Module 3 Chapter 14: Cirrhosis

Question 1

Lab diagnosis for cirrosis

Answer 1

AST>ALP, increased ALP, decreased platelets, increased bilirubin, increased INR, decreased albumin.

Question 2

imaging diagnosis for cirrhosis

Answer 2

nodular liver or evidence of portal hypertension and big spleen.

Question 3

physical exam diagnosis for cirrhosis

Answer 3

hyper dynamic circulation (decreased BP and increased HR), stigmata of chronic liver disease (jaundice, ascites, edema, estrogen issues, encephalopathy)

Question 4

what is mainly responsible for the development of complications? (decompensation)

Answer 4

portal hypertension

Question 5

the child Pugh score is scored ___(5-6), ____ (7-9) or C (10-15). What components does it comprise of?

Answer 5

encephalopathy
ascities
bilirubin
albumin
INR

Question 6

MELD Score

Answer 6

developed to predict survival after trans jugular portosystemic shunt insertion (TIPS).

Includes bilirubin, INR, creatinine.

Used for liver transplant, but now it includes sodium.

Question 7

pathophysiology behind varies

Answer 7

o Varices form in response to portal hypertension and represent the reopening of connections
between the portal and systemic circulation
o They are most commonly seen in the distal esophagus, stomach and rectum

Question 8

clinical presentation of varices

Answer 8

• hematemesis
• melena
• hematoochezia

Question 9

when should screening for varices occur?

Answer 9

cirrhotics should undergo surveillance endoscopy to look for varices.
but they don’t need an endoscopy if platelets are above 150.

Question 10

preventing the first bleeding of esophageal varices

Answer 10

NSBB (nadolol, propanolol) or Banding
BUT: Beta blockers do not prevent the varices from FORMING. they prevent existing varices from BLEEDING.

endoscopy and banding should be done every 2-4 weeks until varices are obliterated.

Question 11

during an active esophageal variceal bleed, what should be given?

Answer 11

• volume expansion (saline) and RBCs if Hb is low.
• 7 days of antibiotics
• octreotide bolus plus infusion 3-5 days
• EGD for banding.
• TIPS for uncontrolled or recurrent bleed.

Question 12

when should TIPS be considered in cirrhotic patients?

Answer 12

when variceal bleeding is uncontrolled or recurrent

Question 13

classification of gastric varices

Answer 13

GOV1 along the lesser curvature
GOV2: along greater curvature

Isolated gastric varices
IGV1= in the fundus
IGV2= else where in the stomach.

Question 14

primary prophylaxis of gastric varices

Answer 14

injection of glue– superior to NSBB in preventing the first bleed.

Question 15

what to do during gastric variceal bleeding

Answer 15

gluing is preferred, as banding in the stomach is difficult.

Question 16

gastric varices secondary prophylaxis

Answer 16

NSBB and gluing or consider TIPS for recurrent bleeding

Question 17

portal hypertensive gastropathy

Answer 17

mosaic pattern in the stomach due to congestion (“snake-skin boot” appearance) and
may have erythema or red spots

Question 18

gastric antra vascular ectasia

Answer 18

red streaks in the antrum (“watermelon stomach”), or a more diffuse
pattern similar to PHG, and is seen with cirrhosis and connective tissue diseases

Question 19

management of Portal hypertensive gastropathy

Answer 19

NSBB, octreotide for acute bleeding, TIPS or liver transplant for refractory bleeding

Question 20

management for Gastric antra vascular ectasia

Answer 20

argon plasma coagulation (APC) or Nd:YAG laser, estrogen therapy, banding might be helpful in antrum, surgery (if not cirrhotic)

Question 21

pathophysiology of ascites in cirrhosis

Answer 21

Cirrhosis leads to portal hypertension → vasodilators (nitric oxide, carbon monoxide) are produced in response to high pressure in liver and portal circulation → vasodilators get into systemic circulation via collaterals → leads to vasodilation in the systemic circulation (hyperdynamic circulation with ↓ BP and ↑ HR) → kidneys respond to this with activation of renin-angiotensin-aldosterone system (RAAS) → sodium and water retention → worsen portal hypertension → ascites eventually is forced through the liver capsule and peritoneal lining into abdominal cavity NOTE: patients often have cirrhotic cardiomyopathy and low albumin, which contribute to ascites formation

Question 22

what must be tested when someone presents with ascites?

Answer 22

spontaneous bacterial peritonitis has a mortality of 20% and can lead to hepatic renal syndrome (must do paracentesis to confirm). SBP may be present with fever and high WBC and high creatinine

Question 23

What must you do with albumin count when someone has ascites?

Answer 23

CALCULATE SEUM ASCITES ALBUMIN GRADIENT= (albumin in serum) - (albumin in the ascites fluid)

Question 24

if ascites is due to Budd chiari syndrome, the protein is ____ and they are at ___ risk for SBP

Answer 24

high protein, low risk for SBP.

Question 25

a diagnosis of SBP would have a high ____ count

Answer 25

high neutrophil count. The culture and sensitivity would also be spiked.

Question 26

first line treatment for asictes

Answer 26

sodium restricted diet
- stop alcohol
- stop NSAIDS
- diuretics (spironolactone)
consider for liver transplant

Question 27

second line treatment for refractory asciets

Answer 27

1. large volume paracentesis
   - consider stopping NSMM, ACE inhibitors because these can LOWER BP and thus WORSEN fluid retention.
2. Add MIDODRINE to increase BP and facilitate renal perfusion.
3. TIPSS (shunt), lowers portal pressure but improves renal perfusion.q

Question 28

when should you NOT do tips

Answer 28

when there’s hepatic encephalopathy. you can worsen neurological symptoms further if you have a shunt

Question 29

treatment for Spontaneous bacterial peritonitis

Answer 29

antibiotics

intravenous albumin

Question 30

definition of hepatorenal syndrom

Answer 30

• cirrhosis with ascites
• high serum creatinine
  -no shock
  can manifest via SBP

Question 31

type II vs type I HRS

Answer 31

o Type II = slow increase in creatinine in
patients with refractory ascites undergoing frequent LVP, which often responds to lowering diuretics
o Type I = rapid deterioration in renal
function, often precipitated by infection or
NSAIDs

Question 32

Treatment for HRS

Answer 32

midodrine to increase BP (also used as a second line ascites treatment)

2. octreotide to lower portal pressure
3. albumin intravenously to improve circulation.

consider TIPS. Prognosis is very poor, HRS is an indication for liver transplant.

Question 33

hepatic encephalopathy

Answer 33

Hepatic encephalopathy (HE) is a brain dysfunction caused by liver insufficiency and/or
portosystemic shunting which manifests as a wide spectrum of neurological or psychiatric abnormalities ranging from subclinical alterations to coma

Question 34

Type A, B and C causes of hepatic encephalopathy

Answer 34

o  Type (underlying disease)
  A = Acute Liver Failure   B = Portosystemic shunt   C = Cirrhosis

Question 35

treatment of hepatic encephalopathy

Answer 35

1. lactulose (remember that this doesn’t help with acute liver failure, but will help with HE via cirrhosis). It is converted to lactic acid in colon creating acidic environment which slows NH3
   absorption
2. antibiotics
3. BCAAs, liver transplantation if refractory

Question 36

T/F: should restrict protein on cirrhotic patient

Answer 36

false.

Question 37

condition where ascites travels through the diaphragm

Answer 37

hepatic hydrothorax. can be complicated by infection/sbp. treat just like ascites

1. reduce salt intake
2. no alcohol
3. dieuretics
4. stop NSAIDs

2nd:

1. paracentesis
2. midodrine
3. consider TIPSS
4. consider stopping ACE inhibitors.

Question 38

T/F can use acetaminophen if cirrhotic

Answer 38

true, as long as they are not using alcohol. should avoid basis as they can cause Gi bleeding and HRS. Opioits can also accumulate and precipitate hepatic encephalopathy