty

43
Q

what is another way of looking at the Pancreatic duct to R/O SOD. It is a more specific exam for pancreatic origins of SOD than CCK/ Microlipid. This is because we are stimulating more of the Pancreatic to secrete bicarbonate.
–
It stimulates the pancreas to
a. emit digestive fluids that are rich in bicarbonate which neutralizes the acidity of the intestines,
b. the stomach to produce pepsin (an enzyme that aids digestion of protein), and
c. the liver to produce bile
•Protocol
–NPO 8-12 hrs.
–Dosage is base on pt’s weight.

A

Pancreas / Secretin (SecreFlo)

44
Q

how is the pancreas/secretin study performed?

what would constitute a significant finding?

A

–
Pt. will have a Hep-Lock placed by a nurse. A nurse will infusion the Secretin over a 5 min period.
–
.2 mcg/ kg is given, MAX dose of 32 mcg.
–
Many time the pt. may go to have an ERCP or other study where they may give IV sedation. Check with the pt. before you pull the Hep-Lock out after the exam, and the pt. has to have another Hep-Lock placed

Increase of Pancreatic duct of > 1mm.

45
Q

what is this?

A

Pancreas / Secretin
•
Notice that you will need to remember where you measured the PD and CBD to accurately reproduce the area.
•
It only takes 1mm to make a positive exam.

46
Q
A

Abdomen II (7 decks)

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