Gi Part 1

Front 1

2 features of the hepatic artery:

Back 1

1. high Pressure

2. low Volume (25%)

- vice versa for portal vein

Front 2

the portal vein brings in 75% of the liver's blood supply; components of this supply:

(3)

Back 2

1. DEoxygenated blood (that's why portal vein is low P)

2. nutrients for the liver

3. waste products/toxins from the intestines/spleen

Front 3

PA's / triads contain:

(3)

Back 3

1. portal venules (no SM)

2. hepatic arterioles

3. interlobular bile ducts

Front 4

2 consequences of cirrhosis, at the lvl of the sinusoids:

Back 4

1. loss of fenestrations (=> no holes)

2. deposition of BM (=> blockage of transfers from blood)

Front 5

what are Kupfer cells and what do they do?

Back 5

macrophages WITHIN sinusoids that attach to endo

- remove bact . coming in from the gut

Front 6

what is the Space of Disse and why is it important?

Back 6

space between hepatocytes and sinusoids

- full of stellate cells, which normally produce Vit. A, but during cirrhosis, synthesize fibrous CT

=> dec. liver function

Front 7

2 markers of hepatocellular injury:

Back 7

ALT,

AST

Front 8

***3 markers of cholestasis:***

Back 8

1. AP

2. GGT

3. total Bilirubin

Front 9

cholestasis =

Back 9

little or no bile secretion

Front 10

3 markers of hepatic synthesis function:

Back 10

1. PT

2. Albumin (produced exclusively in the liver)

3. (bilirubin)

Front 11

PT is an *excellent* measure of liver function b/c:

Back 11

clotting factors have a very short half-life => change in liver function will be noticed almost immediately

Front 12

Bilirubin pathway: RBC's metabolized in the spleen => heme catabolized into:

Back 12

UNconjugated bili (Bu)

Front 13

***3 features of Bu:***

Back 13

1. INSOLUBLE in blood

2. MUST be (non-covalently) bound to albumin for transport to the liver

3. ***NEVER found in the urine***

Front 14

what does the liver do to Bu?

Back 14

conjugates it to glucuronic acid

=> Bc

Front 15

4 features of Bc:

Back 15

1. SOLUBLE

2. excreted into bile

3. CAN be filtered through kidneys => urine

4. NOT NORMAL to be in the urine - indicates disease state

Front 16

from the liver, Bc is excreted into bile and then goes to:

Back 16

the GI tract if needed or to the gallbladder for storage

Front 17

**from the GI tract, Bc of bile is:**

Back 17

*metabolized by bact. of the gut,*

into **urobilinogens**

Front 18

5 features of urobilinogens:

Back 18

1. mostly eliminated in the *feces* as stercobilin

2. => brown color

3. small amount is recycled in the liver

4. should NOT show up in the kidneys

5. (its breakdown product, urobilin, does - gives urine a yellow color)

Front 19

when Bc is HIGH for an extended period of time, it becomes:

Back 19

COVALENTLY bound to albumin

t1/2 becomes 20 days (that of albumin)

=> called Bd

Front 20

when the cause of high lvls of bilirubin are removed, the high lvls of Bu and Bc quickly drop to normal, but:

Back 20

Bd only *gradually* decreases (due to long half-life)

- responsible for persistent bilirubinemia

Front 21

You should NOT see Bd in:

Back 21

the urine

- it's bound to albumin

Front 22

total Bilirubin =

(3)

Back 22

Bu + Bc + Bd

Front 23

direct Bilirubin =

(2)

Back 23

Bc + Bd

- in most cases, Bd is so low that in can be ignored, and direct Bilirubin IS Bc

Front 24

indirect Bilirubin =

Back 24

Bu

Front 25

hyperbilirubinemia occurs in 3 ways:

Back 25

1. pre-hepatic

2 hepatocellular

3. post-hepatic/obstructive

Front 26

pre-hepatic hyperbilirubinemia/jaundice is a result of:

Back 26

TOO MUCH Bu

Front 27

2 potential causes of pre-hepatic hyperbili:

Back 27

1. hemolysis

2. overproduction of Bili

Front 28

does urine change color in pre-hepatic hyperbili?

Back 28

NO

- Bu is NOT excreted in the urine

Front 29

hepatocellular jaundice results from damage to or within the liver, as with:

(2)

Back 29

1. drug toxicity

2. viral hepatitis

Front 30

(remember, damage to liver results in decrease of:

Back 30

uptake, conjugation, and excretion of bilirubin/bile)

Front 31

**result of hepatocellular jaundice ** =

Back 31

MIX of Bu and Bc, depending on where the damage is

=> urine MAY be darkly pigmented, if enough Bc is being excreted by the kidneys

Front 32

when Bc is high in the urine, it's color will be:

Back 32

DARK

Front 33

obstruective/post-hepatic jaundice essentially equals:

Back 33

choledocholithiasis,

obstruction of the CBD

(usually due to gallstones)

Front 34

if the CBD is completely obstructed, bile reach severely-high lvls; at this point, the bilirubin seen will be:

Back 34

almost entirely Bc, and Bd if it persists for several days

Front 35

respective color of urine and stool in obstructive hyperbilirubinemia:

(2)

Back 35

1. urine will be VERY dark

2. stool will be PALE/CLAY-colored, due to LACK of Bc in the intestines => no conversion of Bc into urobilinogens => no stercobilin

Front 36

AST is NOT liver-specific; it's also found in:

Back 36

brain, kidney, etc.

Front 37

the height of ALT lvls roughly estimates:

Back 37

severity of liver parenchymal damage

Front 38

nl aminotransferases lvls do NOT exclude:

Back 38

liver disease

e.g. advanced cirrhosis => LOWER lvls than nl,

while Hep C ~~ fluctuating lvls

Front 39

Alkaline Phosphatase is also found in:

Back 39

*bone and placenta*

=> raised in bone disease, late-stage pregnancy

Front 40

if it IS liver-related, increased AP indicates:

Back 40

cholestasis

Front 41

cholestasis =

Back 41

little or no bile secreted

Front 42

GGT helps to confirm:

Back 42

***hepatic origin of AP***

Front 43

2 other features of GGT:

Back 43

1. nonspecific if by itself

2. induced by alcohol, meds as well as liver damage

Front 44

low lvls of albumin suggest:

Back 44

**decompensation**

- ascites, edema, etc.

Front 45

*hemolysis =>

Back 45

MODerate inc's in tBili

Front 46

a therapeutic dose of Tylenol may be fatal in someone with:

Back 46

cirrhosis

Front 47

2 detox roles of the liver:

Back 47

1. converts ammonia to urea

2. metabolizes EtOH

Front 48

Phase I drug metabolism is achieved via:

Back 48

Cytochrome P450 family

Front 49

cirrhosis is a plumbing problem; there is too much:

Back 49

R

Front 50

activation of Kufer cells following liver injury contributes to:

Back 50

the activation of stellate cells

Front 51

****7 clinical signs of cirrhosis:****

Back 51

1. ascites

2. peripheral edema

3. palmar erythema

4. asterexis (hand pulses when extended)

5. jaundice

6. caput/varices

7. spider naevi on arm

Front 52

SBP ~~ bact from:

Back 52

GUT get into peritoneal fluid

Front 53

portal HTN is defined as:

Back 53

>10-12 mmHg (when clinical symptoms start)

*normal = 5*

Front 54

Pressure =

(equation)

Back 54

Flow x R

Front 55

portal Pressure =

(equation)

Back 55

[in]flow x R [to outflow]

Front 56

"portal R to outflow" is a function of the R of:

(3)

Back 56

1. portal vein

2. hepatic sinusoids

3. hepatic vein

Front 57

collateral vessels become:

Back 57

the sites of varices if portal Outflow is obstructed

Front 58

increased inflow to mesenteric arterioles contrbutes to portal HTN; this increased inflow is a result of:

Back 58

inc. CO and vasodilation, which occur as a result of cirrhosis in the first place

Front 59

fluoroscopy ~~

Back 59

barium

Front 60

**"decompensated" = **

Back 60

has developed ANY complication of cirrhosis

(see Sheet schematic)

Front 61

**what is the most devastating complication of cirrhosis?**

Back 61

*varices*

- high mortality

Front 62

most effective approach to varices =

Back 62

PREVENTION

-screen e/o with cirrhosis or portal HTN with endoscope

Front 63

gastric or esophageal varices are the most common; one problem with them:

Back 63

TOO BIG to tie

- need to use BORTO (balloon obliteration) => inject sclerotherapy
(irritant that causes coagulation and narrowing of the vessel wall)

Front 64

3 causes of ascites:

Back 64

1. cirrhosis (75%)

2. malignancy

3. many other etiologies

Front 65

**what determines ascites etiology?**

Back 65

the Serum Ascites-Albumin Gradient

SAAG

Front 66

HIGH SAAG:

Back 66

>= 1.1

Front 67

***if the SAAG is HIGH, think:***

Back 67

ANATOMICAL etiology:

HF, IVC web, hepatic vein thrombosis, cirrhosis

Front 68

is SAAG is LOW, think:

(3)

Back 68

inf's, malignancies, AI disease

Front 69

2 most common gut pathogens =

Back 69

E. coli,

Kleb

Front 70

secondary prophylaxis against SBP =

Back 70

STANDING antibiotics, lifelong

Front 71

HRS =

Back 71

acute renal failure due to

cirrhosis or fulminant liver failure

~~ dec'd perfusion to kidneys

- an end-stage process

Front 72

3 symptoms for HRS:

Back 72

1. oliguric (low urine)

2. hypotensive

3. hyponatremic

Front 73

4 diagnostic criteria for HRS:

Back 73

1. cirrhosis with ascites

2. serum creatinine >1.5

3. absence of another cause of renal failure

4. no improvement after 2 days of albumin and no other meds

Front 74

Type I HRS is:

Back 74

rapidly fatal

- need transplant ASAP

Front 75

diagnosing Type I HRS:

Back 75

serum clearance doubles in <2 weeks

Front 76

Type II HRS is indolent and usually occurs as a result of:

Back 76

diuretic-refractory ascites

Front 77

prevention is the key to:

Back 77

ALL liver problems

Front 78

HCC is deadly; there is no:

Back 78

great therapy apart from transplant

Front 79

most common cause of HCC in the West =

Back 79

HCV and EtOH combined

Front 80

***special feature of HCC diagnosis:***

Back 80

can be achieved WITHOUT biopsy

- use contrast imaging

Front 81

***diagnosing HCC:***

(2)

Back 81

1. HCC cells are fed EXCLUSIVELY by hepatic artery
=> will light up FIRST

2. as HCC tumor is getting darker, the REST of the liver lights up via portal vein

Front 82

another way of calling the diagnostic pattern of HCC:

Back 82

1. early arterial enhancement

+

2. portal venous washout

Front 83

TIPS = shunt between:

(effect = )

Back 83

portal vein and hepatic vein,

- *rapidly reduces portal HTN*

Front 84

problems with TIPS:

Back 84

*further* loss of flow through portal vein

= further loss of nutrient supply to liver, while gut toxins don't get detoxified

Front 85

3 precipitating factors of hepatic encephalopathy:

Back 85

1. **inf's**

2. metabolic imbalance

3. meds

Front 86

hepatic encephalopathy is a diagnosis of:

Back 86

exclusion

Front 87

serum ammonia is a ____ ______ for encephalopathy

Back 87

BAD test;

ammount does NOT correspond to severity

Front 88

diagnosis of hepatic encephalopathy depends on:

Back 88

clinical symptoms in a "hepatic context"

Front 89

symptoms of high grade Hep. Enceph. =

(3)

Back 89

1. confusion

2. lethargy

3. unable to cooperate

Front 90

which kind of cirrhosis is the best kind to have?

Back 90

Child A

~ best survival

Front 91

Child cirrhosis calculations are based on:

(5)

Back 91

bile,

albumin,

INR,

ascites,

and encephalopathy

Front 92

3 features of the MELD score:

Back 92

1. from 6 to 40

2. determines whether you can get a liver transplant or not

3. higher MELD = gets transplant first

Front 93

MLED is based on:

(3)

Back 93

1. bili

2. INR

3. creatinine

Front 94

liver transplants are the ONLY cure for decompensated cirrhosis/HCC, and VERY effective;

Back 94

you must be able to survive

- so HF is out

Front 95

treatment of variceal bleeding:

(3)

Back 95

primary prophylaxis - prevent the first event from happening

1. screen all cirrhosis pts

2. EV Ligation of varices

3. NON-selective B-blockers

Front 96

2 nonselective B-blockers:

Back 96

propranolol,

nadolol

Front 97

**why do B-blockers have to be NON-selective to treat varices?**

Back 97

b/c cardio-selective ones only decrease CO,

whereas NON-selective ones dec. CO AND vasodilate

=> dec. portal HTN

(all titrated to cause HR or 60)

Front 98

EVL might CAUSE:

Back 98

variceal bleeds

Front 99

a/o with large varices AUTOMATICALLY gets NON-selective B-blocker treatment, as does anyone with:

Back 99

**with small varix AND decompensated cirrhosis**

- all others get monitored

Front 100

for ACUTE variceal bleed, focus on:

(ABC's)

Back 100

Airway

Breathing

Circulation

Drugs

Endoscopy

- in that order

Front 101

***3 drugs for acute variceal bleed***

Back 101

1. Octreotide (IV)

2. PPI's

3. antibiotics

Front 102

Octreotide =

Back 102

long-acting analogue of somatostatin

Front 103

***what does Octreotide do?***

Back 103

inhibits vasodilatory hormones,

which decreases the inflow into the already- hypertensive portal system,

by effectively increasing vasoconstriction of mesenteric arteries

**doesn't affect SYSTEMIC vessels/BP**

Front 104

why aren't B-blockers given in an ACUTE variceal bleed?

Back 104

they are anti-hypertensive, which is no good when you're bleeding AND hypotensive already

Front 105

why are PPI's given with acute variceal bleeds?

Back 105

to hedge against possible peptic ulcer bleed

- many cirrhotics have peptic ulcers => you don't know whether the bleed is coming from the ulcer or the varices

Front 106

why are antibiotics given for acute variceal bleed?

(3)

Back 106

1. dec. risk of re-bleeding (due to inflammation)

2. dec. risk of SBP

3. dec. risk of encephalopathy (a little)

Front 107

secondary prophylaxis prevents recurrent variceal bleeds; treatment =

(2)

Back 107

combination of band therapy/obliteration

AND

life-long B-blockers

Front 108

treatment for ascites:

(3)

Back 108

1. low-sodium diet (<2,000 mg/day)

2. diuretics

3. large volume paracentesis if refractory to diuretics

Front 109

**which diuretics are used in ascites, and why?

Back 109

1. Furosemide, for volume reduction

2. Spironolactone, to inhibiti RAA

in a 20/50 ratio

- watch for hyponatremia

Front 110

treatment for SBP = primary prophylaxis =

Back 110

WEEKLY antibiotics

- ciprofloxacin (a Q) + albumin to protect kidneys

Front 111

primary prophylaxis of SBP is indicated in:

(3)

Back 111

1. ascites

2. Child C

3. hyponatremia

Front 112

acute SBP: early therapy saves lives; if you see cirrhosis/ascites with _______(3)__________, start antibiotics

Back 112

cirrhosis/ascites with

1. fever

2. abdominal pain

or

3. altered mental status

Front 113

if you DON'T see fever/abd pain/AMS in cirrhosis/ascites pt, wait for:

Back 113

cell count to come back before deciding on antibiotics

Front 114

***pertinent cell count for starting early therapy in acute SBP:***

Back 114

>250 PMN's/cc

- NEEDS antibiotics

Front 115

antibiotics for treatment of ACUTE SBP:

Back 115

3rd-gen cephalosporins for 5 days, + albumin

- cefotaxime, ceftriaxone

- longer if blood cultures remain positive after 5 days

Front 116

secondary prophylaxis for SBP =

(2)

Back 116

ciprofloxacin or TMP/SMZ

- long-standing

Front 117

treatment for HRS:

(5)

Back 117

1. liver transplant

2. Midodrine + Octreotide + albumin

3. NOR or VP in severe cases

4. dialysis is only a BRIDGE (devastating alone)

5. TIPS doesn't work!

Front 118

**what do Midodrine and Octreotide do, respectively?**

Back 118

Mido vasoconstircts splanchnic/mesenteric arteries/arterioles;

Octreo inhibits vasodilation

Front 119

**effect of Mido + Octreo = **

Back 119

blood is shunted back toward the kidneys

Front 120

splanchnic means:

Back 120

of the organs

Front 121

Terlipressin =

Back 121

analogue of VP

- it too shunts flow back to kidneys,

- but also causes cardiac vasoconstriction => MI, a-fib

Front 122

we can reverse HRS, but can't:

Back 122

cure it

Front 123

general treatment of hepatic encephalopathy =

Back 123

reduce Nitrogen load from the gut

Front 124

treatment of encephalopathy:

(3)

Back 124

1. catharsis/pooping via lactulose

2. antibiotics

3. downsizing/closure of shunts/TIPS

Front 125

Rifaxamin and metronidazole are used to treat:

Back 125

encephalopathy

Front 126

other therapies for encephalopathy (grasping at straws):

(3)

Back 126

1. ornithine aspartate

2. zinc

3. short-medium-chain branched FA's

Front 127

with encephalopathy, do NOT:

Back 127

restrict prot

- just animal prot

- bean/veggy prot, is good