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DEMS Exam 1 > Cirrhosis > Flashcards

Cirrhosis Flashcards

1
Q

in which patients should we suspect Cirrhosis

A

Any patient with chronic liver disease ->

Chronic abnormal aminotransferases (ALT) and/or alkaline phosphatase (alk phos)

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2
Q

what is an early, more sensitive lab finding suggestive of cirrhosis that occurs as a result of portal hypertension and hypersplenism

A

low platelet count

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3
Q

Liver biopsy for cirrhosis is not necessary in the presence of any of the following:

A

1) Decompensated cirrhosis (variceal hemorrhage, ascites, encephalopathy)
2) CT scan diagnostic of cirrhosis

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4
Q

what can be seen on CT scan to diagnose cirrhosis

A

The contour of the liver is irregular,
Splenomegaly,
Presence of collaterals indicates portal hypertension and secures the diagnosis of cirrhosis.

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5
Q

The Model for End-stage Liver Disease ( MELD) is a mathematical model that estimates the risk for 3-month mortality. It is derived from the ______

A

serum total bilirubin, serum creatinine, and INR for prothrombin time.

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6
Q

Portal hypertension can result from what 2 mechanisms:

A

1) Increase in resistance to portal flow and/or

2) Increase in portal venous inflow

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7
Q

The deposition of fibrous tissue and the formation of nodules, disrupts the architecture of the liver, leading to an increased resistance to flow and to _____. Vessels that normally drain into the portal system, such as the coronary vein (left gastric vein), reverse their flow and become_____. Additionally, with portal hypertension, the spleen increases in size and sequesters platelets and other formed blood cells leading to hypersplenism.

A

portal hypertension,

porto-systemic collaterals

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8
Q

what is an example of Pre-hepatic portal hypertension

A

Portal or splenic vein thrombosis

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9
Q

what is an example of Post-hepatic portal hypertension

A

Budd-Chiari syndrome (Hepatic Vein Thrombosis)

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10
Q

what is an example of pre-sinusoidal portal hypertension

A

(Schistosomiasis) freshwater parasitic worms

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11
Q

what is Sinusoidal Obstruction Syndrome (formerly Hepatic Venooclusive Disease)

A

Condition in which small hepatic veins are obstructed

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12
Q

when does Sinusoidal Obstruction Syndrome (formerly Hepatic Venooclusive Disease) most commonly occur?

A

Occurs most commonly as a complication of myeloablative regimens used to prepare patients for bone marrow transplantation

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13
Q

IN THE NORMAL LIVER, ______ PLAYS AN IMPORTANT ROLE IN THE REGULATION OF INTRAHEPATIC RESISTANCE

A

NITRIC OXIDE

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14
Q

IN CIRRHOSIS, ______ ACTIVITY IS REDUCED AND THE ACTIVITY OF VASOCONSTRICTORS IS INCREASED

A

NITRIC OXIDE

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15
Q

Elevated portal pressure leads to an increase in shear stress in the splanchnic vasculature. Shear stress gives rise to an ________, splanchnic vasodilatation and increased portal flow.

A

increase in nitric oxide (NO) production

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16
Q

how is portal pressure measured

A

portal pressure is measured as the gradient between portal and inferior vena cava pressures

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17
Q

which types of portal hypertension will have increased hepatic venous pressure gradients (HVPG)

A

sinusoidal,

post-sinusoidal

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18
Q

________ consists of the placement of rubber rings on variceal columns with the objective of interrupting blood flow and subsequently developing necrosis of mucosa and submucosa and replacement of varices by scar tissue.

A

Endoscopic variceal ligation

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19
Q

Bleeding controlled in ____ of patients who undergo Endoscopic Variceal Band Ligation

A

90%

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20
Q

what does TIPS mean?

A

Transjugular Intrahepatic Portosystemic Shunt
It is a intrahepatic stent that connects a branch of the portal vein with a branch of an hepatic vein, bypassing the liver to relieve portal hypertension

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21
Q

what are possible complications of a TIPS procedure?

A

complications related to diversion of blood flow away from the liver, namely portal-systemic encephalopathy and liver failure (ischemia).

22
Q

_____ is the Most Sensitive Method to Detect Ascites

A

Ultrasound

23
Q

what is a routine workup for AscitesDiagnostic Paracentesis

A

the fluid should be routinely evaluated for:
Albumin (with simultaneous estimation of serum albumin, total protein),
Polymorphonuclear (PMN) blood cell count,
Bacteriological cultures (shown in yellow).

24
Q

what are indications for Diagnostic Paracentesis

A 
New-onset ascites
Admission to hospital
Symptoms/signs of abdominal or systemic infections
Renal dysfunction
Unexplained encephalopathy
25
Q

THE SERUM-ASCITES ALBUMIN GRADIENT (SAAG) CORRELATES WITH _______

A

SINUSOIDAL PRESSURE

26
Q

how do you calculate the Serum-Ascites Albumin Gradient

A

serum albumin minus ascites albumin

27
Q

what is the Tx for Portal Hypertension with No ascites

A

No specific therapy

Consider salt restriction

28
Q

what is the Tx for Uncomplicated ascites

A

1) Salt restriction + diuretics

2) Large volume paracentesis (LVP) with tense ascites

29
Q

what is the Tx for Refractory ascites

A

1) LVP + albumin

2) TIPS

30
Q

what are the Definitions and Types of Refractory Ascites

A

Diuretic-intractable ascites (80%):
Therapeutic doses of diuretics cannot be achieved because of diuretic-induced complications

Diuretic-resistant ascites (20%):
No response to maximal diuretic therapy (400 mg spironolactone + 160 mg furosemide/day)

31
Q

describe Type 1 hepatorenal syndrome:

A

Rapidly progressive renal failure (2 weeks)

Doubling of creatinine to >2.5 or halving of creatinine clearance (CrCl) to <20 ml/min

32
Q

Describe type 2 hepatorenal syndrome

A

More slowly progressive
Creatinine >1.5 mg/dL or CrCl < 40 ml/min
Associated with refractory ascites

33
Q

Median survival in HRS type 2 is ______ compared to only _____ in HRS type 1.

A

6 months,

2 weeks

34
Q

what are the MANY CONDITIONS OTHER THAN HEPATORENAL SYNDROME THAT CAN LEAD TO RENAL FAILURE IN PATIENTS WITH CIRRHOSIS

A 
1) decreased arterial resistance:
     Vasodilators
     LVP w/o albumin
     Infection
2)decrease effective blood volume:
     Diuretics
     Diarrhea
     Hemorrhage
3) increase renal constriction:
     NSAID use
4) nephrotoxic: aminoglycosides
35
Q

_______ is universal in patients with HRS.

A

Ascites (If ascites is absent, renal failure is more likely due to other causes )

36
Q

_________ is almost universal in HRS.

A

Hyponatremia (If serum sodium is normal, diagnosis of HRS is unlikely)

37
Q

The only definitive treatment of HRS is _______

A

liver transplantation.

38
Q

________ is the Most Common Infection in Cirrhotic Patients

A

Spontaneous Bacterial Peritonitis (SBP)

39
Q

what is the main mechanism for Spontaneous Bacterial Peritonitis (SBP)

A

Bacterial Translocation (BT) which is the migration of viable microorganisms from the intestinal lumen to mesenteric lymph nodes and other extraintestinal organs and sites

40
Q

how is the diagnosis for spontaneous Bacterial Peritonitis (SBP) made?

A

Diagnosis based on ascitic fluid

PMN count >250/mm3

41
Q

what is the most common isolated organism in SBP

A

Gram-negative bacilli (72%)

->(Escherichia coli 47%)

42
Q

what is the Recommended antibiotics for initial empiric therapy of SBP

A 
i.v. cefotaxime, amoxicillin-clavulanic acid
oral ofloxacin (uncomplicated SBP)
43
Q

which antibiotic should be avoided in SBP therapy?

A

aminoglycosides

44
Q

________ Decreases Renal Dysfunction and Short-term Mortality in Spontaneous Bacterial Peritonitis

A

Albumin

45
Q

Patients who have recovered from an episode of SBP have a ______ chance of developing another episode within the first year

A

70%

46
Q

________ REDUCES RECURRENCE OF SPONTANEOUS BACTERIAL PERITONITIS (SBP)

A

NORFLOXACIN (fluoroquinolone antibiotic)

47
Q

antibiotic prophylaxis is not justified in patients with ______

A

high-protein ascites.

48
Q

The diagnosis of hepatic encephalopathy is based on history and physical exam findings. _____ levels are unreliable, and there is a poor correlation between the stage of encephalopathy and blood level of _______. Therefore, measurements of ______ are not necessary

A

Ammonia X3

49
Q

Precipitating factors for hepatic encephalopathy include:

A

High protein load,
Gastrointestinal bleeding or constipation,
Infection,
overdiuresis (leading to azotemia and hypokalemia). Narcotics and sedatives by directly depressing brain function.
Transjugular intrahepatic porto-systemic shunt (TIPS).

50
Q

what is the treatment of Hepatic encephalopathy?

A

1)Identify and treat precipitating factor:
(Infection, GI hemorrhageconstipation etc…)
2)Lactulose (adjust to 2-3 bowel movements/day)
3)Protein restriction, short-term (if at all)

51
Q

describe the mechanism of action of lactulose

A

The acidic pH decreases urease-producing bacteria which produce ammonia. The proton H+ produced combines with NH3 to give NH4, which is non-absorbable, and results in ammonia excretion in stool

DEMS Exam 1 (28 decks)

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