Icm Winter 3 Pancreatitis Liver Enzymes

Front 1

where is there lots of ALK phos

Back 1

liver
bone
intestine
kidney
WBC
placenta

**work in alkaline environment

Front 2

where is tehre lots of GGT

Back 2

lots of places but high conc in bile ductule cells

Front 3

what protein does the liver makle

Back 3

ALL except Ig

albumin, protime, bili, cholesterol

Front 4

whats normal

AST
ALT
AP
TB

Back 4

AST- 10-40
ALT- 15-40
AP-25-165
TB0.5-1 (about 1/3 is conjungated, direct)

Front 5

what form of bili is lipd solible? what about water

Back 5

Lipid- unconjungated

Water- conjungated (direct)

**bili is made from catabolism of heme

Front 6

make more bili when...

Back 6

1. hemolysis
2. ineffetive Erythropoeisis
3. mm injury

**all result in UNCONG bili

Front 7

make less bili when...

Back 7

1. liver diseae
2. obstruction, cong bili

Front 8

what does GGT tell us

Back 8

it is not specific for liver, BUT it is sensitive for liver/bile with ALK PHOS is also increased

Front 9

what clotting factor is NOT made in teh liver

Back 9

8, made in endo cells

**so when liver is not making protein there is an increase in bleeding time and prothrombin time

**extrinsic, 2 5 7 10

Front 10

when PT is increased whats on DDX

Back 10

1. Vit K deficit (2 7 9 10)

2. Warfarin

3. DIC

4. Liver disease , not making clotting factors

5. rare congenital things

Front 11

what is a better test for assessing the synthetic ability of the liver

PT or Albumin

Back 11

PT-

ALbumin has a long half live (20 days) so takes a while to show deficit

Front 12

ok so lets rank the severity of disease

in a mild, mod, severe disease whats the relative increase in:
AST/ALT
ALK Phos
GGT

Back 12

Mild: AST ALT x3, AP x2, GGT x3

Mod: AST/ALT x20, AP x5, GGT x 10

Severe: AST/ALT x 20++, AP x5++, GGT x10+++

Front 13

when might we see HUGE increase in ALT AST >2000

Back 13

1. Drugs
2. ischemic liver
3. acute viral hepatitis
4.

Front 14

when might we see mod increase in liver enzymes ALT ande AST 205-1000

Back 14

less specific
all liver disease
Wilson
A 1 antitryptin deficit
autoimmune
OTC meds
HSV

Front 15

what can cause a mild increase in liver enzymes

Back 15

1. any kind of liver disease with mild inflammatino/necrosis
2. non EtOh fatty liver- SUPER common
3. steatosis, EtOH, chronic viral hep, colestasis, cancer, hemachromatosis

Front 16

whats cholestasis

Back 16

impaired bile flow

can be drugs, viral, toxins
or stones, tumor, stricture

*sx: itch, yellow, abd pain, fever

Front 17

what LFT are incereased with cholestasis

Back 17

AP
GGT
Bili- cong
cholesterol
PT

Front 18

tell em about uncong bili

Back 18

its the majority, lipid soluble

increased when increased production of bili and increased in GILBERTS syndrome

rarely more than 5

Front 19

tell me about cong bili

Back 19

its in teh minority, water soluble

increased when there are inherited defects in hepatic secretion, regurg of bili from liver cells to serum

Front 20

AST/ALT ++
Bili +
albumin -
PT +
CHolesterol -

Back 20

hepatocellul;ar injury

Front 21

what does LFT look like for hepatocellular injuy

Back 21

increase in ALT/AST, as well as bili and PT

decrease in albimun adn cholesterol

Front 22

whats a liver infiltrative disease

Back 22

when things like fat, tumor, granuloma, cyst abcess, amyloid accumulate in liver

RUQ pain, weight loss, fever etc

AP increase (more than bili) , GGT increase

Front 23

what are LFT for infiltrative disease

Back 23

ALT AST +/-
AP ++
GGT++

Front 24

+/- ALT AST
AP++
GGT ++
bilib+
PT+
Cholesterol +/-

Back 24

infiltrative disease


Hepatocellular:
ALT/AST ++
AP+/-
GGT+/-
bili +
PT+
albumin -
cholesterol +/-

Front 25

doe the pancreas have protein producing capacity

Back 25

OH YA! more than liver and reticuloendothelial systemCOMBINED

Front 26

does EtOH cause acute or chronic pancreatitis

Back 26

both but chronic is much more liket to be EtOH

Acute can have lots of things besides EtOH (gallstones and EtOH is most common)

Front 27

whats a mild acute pancreatitis

Back 27

self limited, edematous intersitial pancreas

Front 28

what is a severe acute pancreatitis

Back 28

pancreatic necrosis, can lead to multi organ failure and local complications

Front 29

what causes acute pancreatitis

Back 29

EtOH
gallstoens
nothing
trauma
hypertryceridemia
CF

THIS is BAD
Trauma
Hypertriglycerides
Idiopathis
Scorpion bites
Biliary
Alcohol
Drugs
reyes

Front 30

what are some drugs assoc w/acute pancreatitis

Back 30

azathioprine
sulfa
tetracycline
valproic acid
ASA

Front 31

what race is pancreatits more common in

sex

other conditions

Back 31

black
M=W
AIDS

seen in older ppl

Front 32

55 to AA male has a sudden onset of epigastric pain that radiates to the back, it is constant dull and achy, there is NV. amylase is high as is lipase. the ALT is 300. whats the deal;

but then you see that HCT is 47% what does this make you think

Back 32

acute pancreatitis

ALT is more than 150 so it suggests GALLSTONE pancreatitis

HCT >47- severe necrotixing pancreatits

Front 33

what suggests gallstone pancreatitis

what about severe necrotizing pancreatitis

Back 33

ALT >150

HCT >47%

Front 34

pancreatitis and...

1. ALT
2. CRP
3. HCT

Back 34

1. ALT >150 gall stone pancreatits
2. CRP: >150 severe pancreatits
3. HCT >47 necrotizing pancreatits

Front 35

is serum amylase always increased in pancreatits

Back 35

nope, it is in like 75%

Front 36

tell me about ransons criteria

Back 36

determines prognosis of pancreatitis, you get pts for differnt sx (age, WBC, glucose, LDH, AST, HCT, BUN, Ca+, PO2, etc)

0-2 pts: 0-3 mortality
3-5 15%
6-11 >40%

Front 37

tell me about balthazar grading system

Back 37

uses a contract CT of pancrease to determine severity

Grade A-E based on fluid collection

Front 38

a score of more than what on the APACHE II pancreas grading scale indicated SAP

Back 38

>8

Front 39

what is teh most important thing to treat pancreatitis

Back 39

fluid replacement

also tx with AB, enteral nutrution

Front 40

whats teh deal with fine needle aspirate and pancreatitis

Back 40

do it when there is infected necrosis

Front 41

what labs are ordered for pancreatitis

Back 41

1. amylase,
2. Lipase
3. CBC
3. CMP
4. GGT

Front 42

when is CRP used for pancreatitis marker

Back 42

36-48 hrs

if >150 its severe

Front 43

when do you give AB for pancreatits

Back 43

first sign of infection

Front 44

in acute pancreatitis when is ERCP useful

Back 44

when AST, ALT and bili are increased

alonse US is NOT sensitive for CBD stones

Front 45

whats the def of chronic pancreatisi

Back 45

Chronic inflammation, fibrosis and cell loss due to ductal obstruction from strictures resulting from proteinaceous plug formation leading to ductal calcifications and/or stones

Front 46

what causes chronic pancreatitis

Back 46

1. EtOH
2. high lipids
3. congenital thigns like CF
3. autoimmune- ALE, PBC, sjogrens
5. Idiopathic

Front 47

whats the deal

your pt drinks a tin and has chronic intermittent back.abd pain that radiates to back. he has N often with some V, steatorrhea

whats the deal

Back 47

chronic pancreatitis

+/- increase amylase, lipase, Obstructed LFT, acquired DM late

Front 48

what does the pancreas with chronic pancreatitis look like

Back 48

strictures, calcifications,

Front 49

we know for acute pancreatitis the tx is AB and FLUID, what about chronic

Back 49

no EtOH
pain meds
decrease fat intake
give oral pancreatic enzymes
ductal decompression
resection of isolated section