Goljan: Hepatobiliary And Pancreatic Disorders

Front 1

VHY**
First and second most common cause of Jaundice

Back 1

Viral hepatitis and second is gilberts

Front 2

Most of the bilirubin in the body is in what form

Back 2

Uncojugated usually from the breakdown of RBC's

Front 3

Briefly describe Bilirubin metabolism/coure?

Back 3

RBCs are phagocytized by splenic RBCs (after about 120 days normally)...UCB is the end product of heme degradation in splenic macrophages...comibines w/ albumin and is taken up by the hepatocytes...Conjugated bilirubin is produced (glucuronidation)..CB is stored in the gallbladder...intestinal bacteria make CB into urobilinogen...spontaneosly oxidizes into urobilin (brown color of stool)...small amount is recycled to liver and kidneys giving urine its color

Front 4

VHY**
What is the color of stool and urine?

Back 4

urobilin

Front 5

What is jaundice caused by and how is it classified?

Back 5

due to an increase of UCB or CB and is based on percent of CB.

Front 6

If CB is found in the urine what does this mean?

Back 6

pathology

Front 7

In what situations would you see a pateint w/ less than 20% unconjugated bilirubin (i.e. high UCB)?

Back 7

Hemolytic anemias (spherocytosis, sickle cell disease)

Rh and ABO HDN (hemolytic dissease of the newborn), RBCs are destroyed by macrophages

Gilberts and Criler Najar syndromes (defect in cojugating liver enzymes)

Front 8

VHY**
Patient becomes jaundice after FASTING, CB<20%, no other symptoms, DX?

Back 8

Gilbets syndrome (defect in uptake of UCB and little bit in conjugation)

AD, benign

Front 9

In what situations do you see CB% between 20-50%, and dark urine? why?

Back 9

Viral hepatitis, and alcoholic hepatitis

UCB increases because the liver has dec. uptake.

increase CB because inflammation and necrosis (destroyed architecture) of the liver causes CB to spill into blood, and reabsorbed urobilin is directed away from the liver and to the kidneys

Front 10

VHY***
CB>50%, white colored stools and dark yellow urine (CB is elevated not the UBG)?

Back 10

intrahepatic cholestasis

extrahepatic cholestasis (stone in common bile duct, MCC) or canrcinoma of the head of the pacnreas)

Front 11

Why is CB so high is hepatic obstruction?

Back 11

CB backs up because it can't get out via the bile ducts and spills into the blood (that why your urine is dark and, stool is white and CB% is so high in the blood)

Front 12

VHY
How do you tell viral VS Alcoholic hepatitis on the basis of liver enzymes

Back 12

ALT>AST - viral

AST>ALT - Alcoholic (alcohol damages the liver where AST is found)

Both are liver cell necrosis markers

Front 13

What is the most common casue of jaundice?

Back 13

Hepattis A - most common viral hepatitis

Front 14

Which liver enzyme is elevated in viral hepatitis, where else is this enzyme found?

Which one is elevated in alcoholic liver disease

Back 14

ALT - also found in Muscle, liver and RBCS

AST - found in the liver mitochondria and GGT (SER increases to help detoxify alcohol)

Front 15

Which liver enzymes are elevated in obstruction (cholestasis)

Back 15

GGT - serum gamma-glutamyl transferase (found in the SER)

ALP - serum alkaline phosphatasse

MUST SEE THE TWO Two-together elevated, probably need to do a ERCP

Front 16

Where else is ALP made

Back 16

placenta and bone

Front 17

What are the two best test to check liver severtiy?

Back 17

Serum albumin - can't make it in severe liver disease

Prothrombin time (PT) is increased because not making cagulation factors. all but vWF coagulation factors are made in the liver

Front 18

What autoantibody is elevated in primary biliary cirrhosis?

Back 18

Antimitochondrial antibody

Front 19

What tumor marker is elevated in hepatocellular carcinoma?

Back 19

Alpha-fetoprotein (AFP)

alpha 1 anti

Front 20

CB 20-50% and AST elevated, DX?

Back 20

VIRAL hepatitis

Front 21

CB 20-50%, ALT and GGT are elevated, DX?

Back 21

Alcoholic hepatitis

Front 22

CB>50%, GGT and ALT are elevated, DX?

Back 22

Obstruction of liver of some sort. light colored stool and dark urine

Front 23

CB<20%, really dark stool and urine, DX?

Back 23

extravascular hemolysis

Front 24

What is the first antigen to appear (first sign of infection) and the last to leave in hepatitis B?

Back 24

HBsAg (surface antigen)

Front 25

What are the infective particles of Hepatitis B?

Back 25

HBeAg (envelope) and HBV DNA

Front 26

What do the following serological test tell you:
HBsAg, HBV DNA and HBeAg and Anti-HBc-IgM positive (c=core)?

Back 26

Acute infection

Front 27

VHY**
What do the following serological test tell you:
Anti-HBc-IgM positive?

Back 27

Patient is in the window phase or serological gap phase, they are in the recovery phase but have not transitioned to making anti-HBc-Ig

Front 28

What do the following serological test tell you:
Anti-HBs?

Back 28

Immunized

Front 29

What do the following serological test tell you:
Anti-HBc-IgG, and Anti-HBs positive?

Back 29

Recovered from HBV

Front 30

What do the following serological test tell you:
HBsAg (for six months) and anti-HBc-IGg positive?

Back 30

"Healthy carrier" if HBsAg for more than six months

Front 31

What do the following serological test tell you:
HBsAg (for six months), HBV DNA, HBeAg and Anti-HBc-IgG positive?

Back 31

Chronic infective carrier

Front 32

What do the following serological test tell you:
anti-HAV-IgM?

Back 32

active hapatits A infection

Front 33

What do the following serological test tell you:
anti-HAV-IgG?

Back 33

Recovery or immunization form Hep A virus

Front 34

How do the levels of urine urobilinogen and Conjugated bilirubin differ in viral hepatits Vs extravscular hemolysis VS cholestasis?

What will the color of the stool and urine be in each case?

Back 34

Extravascular hemolysis - urobilinogen will be elevated but CB will be abscent have dark colored stool and urine )

Viral hepatits - CB will be elevated and urobilinogen (dark urine, normal stool color)

Cholestasis - CB will be elevated but urobilinogen will be abscent (dark urine but light stool)

Front 35

What do the following serological test tell you:
anti-HCV-IgG?

Back 35

indicates infection or recovery

IT IS NOT A PROTECTIVE ANTIBODY

Front 36

what are the clinical findings in acute viral hepatits?

Back 36

Fever

painful hepatomegaly

serum transaminases (ALT>AST) increases steadily and peak just before jaundice

atypical lymphocytes

increased urine urobilinogen and bilirubin

Front 37

Which of the viral hepatitis need requires co-infection w/ hepatits B (needs HBsAg)?

Back 37

Hepatitis D

Front 38

Which of the viral hepatits has no chronic state?

Back 38

Hep A

Hep E - only if pregnant women can develop chronic (fulminant hepatits)

Front 39

How do you confirm hepatitis C?

Back 39

RIBA recombinant immunoblot essay

Front 40

VHY*****
Flasked shaped ulcers in cecum, bloody diarrhea, gets into the blood and goes to the liver and forms anchovy paste abscess, in the right lobe, DX and treatment?

Back 40

Amebiasis - caused by entamoeba histolytica (resistant to stomach acid)

Metranidazole

Front 41

VHY***
Only protozoa that can phagotasize RBCs?

Back 41

Entameba histolytica

Front 42

What is metranidazole used in the treatment of?

Back 42

Giardia, C. difficile and amebiasis, bacterial vaginosis and trichimonis

Front 43

Definitive host

Intermediate host

Back 43

D-can mate and lay eggs (sexually active)

I-not sexually active

Front 44

Sheepherder's disease (echinococcisis) what are the definitive and intermediate hosts

Back 44

sheepherder and sheep are intermediate hosts

dog - definitive host

Front 45

What are the characteristics of sheep herders disease (echinococcus granulosus)

Back 45

single or multiple cysts containg larval forms...rupture of the cysts can produce anaphylaxis

Front 46

Patient (intermediate host) ingest food or water containing eggs, eggs develop into,larval forms (cysticerci) that invades into the brain producing seizures, DX?

Back 46

Cystercercosis (see multiple cysts in the brain on a picture) caused by tenia solium

IF an adult eats the infected pig they can become a definitive host (tenia cysts in the muslce)

Front 47

What is the cause of spontaneous peritoniitis in adults and childern

Back 47

Adults - E. coli

Children - strep. pneumoniae

Front 48

This pathogens eggs cause a fibrotic response in the portal vein (pipestem cirrhosis)...resulting in cirrhosis, they will have portal HTN, ascites and esophageal varices, DX?

Back 48

Shistosomiasis (shistosomiasis mansoni)

Front 49

VHY***
Patient has ascites, portal HTN, splenomegaly and varices but no hepatomgegaly, where is the thrombis?

Back 49

Portal vein thrombosis

Front 50

Why is hepatic artery infarction uncommon?

Back 50

Dual blood supply

Front 51

VHY****
Patient has enlarged, painful liver (they show a picture of a nutmeg liver), portal HTN, ascites and splenomegaly, where is the thrombosis?

Back 51

HEPATIC vein thrombosis (bud chiari syndrome)

Front 52

VHY**
What is the most common cause of hepatic vein thrombosis?

what is the second most common cause?

Back 52

POLYCYTHEMIA VERA

Birth control pills

Front 53

Treatment for bud-Chiari/hepatic vein thrombosis?

Back 53

surgical emergency if you don't operate they die

Front 54

What it the most common type of liver disease? Patient presents w/ tender hepatomegaly, but no fever or neutrophilic leukocytosis?

Back 54

Fatty change - substrates from alcohol metabolism are used to synthesize liver TG's

Front 55

patient presents w/ portal HTN, varices, ascites and splenomegaly. Imaging studies show air in the biliary tree, DX?

Back 55

Portal vein thrombosis caused by inflammation of the portal vein (pylephlebitis) from the E. coli that got there from acute appendicitis

Front 56

What produces the nutmeg liver appearnce?

Back 56

Congestion - specifically of the central veins and sinusoids causing necrosis of the hepatocytes around the central vein

Front 57

Patient presents w/ painful hepatomegaly, fever, neutrophilic leukocytosis, ascties and hepatic encephalopathy, hight AST>ALT, DX?

Back 57

Alcoholic hepatitis, they can die if they don't stop drinking, this is where you see mallory bodies

Front 58

Is fatty change reversible

Back 58

yes, completley if you stop drinking

Front 59

VHY**
What is it that actually damges the liver in alcohol?

Back 59

Acetaldehyde...stimulates ito cells (used to store vitamine A) to put down fibrotic tissue.

Front 60

VHY**
What is a mallory body?

Back 60

Damaged cytokeratin intermediate filament seen in alcoholic hepatits

Front 61

What is cholestatic liver disease?

Back 61

Obstruction liver disease

Front 62

What is intrahepatic Vs extrahepatic cholestasis?

Back 62

Intra - blockage of the intrahepatic bile ducts

Extra - blockage of the Common bile duct (CBD)

Front 63

What is the most common cause of extrahepatic cholestasis?

Back 63

Stone in the CBD

Front 64

VHY**
Patient presents w/ jaundice, pruritis, steatorrhea (light colored as well), urine is yellow and cholesterol deposits in the skin? Gross of the liver shows it to been green, DX?

explain the clinicial manifestations

Back 64

Cholestatic liver disease.

Jaundice - CB getting into the blood

Pruritis - reflux bile and gets into blood and into skin

Malabsorption (steatorrhea) - can't bind fats to be absorbed

Cholestrol in the skin - cholesterol is refluxed and gets into blood and deposited in the skin (patients usually have hypercholesterolemia)

yellow urine from CB not urobilin in the urine.

Front 65

Patient presents w/ Bile duct surrounded by fibrous tissue, bloody diarrhea, and left lower quandrant,DX?


What cancer can occur in this stiuation?

Back 65

primary sclerosing cholangitis strong association w/ UC (as is the case in this question)

Cholangiocarcinoma (MCC in US)

Front 66

VHY**
What is the most common cause of cholangiocarcinoma in 3rd world country?

Back 66

Clonorchiasis - clonorchis sinesis (chineese liver fluke)...get this by ingesting encysted larvae in fish...larvae travel to common bile duct and become adults

Front 67

VHY****
50 yr old women has generalized itching, bilirubin is normal, GGT and ALP are off the charts, and she has hepatomegaly but no jaundice, DX, what test should you order?

Back 67

Primary biliary cirrhosis - autoimmune granulomatis destruction of the portal triads...later they will get jaundice.

anti-mitochodrial antibody and IgM

Front 68

What can oral contraceptives and anablic steroids both do to the liver?

Back 68

Blockage of the intrahepatic bile ducts (cholestasis,goes away when you stop the drugs) also produce hepatic adenoma (benign but have a tendancy to rupture.)

Front 69

VHY**
Weight lifter who suddenly becomes hypotensive and colapses, abdomen is distended and find blood in peritoneum, spleen is ok, what is the most common cause?

Back 69

liver cell adenoma ruptures cause by anabolic steroids

Front 70

Most common hepatitis in day care centers and jails

Back 70

Hepatitis A

Front 71

Most common hepatitis in accidental needle stick and IV drug abusers

Back 71

Hepatitis B

Front 72

VHY***
Diffusley hyperpigmented person who is diabetic, Diagonis and cause of symptoms?

Back 72

hemochromatosis - bronze diabetes (Iron leads to destruction of endocrine and exocrine pancreas, patient is diabetic, hyperpigmented and has malabsorption)

Front 73

What supplement is contraindicated in older persons?

Back 73

Iron - get overloaded

Front 74

what is Hemosiderosis?

Back 74

secondary or aquired iron overload (e.g alcohol abuse, blood transufions, water from wells (iron pipes)...the iron deposits will be more prominent in Macrophages that in parenchymal tissue (hemochromatosis)

Front 75

VHY***
What is hemochromatosis?

What are the genetics

Back 75

Unrestriceted reabsorption of iron, AR disease**

Front 76

VHY***
What is the target organ in hemochromatosis?

they might show you a prussian blue stain.

What does the iron do?

Back 76

liver - produces hydroxyl free radicals causing destruction of the liver leads to cirrhosis and increased risk of hepatocellular carcinoma

Front 77

VHY***
What other places does iron go to in hemochromatoisis?

Back 77

pancreas (destroys endocrine and exocrine pancreas), heart (restictive cardiomyopathy), joints (DJD), skin and pituitary

Front 78

VHY****
How do you screen for iron overload and what is the treatment?

Back 78

serum ferritin - increased
other test show:
serum iron - high
TIBC - decreased
% saturation - increases

PHlebotamy

Front 79

VHY
Patient has hepatitis (that will progress to cirrhosis), kayser flesher ring, movement disorders and dementia, DX, what lab value is decreased?

Back 79

Wilsons disease

dec. ceruloplasmin

Front 80

VHY
WHat is a Kayser-Fleishcer ring?

Back 80

Excess copper in the Descemet's membrane

Front 81

VHY
WHy do the following Centeral nervous system symptoms develop in wilsons disease:
Movements resembling parkinsons, hemibalism and dementia

Back 81

Parkinsons like movemnts - copper int he putamen

Hemibalism - copper in the subthalamic nucleus

Dementia - copper deposits in the cortex

Front 82

VHY
What is the problem in wilsons disease?

How does this cause the characteritic symptoms

Back 82

dec. production of ceruloplasmin and dec. excretion of copper in Bile


Accumulation of copper in the liver results in free radicals and damage of the liver...eventually cirrhosis resutls in dec. production of cerulplasmin and inc. free copper in the blood...w/in a few years copper significatly deposits in the brain, kidney, cornea...

Front 83

VHY
What is the normal metabolsim of copper?

Back 83

most (95%) is usually bound to ceruloplasmin w/ 5% being bound to albumin...eventually it is taken up and degraded by the liver. Copper that was bound to ceruloplasmin is excreted into the bile.

Front 84

VHY
What is the total copper level in a patient w/ wilsons disease?

Back 84

TOTAL IS LOW but free level is increased.

Remember most is bound to ceruloplasmin but when the liver is damaged by copper and udergoes cirrhosis it stops making ceruloplsamin and the total level goes down but the free level goes up.

Front 85

What is cirrhosis?

Back 85

Irreersible diffuse fibrosis of the liver w/ formation of regenerative nodules

Front 86

Treatment for wilsons disease?

Back 86

penicillamine - binds up free copper

Front 87

WHat is cirrhosis?

What are regenerative hepatocytes?

Back 87

Irreiversible diffuse fibrosis of the liver w/ formation of regenerative nodules.

Hepatocyte reaction to injury, lack normal liver architecture (lack portal triads and sinusoids)....this is why you get portal HTN

Front 88

Intrasinusoidal hyptertension is produced by?

Back 88

Regenerative nodules

Front 89

Gynecomastia in a 13 yr old male?

Back 89

normal leave it alone, its not cancer...

Front 90

What is the most common cause of cirrhosis?

Back 90

alcoholic liver disease

other causes include: Hepatitis B and C (post necrotic cirrhosis), primary biliary cirrhosis (autoimmune), metabolic (hemochromatosis, wilsons, alpha 1 antitrypsin)

Front 91

What are the complications associated w/ cirrhosis?

Back 91

1.Hepatic failure
2.Portal Hypertension
3.Ascites
4.Hepatorenal syndrome
5.Hyperestrinism

Front 92

VHY**
Why does hyperestrinism result if a patient has cirrhosis?

What does it cause in males?

Back 92

Liver can't degrade estogen and 17-ketosteroids (e.g androstenedione, converted to estrogen by adipose tissue)

VHY: Causes GYNECOMASTIA, SPIDER TELANGIECTASIAS and Female distribution of hair

Front 93

Why does Hepatorenal syndrome result in patients w/ cirrhosis?

Back 93

It is renal failure w/o renal parenchymal disease...results from a decrease in blood flow w/ preservation of renal tubular function

Front 94

VHY
WHat is a compliation of acities in adults and kids?

Ascites presents w/ abdominal distension and a fluid wave

Back 94

spontaneous peritonitis caused by E. coli.

strep pneumoniae if it is a kid.

Front 95

VHY
What are the causes of ascites?

Back 95

Transudate due to alterations in the starling pressures (from portal HTN or hypoalbuminemia) + secondary hyperaldosteronism (Na and water retention)

Front 96

VHY
What makes up the portal vein?

Back 96

Superior mesenteric vein and splenic vein

Front 97

What is the most common cause hepatocellular carcinoma?

Back 97

Cirrhosis caused by HBV and HBC

Front 98

VHY***
Patient presents has had cirrhosis, ascites but comes to the doctor because of unintentional weight loss and worsening ascites. They do a peritoneal tap and find blood in peritoneum, what test would you do to make the diagnosis?

What other labratories findings are possible

Back 98

Look for increased alpha-fetoprotein (AFP) to make the call of hepatocellular carcinoma

Cancer can produce ectopic hormones like erythropoietin (secondary polycythemia) and insulin like growth factor (hypoglycemia)

Front 99

VHY**
What is the most common cancer of the liver?

What is the most common primary cancer of the liver

Back 99

Metastasis; lung is the most common primary site.

hepatocellular carcinoma usually in pre-existing cirrhosis

Front 100

Exposure to vinyl chloride or arsenic can cause?

Back 100

angiosarcoma of the liver

Front 101

what are the gross and microscopic findings of hepatocellular carcinoma?

Back 101

Gross - multifocal, diffusley infiltrating cancer

Micro - bile in neoplastic cells is characteristic

Front 102

VHY
Patient is a non-smoker and they show a picture of liver w/ mets, what is the most likely primary cancer

Back 102

colon cancer

Front 103

VHY
Pathogenesis of the stones

Back 103

VHY
to much cholesterol or to little bile salts and lethicin, predisopose to stones

cholesterol stones are the most common type (yellow color)

Front 104

VHY***
25 year old female presents w/ RUQ pinpoint pain, normocytic anemia, 8% corrected reticuloctye count, splenectomy when she was young, leukocytosis, and the ultrasound shows stone, DX?

Back 104

Hereditary spherocytosis causing cholelithiasis - from hemolysing RBCs she created bile that was saturated w/bilirubin creating calcium bilirubinate stones (THEY ARE JET BLACK)

Front 105

VHY
Screening test of choice for stones is

Back 105

ultarsound

Front 106

VHY
Screening test of choice for anything in the pancreas is?

Back 106

CT - because bowel overlies it and obscures ultrasound

Front 107

What is the growth alteration that results from cystic fibrosis on the pancreas?

Back 107

Atrophy - from back pressure

Front 108

Most common gallstone?

Back 108

cholesterol stones

Front 109

Black pigmented stones are a sign of what?

Back 109

Extravascular hemolysis

Front 110

VHY
Patient presents w/ obstrutive jaundice (CB>50%...) and a palpable gallbladder, DX, and most common cause?

Back 110

cholangiocarcinoma - primary sclerosing pericholagnitis (obliterative fibrosis of intra/extrahepatic bile ducts)

Not the same as primary biliary cirrhosis where there is autoimmune destruction of the bile ducts in the triads.

Front 111

How does cirrhosis result in alpha1-antitrypsin deficeincy?

Back 111

Mutant AAT cannont be secreted from by the liver cells...

Front 112

What effects does cirrhosis have on BUN and ammonia?

Back 112

dec. BUN (disrupts urea cycle) and increased serum ammonia

Front 113

Why does hypocalcemia result in the setting of cirrhosis?

Back 113

dec. vitamin D conversion (so dec. vitamin D) and dec. serum albumin

Front 114

Brown pigmented gallstones is a sign of?

Back 114

Commmon bile duct infection

Front 115

What is the inheritance of cystic fibrosis?

Back 115

Autosomal recessive, primarily effects whites

Front 116

VHY**
What is the pathogenesis in cystic fibrosis?

Back 116

Three nucleotide deletion of chromosome 7, normaly codes for phenylalanine...results in defective transmembrane conductance regulator (CFTR) for chloride ions

Front 117

VHY**
Why is CFTR not effective in cystic fibrosis?

Back 117

The defective CFTR CL- is degraded in the GOLGI APPARATUS do to defictive protein folding.

Front 118

What happens to the sweat glands in cystic fibrosis?

Back 118

Loss of CFTR CL- causes decreased Na and Cl- reabsorption in the sweat glands...basis of the sweat test (decreased sweat).
Can become salt defecient if severly dehydrated.

Front 119

What does CFTR normally do?

Back 119

transports Cl- ions across epithelial cell surfaces

Front 120

What is the effect of loss CFTR on secretions in the body?

Back 120

Increased Na and water reabsorbion from the luminal secretions and decreased Cl- secretion out of epithelial cells into luminal secretions resulting in dehydration of body secretions due to lack of NACL. (concrete/thick secretions) Because you took out the two important ingredients

Front 121

VHY**
loss of NaCl in sweat and luminal secretions (dehydrated) is seen in what disease?

WHer do you commonly see the problems

Back 121

cystic fibrosis

dehydrated secretions in the bronchioles, pancreatic ducts, bile ducts, meconium and seminal fluid

Front 122

VHY
What is the most common cause of death in CF patients?

Back 122

Respiratory infections - due to sodium

Front 123

VHY**
What is the percent chance of a cystic fibrosis male producing offspring?

Back 123

0-5%

Front 124

What are the major clinical findings in a patient w/ cystic fibrosis?

Back 124

Nasal polyps (25%)
respiratory infections/failure
Chronic pancreatitis and atrophy (malabsorption and type I diabetes)
Infertility in males
Meconium ileus
Secondary biliary cirrhosis

Front 125

VHY**
Alcoholic presents w/ epigastiric pain radiating to the back, DX?

Why do you see these symptoms

Back 125

Acute pancreatitis - because it is a retroperitoneal organ

Front 126

What are the two common causes of acute pancreatitis?

Back 126

Stones and alcohol abuse

Front 127

History of acute pancreatis, later you fill a mass in the abdomen, DX?

Back 127

pseudocyst

Front 128

When you see a calcifications on a CT in the area of the pancreas you should be thinking of?

Back 128

Pancreatitis - dystrophic calcification

Front 129

What is the cause of acute pancreatitis?

Back 129

Activation of pancreatic pro-enzymes - leads to autodigestion of the pancreas

Front 130

How can pancreatic enzymes be activated? Think of the things that

Back 130

1.Obstruction of pancreatic or terminal CBD
2.Chemical injury of acinar cells (thiazides, alcohol, TG)
3.INfectious injury of acinar cells (CMV, MUMPS, coxsackie)
4.Mechanical injury of acinar cells
5. Metabolic activatio of proenzymes (hypercalcemia, ischemia, shock)

Front 131

VHY****
what is the most common cause of pancreatitis is children?

Back 131

seat belt trauma

Front 132

How does tetany result from actue pancreatitis?

Back 132

Hypocalcemia results from enzymatic fat necrosis, calcium binds to fatty acids leading to decrease in ionized calcium

Front 133

VHY**
What is the best labratory test for diagnosing acute pancreatitis?

Back 133

Serum lipase

Amylase is not specific (can be elevated in mumps, small bowel infarction and ruptrued ectopic pregnancy)

Front 134

VHY***
What is the gold standard for pancreatic imaging?

Back 134

CT

Front 135

painless jaudice, light colored stools palpable gallbladder (courvoisiers sign), primary conjugated Bilirubin (>50%), DX?

What do you see on barium imaging?

Back 135

Carcinoma of the head of the pancreas. - blocks the CBD causing jaundice

C-sign from the cancer indenting the duodenum

Front 136

VHY***
What is the MCC of adenocarcinoma of the pacnreas?

What is the second MCC?

What is the most common location?

Back 136

1. SMOKING
2. CHRONIC PANCREATITIS

HEAD OF THE PANCREAS

Front 137

What is the gold standard tumor marker in adenocarcinoma of the pancreas?

Back 137

CA19-9

Front 138

VHY
How does the bowel react to inflammation next to it like in actue pancreatitis? What would you see on X-ray

Back 138

Localized illeus (inflammation stops peristalsis)

Sentinal sign- air next to the area where the bowel is not moving (can also see this in acute appendicitis)

Front 139

What is the most common cause of chronic pancreatitis?

What sit he pathogenesis

Back 139

Alcohol abuse

repeated attacks of acute pancreatis produce duct obstruction (see calcified concretions)

Front 140

What should you think of if you have persistant elevated serum amylase and an abdominal mass?

Back 140

pancreatic pseudocyst - collection of digested pancreatic tissue around pancreas

amylase is elevated because the amount released surpasses renal clearnce

Front 141

Patient presents w/ fever, nauses, vomitting, initial midepigastric pain that shits to the RUQ, pain is constant and dull, and radiates tot he right scapula?

Back 141

Cholecysitis

Front 142

What is the MCC of acute cholecysitis?

Back 142

Obstruction of cystic duct by a stone

Front 143

What are teh complication fo stones (cholelithiasis)?

Back 143

Cholecysitis most common

CBD obstruction

gallbladder obsturciton

actue pancreatitis

Front 144

What is the pathogenesis of actue cholecystis?

Back 144

increased intraluminal pressure and ishcemia to the gallbladder, irritation of the gallbladder from conversion of lecithin to lysolecithin

Front 145

What is the most common symptomatic disorder of teh gallbladder?

Back 145

Chronic cholecystitis - resulsts from cholelithiasis w/ repeated attacks fo minor inflammation

Front 146

What are the clinicial findings in chronic cholecystitis?

Back 146

Severe, persisitant pain 1 to 2 hours postprandially

recurrent epigastric distress, bleching and bloating