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pharmacotherapy 2 > liver cirrhosis > Flashcards

liver cirrhosis Flashcards

1
Q

define cirrhosis

A

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

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2
Q

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

A

fibrous scar tissue

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3
Q

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

A

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

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4
Q

cirrhosis it the result of ________________.

A

constant insult to the liver

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5
Q

when does cirrhosis become clinically evident

A

not until the fourth decade of life

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6
Q

what are the most common causes of cirrhosis

A

alcohol ingestion and viral hepatitis B and C infection

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7
Q

what type of viral hepatitis leads to cirrhosis

A

chronic infection with hepatitis B or C virus

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8
Q

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

A

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

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9
Q

what is the normal portal vein pressure

A

5-10mm Hg

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10
Q

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

A

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

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11
Q

what is the most common cause of portal htn

A

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

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12
Q

reduced hepatic blood flow ______________ and ______________. eg. ________

A

alters the metabolism and decreases protein synthesis eg. albumin

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13
Q

what happens when hepatic drug metabolism is reduced.

especially with what kind of drugs

A

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

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14
Q

how can reduced hepatic metabolism cause therapeutic failure

A

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

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15
Q

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

A

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)

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16
Q

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

A

urobilinogen

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17
Q

what is ascitis

A

ascitis is the accumulation of fluid in the peritonium

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18
Q

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

A

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

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19
Q

the pathophysiology of which 3 conditions are interrelated

A

ascitis, portal htn and cirrhosis

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20
Q

Cirrhotic changes and subsequent decreases in synthetic function lead to ______________

A

hypoalbuminemia

21
Q

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

A

low serum bilirubin, increased hydrostatic pressure, increased capillary permeability

22
Q

what does lowered effective intravascular volume cause

A

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

23
Q

what are varices

A

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

24
Q

what is the most important RESULT of portal htn

A

development of varices

25
Q

why do varices develop. in which parts could it develop

A

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

26
Q

when are patients with cirrhosis at risk of varices

A

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

27
Q

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

A

25% to 40%

25% to 30%

28
Q

what is hepatorenal syndrome

A

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.

29
Q

what is the risk associated with HRS if untreated

A

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

30
Q

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

A

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

31
Q

what is SBP

A

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

32
Q

Up to _____ of patients with ascites develop SBP

A

30%

33
Q

The most common bacteria isolated from patients with SBP are

A

gram -ve = e.coli, klebsiella pneumoniae

gram +ve = streptococcus pneumoniae

34
Q

what is HE caused by

A

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

35
Q

what is HE

A

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.

36
Q

In cirrhosis, conversion to____ is reduced and _________ accumulates

A

urea

ammonia

37
Q

Patients with HE commonly have _________________ (lab)

A

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

38
Q

Patients with cirrhosis may be___________ until_____ __________ develop.

A

asymptomatic

acute complications

39
Q

Clinical Presentation of Cirrhosis

S&S

A

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

40
Q

Clinical Presentation of Cirrhosis

Laboratory tests

A

Laboratory tests

Hypoalbuminemia
Elevated prothrombin time
Thrombocytopenia
Increased bilirubin concentration 
Elevated liver enzymes: aspartate aminotransferase (AST), alanine aminotransferase (ALT), and γ -glutamyl transpeptidase (GGT)
41
Q

why do models exist for classification of liver disease

give eg. of a model

A

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

42
Q

child turcotte pugh model readings

as many as you remember

A 
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%

43
Q

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

A

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

44
Q

ttt for portal htn

A

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

45
Q

what are the goals in ascitis

A 
Mobilize ascitic fluid
Diminish abdominal discomfort, back pain, and difficulty in movement
Prevent complications (bacterial peritonitis & respiratory distress).
46
Q

ttt in ascitis should be done gradually. why?

A

the allow the ascitic fluid to equilibrate with intravascular fluid

47
Q

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

A

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

48
Q

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

A

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.
49
Q

Treatment options for varices:

A 
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

pharmacotherapy 2 (8 decks)

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