liver cirrhosis

Question 1

define cirrhosis

Answer 1

Cirrhosis is defined as fibrosis of the hepatic parenchyma resulting in nodule formation, altered hepatic function, restricted venous outflow, and portal hypertension

Question 2

Cirrhosis involves replacement of normal hepatic cells with ______________ and progressive deterioration of liver function.

Answer 2

fibrous scar tissue

Question 3

is cirrhosis reversible or irreversible. what does it lead to.

Answer 3

irreversible. it leads to portal hypertension responsible for the complications of advanced liver disease.

Question 4

cirrhosis it the result of ________________.

Answer 4

constant insult to the liver

Question 5

when does cirrhosis become clinically evident

Answer 5

not until the fourth decade of life

Question 6

what are the most common causes of cirrhosis

Answer 6

alcohol ingestion and viral hepatitis B and C infection

Question 7

what type of viral hepatitis leads to cirrhosis

Answer 7

chronic infection with hepatitis B or C virus

Question 8

how are hepatitis B & C transmitted. what is the more common route for hepatitis B

Answer 8

both are transmitted through IV drug use but sexual contact is more common for hepatitis B

Question 9

what is the normal portal vein pressure

Answer 9

5-10mm Hg

Question 10

what causes portal HTN. when does it occur (pressure)

Answer 10

increased resistance to hepatic blood flow. occurs when portal pressure exceed 10-12 mm Hg

Question 11

what is the most common cause of portal htn

Answer 11

intrahepatic damage

Portal hypertension results from fibrotic changes within the hepatic sinusoids, changes in the levels of vasodilatory and vasoconstrictor mediators, and an increase in blood flow to the splanchnic vasculature

Question 12

reduced hepatic blood flow ______________ and ______________. eg. ________

Answer 12

alters the metabolism and decreases protein synthesis eg. albumin

Question 13

what happens when hepatic drug metabolism is reduced.

especially with what kind of drugs

Answer 13

drug concentrations increase systemically and half lives are extended which were normally excreted by the liver. especially those with high first pass metabolism.

Question 14

how can reduced hepatic metabolism cause therapeutic failure

Answer 14

decreased hepatic metabolism can lead to reduced prodrug activation or delayed response leading to therapeutic failure

Question 15

what signs and symptoms are observed in hepatic metabolism failure (failure to excrete waste products)

Answer 15

accumulation of bilirubin ( due to enzymatic breakdown of heme and not metabolized by the liver), jaundice yellowing of skin, scleral icterus - yellowing of sclera and tea-coloured urine ( urinary bilirubin excreted as urobilinogen)

Question 16

what is urinary bilirubin excreted as in hepatic metabolism failure (failure to excrete waste products)

Answer 16

urobilinogen

Question 17

what is ascitis

Answer 17

ascitis is the accumulation of fluid in the peritonium

Question 18

what is the most common condition associated with cirrhosis. does it have a good or poor prognosis

Answer 18

ascitis is the most commonly associated condition with cirrhosis. it has a poor prognosis

Question 19

the pathophysiology of which 3 conditions are interrelated

Answer 19

ascitis, portal htn and cirrhosis

Question 20

Cirrhotic changes and subsequent decreases in synthetic function lead to ______________

Answer 20

hypoalbuminemia

Question 21

what allows the fluid to leak from the vascular space into body tissues

Answer 21

low serum bilirubin, increased hydrostatic pressure, increased capillary permeability

Question 22

what does lowered effective intravascular volume cause

Answer 22

decreased renal perfusion. kidneys activate RAAS, increasing plasma renin activity. increased aldosterone production. increased sodium and water retention.

Question 23

what are varices

Answer 23

varices are weak superficial vessels that protrude intot he gastric lumen and may rupture or bleed due to any additional increase in pressure

Question 24

what is the most important RESULT of portal htn

Answer 24

development of varices

Question 25

why do varices develop. in which parts could it develop

Answer 25

development of varices occurs to overcome resistance to drainage originating from the organ esophagus, stomach and rectum due to compensate for increased blood volume

Question 26

when are patients with cirrhosis at risk of varices

Answer 26

when the portal pressure exceeds the vena cava pressure by greater than or equal to 12 mm Hg

Question 27

Hemorrhage from varices occurs in________ of patients with cirrhosis Each episode of variceal bleeding carries a _______risk of death.

Answer 27

25% to 40% 25% to 30%

Question 28

what is hepatorenal syndrome

Answer 28

hepato renal syndrome is the decline in renal function in cirrhosis the cause of which is not intrinsic renal diseas.e It is caused by rapid deterioration of renal function in the presence of cirrhosis.

Question 29

what is the risk associated with HRS if untreated

Answer 29

rapidly fatal with a 50% mortality rate at 14 days.

Question 30

how do the kidneys in HRS counteract the drop in renal perfusion

Answer 30

by activating the RAAS, increasing renin activity, causing fluid retention and peripheral vasoconstriction in attempt to increase renal blood flow

Question 31

what is SBP

Answer 31

SBP is acute bacterial infection of the peritoneal ascitic fluid in absence of intra abdominal infection or intestinal perforation

Question 32

Up to _____ of patients with ascites develop SBP

Answer 32

30%

Question 33

The most common bacteria isolated from patients with SBP are

Answer 33

gram -ve = e.coli, klebsiella pneumoniae | gram +ve = streptococcus pneumoniae

Question 34

what is HE caused by

Answer 34

oesophageal bleeding, PUD, Excessive protein intake, Sedatives & Opioids.

Question 35

what is HE

Answer 35

In severe hepatic disease, systemic circulation bypasses the liver; substances that are normally hepatically metabolized accumulate in the systemic circulation. These metabolic by-products, especially nitrogenous waste, are neurotoxic. Ammonia (NH3) is the main toxin implicated in HE. Ammonia is a metabolic by-product of protein catabolism & is also generated by bacteria in the GIT.

Question 36

In cirrhosis, conversion to____ is reduced and _________ accumulates

Answer 36

urea | ammonia

Question 37

Patients with HE commonly have _________________ (lab)

Answer 37

elevated serum ammonia concentrations, but ammonia levels do not correlate with the degree of CNS impairment (because other toxins are involved).

Question 38

Patients with cirrhosis may be___________ until_____ __________ develop.

Answer 38

asymptomatic | acute complications

Question 39

Clinical Presentation of Cirrhosis | S&S

Answer 39

-hepatomegaly, splenomegaly -pruritis, jaundice, palmar, erythema, spider angiomata, hyperpigmentation - gynecomastia, decreased libido - Malaise, anorexia and weight loss encephalopathy

Question 40

Clinical Presentation of Cirrhosis | Laboratory tests

Answer 40

Laboratory tests ``` Hypoalbuminemia Elevated prothrombin time Thrombocytopenia Increased bilirubin concentration Elevated liver enzymes: aspartate aminotransferase (AST), alanine aminotransferase (ALT), and γ -glutamyl transpeptidase (GGT) ```

Question 41

why do models exist for classification of liver disease | give eg. of a model

Answer 41

to determine severity of end stage liver disease and need for transplantation eg. child turcotte pugh model

Question 42

child turcotte pugh model readings | as many as you remember

Answer 42

``` serum bilirubin not more than 3 (more than 3 severe) serum albumin not less than 2.8 prothrombin time not greater than 6s HE mild mod adv ascitis mild mod advace ``` scores 5-6 pts = 1yr 100% 2yr 85% 7-9 pts = 80% 60% 10-15pts = 45% and 35%

Question 43

what are the desired outcome in ttt of liver cirrhosis. is it reversible? what are the immediate ttt goals

Answer 43

liver cirrhosis is irreversible so ttt is aimed at treating underlying cause, preventing disease progression and avoiding complications imm ttt goals are stop variceal bleeding and prevent SBP

Question 44

ttt for portal htn

Answer 44

non selective beta blockers eg. propanolol nitrates eg. isosorbide mononitrate nitrates when used alone cause mortality

Question 45

what are the goals in ascitis

Answer 45

``` Mobilize ascitic fluid Diminish abdominal discomfort, back pain, and difficulty in movement Prevent complications (bacterial peritonitis & respiratory distress). ```

Question 46

ttt in ascitis should be done gradually. why?

Answer 46

the allow the ascitic fluid to equilibrate with intravascular fluid

Question 47

ttt of ascitis what is the goal of weight loss aggressive diuresis should be avoided unless how is it acutely ttt? how much fluid removed if volume exceeding 5L removed what is done

Answer 47

Spironolactone (an aldosterone antagonist) with or without furosemide forms the basis of pharmacological treatment of ascites. 0.5 - 1 kg/day or 0.5-1L fluid loss aggressive diuresis should be avoided unless patient has concomitant peripheral edema acute discomfort resolved by paracentesis, 1-2 L removed albumin infusion post paracentesis

Question 48

Treatment goals for an acute bleeding in varices are: Risk factors for early rebleeding are: Risk factors for late rebleeding are:

Answer 48

Volume resuscitation Acute treatment of bleeding Prevention of recurrence. Age >60 years Acute renal failure Severe initial bleeding (defined as hemoglobin <8 mg/dL). ``` Severe liver failure Continued alcohol abuse Large variceal size Renal failure Hepatocellular carcinoma. ```

Question 49

Treatment options for varices:

Answer 49

``` Splanchnic vasoconstrictors e.g. Somatostatin or octreotide Endoscopic Interventions: Sclerotherapy (injecting sclerosing agent e.g. ethanolamine into the varix) Band Ligation (placement of rubber bands around the varix) ``` Combination of vasoconstrictor and variceal ligation to manage bleeding is recommended. Balloon tamponade is used as a temporary measure (maximum of 24 hours) to stop massive bleeding. Surgical intervention: in patients who have failed repeated endoscopy and vasoactive drug therapy Guidelines recommend 7 days of antibiotic prophylaxis for prevention of Spontaneous Bacterial Peritonitis in patients with variceal hemorrhage