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DEMS I > cirrhosis and complications > Flashcards

cirrhosis and complications Flashcards

1
Q

cirrhosis

A

·Late stage of progressive hepatic fibrosis

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2
Q

cirrhosis histology

A

·regenerative nodules surrounded by fibrous tissue

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3
Q

types of cirrhosis

A

Compensated (no complications) OR Decompensated (complications)

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4
Q

Transition from compensated to decompensated cirrhosis

A

development of variceal hemorrhage, ascites, hepatic encephalopathy and/or jaundice

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5
Q

Cirrhosis leads to what two clinical syndromes

A

portal hypertension and liver insufficiency. Portal hypertension cuases variceal hemorrhage, ascites and encephalopathy. Liver insufficiency causes encephalopathy and jaundice

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6
Q

complications of ascites

A

infection (spontaneous bacterial peritonitis) and the development of a functional renal failure (hepatorenal syndrome).

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7
Q

In whom should we suspect cirrhosis

A

any patient with chronic liver disease- chronic abnormal ALT and/or Alk phosp

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8
Q

etiologies of cirrhosis

A

viral (Hep C and B), alcoholic liver dz, autoimmune (PBC, PSC, autoimmune hepatitis), metabolic (hemochromatosis, wilsons dz, alpha1 antitrypsin), vascular (Budd-Chiari syndrome, CHF), non alcoholic fatty liver dz

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9
Q

cirrhosis physical exam findings

A

jaundice, spider angiomata, enlargement of the left lobe of liver, caput medusae, ascites, dupuytrens contracture, muscle wasting and splenomegaly.

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10
Q

cirrhosis lab findings

A

Hypoalbuminemia, prolonged INR, hyperbilirubinemia, Low platelet count

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11
Q

cirrhosis radiological findings

A

nodular liver with caudate lobe hypertrophy, ascites, splenomegaly, venous collaterals, recanulization of the umbilical vein and hepatocellular carcinoma.

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12
Q

is liver biopsy required for confirming cirrhosis

A

No- not in the presence of decompensation or physical exam, laboratory and radiologic findings compatible with cirrhosis. Also not needed for transplant

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13
Q

What child-Turcotte-Pugh score is required for liver transplant

A

7 or greater

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14
Q
  1. Recognize the components of the Model for End-Stage Liver Disease (MELD score)
A

A mathematical model that estimates the risk for 3-month mortality. It is derived from the serum total bilirubin, serum creatinine, and INR for prothrombin time.

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15
Q

describe the MELD score use

A

Determines priority for liver transplant in cirrhosis: Among patients with the same blood type, the patient with the highest MELD score gets the priority. Waiting times are used only to break ties when patients have identical MELD scores. MELD scores are updated at regular intervals

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16
Q

Who gets highest priority for liver transplants

A

fulminant hepatic failure

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17
Q
  1. Describe the mechanism of portal hypertension in cirrhosis
A

Initial mechanism: increased intrahepatic sinusoidal resistance (nl liver has almost no resistance to flow) from deposition of fibrous tissue and active vasoconstriction leads to reversal of vessels draining into portal system and spleen increases in size. Then: increased shear stress in splanchnic vasculature > increased NO > splanchnic vasodilation > increased portal blood inflow > increased portal HTN

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18
Q

What causes vasoconstriction in cirrhosis

A

reduced endothelial nitric oxide release and increase in endogenous vasoconstrictors endothelin-1 and increased endothelin-1 receptor density

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19
Q

Diagnosis of portal hypertension

A

Measure portal pressure via hepatic vein catheterization. The hepatic venous pressure gradient (HVPG) is obtained by subtracting the free hepatic venous pressure (FHVP) from the wedged hepatic venous pressure (WHVP). Normal HVPG is 3-5mmHg

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20
Q

compare HVPG is pre vs post hepatic portal hypertension

A

Presinusoidal and pre-hepatic: HVPG is normal. Sinusoidal: HVPG increased. Post sinusoidal: HVPG increased. Post hepatic: HVPG normal

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21
Q
  1. Describe how portal hypertension leads to varices formation.
A

varices: Portal HTN causes formation of portal-systemic collaterals. Dilation of coronary and gastric veins constitue gastroesophageal varices.

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22
Q

causes of pre-hepatic portal hypertension

A

portal vein thrombosis and splenic vein thrombosis.

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23
Q

causes of pre-sinusoidal portal hypertension

A

schistosomiasis - increased resistance at portal venules in the portal triad where eggs are trapped

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24
Q

causes of post-sinusoidal portal hypertension

A

veno-occlusive disease- fibrosis occludes central vein

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25
Q

causes of post-hepatic portal hypertension

A

Budd-Chiari syndrome (hepatic vein thrombosis)- increased resistance distal to liver

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26
Q

rate of development and growth of varices

A

7-8% per year

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27
Q

Risk factors for variceal growth in cirrhosis

A

Child B/C cirrhosis, alcoholic etiology and presence of red wale marks on initial endoscopy.

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28
Q

Predictors of variceal hemorrhage

A

large variceal size (expanding force exceeds maximal wall tension, as radius increases variceal wall becomes thinner), Child B/C and the presence of red wale markings on varices.

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29
Q

What will decrease risk of variceal rupture

A

decreased portal pressure

30
Q

List Variceal therapies

A

Vasoconstrictors, venodilators, vasoconstrictors + venodilators, endoscopic therapy, TIPS/shunt surgery

31
Q

MOA of vasoconstrictors for varices

A

Cause splanchnic vasoconstriction, reducing portal blood inflow. Intrahepatic resistance is slightly increased b/c decreased flow through collaterals so they only moderately decrease portal pressure.

32
Q

MOA of venodilators for varices

A

Cause intrahepatic vasodilation, reducing intrahepatic resistance and moderately decreasing portal pressure

33
Q

MOA of vasoconstrictors plus venodilators for varices

A

Reduces both splanchnic flow and intrahepatic resistance, with a marked decrease in portal pressure.

34
Q

TIPS/ Shunt surgery MOA and side effects

A

Bypasses the liver to maximally reduce resistance and leads to normalization of portal pressure. Blood from hypertensive portal vein and sinusoidal bed is shunted to hepatic vein. Can lead to encephalopathy and liver failure tho

35
Q

Prophylaxis of variceal hemorrhage

A

Beta blocker or endoscopic variceal band ligation

36
Q

Endoscopic variceal band ligation MOA

A

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.

37
Q

Mechanism of ascites formation in cirrhosis

A

Portal HTN causes NO production in splanchnic and systemic circulations. This causes vasodilation, decreased effective arterial blood volume, activation of neurohumoral systems (renin, angiotensin, aldosterone) and sodium and water retention, a key element in the pathogenesis of ascites. Additionally, in more advanced cirrhosis there is an increase in translocation of bacteria from the gut that leads to a further increase in NO production

38
Q

Diagnosis of ascites

A

ultrasound is most sensitive.

39
Q

Hepatorenal syndrome- cause

A

Ascites which progresses due to renal vasoconstriction and even higher levels of plasma renin activity and aldosterone levels, leading to functional renal failure

40
Q

natural history of ascites and levels of vasodilation

A

portal HTN w/out ascites (HVPG uncomplicated ascites (HVPG >10, moderate vasodilation) > refractory ascites (HVPG >10, severe vasodilation) > hepatorenal syndrome (HVPG >10, extreme vasodilation)

41
Q

what does diagnostic paracentesis detect

A

in ascites- PMN count and culture to look for bacterial infection, protein/albumin for cirrhotic ascites. OPTIONAL : glucose for secondary infection, amylase for pancreatic ascites, cytology for malignancy

42
Q

serum-ascites albumin gradient correlates with …

A

sinusoidal pressure.

43
Q

serum-ascites albumin gradient for different causes of ascites

A

SAAG>1.1: hepatic sinusoid HTN cause. SAAG<1.1: peritoneum cause

44
Q

ascites protein level and SAAG level for sinusoidal HTN

A

SSAG>1.1 and ascites protein <2.5 (sinusoids are capillarized and don’t allow loss of proteins). This is seen in Cirrhosis and late Budd Chiari

45
Q

ascites protein level and SAAG level for post- sinusoidal HTN

A

SAAG > 1.1 and ascites protein >2.5 (normal leaky sinusoids). Seen in cardiac ascites, eraly Budd-Chiari and veno-occlusive dz

46
Q

ascites protein level and SAAG level for peritoneal pathology

A

SAAG 2.5 (peritoneal lymph). Seen in malignancy and tuberculosis

47
Q

treatment of ascites- general

A

diuretics and Na restriction, large volume paracentesis (removes fluid directly), albumin to increase effective arterial blood volume and TIPS (decreases sinusoidal pressure and increases effective arterial blood volume)

48
Q

treatment of uncomplicated ascites

A

salt restriction, diuretics, then large volume paracentesis

49
Q

treatment of refractory ascites

A

large volume paracentesis + albumin, then TIPS

50
Q

types of refractory ascites

A

diuretic intractable (80%): Therapeutic doses of diuretics cannot be achieved because of diuretic-induced complications. Diuretic resistant: which no response is achieved despite maximal diuretic therapy

51
Q

Hepatorenal syndrome

A

It is a functional renal failure, that is, the kidneys of these patients have no significant histological abnormalities. Renal failure occurs as a result of renal vasoconstriction that in turn occurs as a result of extreme peripheral vasodilatation.

52
Q

types of hepatorenal syndrome

A

type 1: Rapidly progressive renal failure (2 weeks), Doubling of creatinine to >2.5 orhalving of creatinine clearance (CrCl) to 1.5 mg/dL or CrCl < 40 ml/min, Associated with refractory ascites

53
Q

List conditions that can cause renal failure in cirrhosis, NOT hepatorenal syndrome related

A

NSAIDS increase renal vasoconstriction. Vasodilators, LVP w/o albumin and infection cause vasodilation. Diuretics, diarrhea and hemorrhage decrease effective arterial blood volume

54
Q

hepatorenal syndrome diagnosis- major criteria

A
  1. Advanced hepatic failure and portal hypertension. ascites and hyponatremia 2. Creatinine > 1.5 mg/dL or creatinine clearance < 40 ml/min. 3. Absence of shock, bacterial infection, or nephrotoxic drugs. 4. Absence of excessive gastrointestinal or renal fluid loss. 5. No improvement in renal function after plasma volume expansion with 1.5 L of isotonic saline. 6. Urinary protein < 500 mg/dL and normal renal ultrasound
55
Q

minor criteria of hepatorenal syndrome

A 
Urine sodium  plasma osmolality
Serum sodium < 130 mEq/L
Urine volume < 500 ml/day
Urine RBCs < 50/HPFUrine sodium  plasma osmolality
Serum sodium < 130 mEq/L
Urine volume < 500 ml/day
Urine RBCs < 50/HPF
56
Q

natural history of hepatorenal syndrome

A

type 2 > spontaneous bacterial peritonitis > type 1

57
Q

in cirrhosis, sodium retention cuases _____________, renal vasoconstriction causes _________ and water retention causes __________`

A

ascites, hepatorenal syndrome, hyponatremia

58
Q

hepatorenal syndrome treatment

A

Liver transplant - only proven.

59
Q

spontaneous bacterial peritonitis

A

infection of ascitic fluid that occurs in the absence of a hollow viscus perforation and in the absence of an intra-abdominal inflammatory focus such as an abscess, acute pancreatitis or cholecystitis. Can precipitate hepatorenal sndrome

60
Q

SBP mechanism

A

Bacteria can migrate from the intestinal lumen to mesenteric lymph nodes and other extraintestinal sites, a process called bacterial translocation (BT).

61
Q

SBP presentation

A

are fever, jaundice and abdominal pain. However, patients with SBP can present atypically with only encephalopathy or with evidence of shock. Importantly, up to one-third of the patients may be entirely asymptomatic.

62
Q

SBP diagnosis

A

diagnostic paracentesis - ascitic fluid polymorphonuclear count (PMN) greater than 250/mm3.

63
Q

SBP common organisms

A

gram negative enteric organisms usually. E coli most common.

64
Q

SBP treatment

A

third-generation cephalosporins (cefotaxime and ceftriaxone have been the most utilized) or amoxicillin-clavulanic acid, administered intravenously. If uncomplicated, oral ofloxacin.

65
Q

What Abx should be avoided in SBP

A

aminogycosides- cause renal toxicity

66
Q

hepatic encephalopathy

A

neuropsychiatric manifestations of cirrhosis of the liver.

67
Q

hepatic encephalopathy cause

A

Ammonia, which crosses the blood-brain barrier, results in up-regulation of astrocytic peripheral-type benzodiazepine receptors which are the most potent stimulants of neurosteroid production. Neurosteroids are the major modulators of GABA, which results in cortical depression and hepatic encephalopathy.

68
Q

Hepatic encephalopathy diagnosis

A

history and PE

69
Q

precipitating factors of hepatic encephalopathy

A

high protein load, gastrointestinal bleeding or constipation, as well as infection and over diuresis (leading to azotemia and hypokalemia), Narcotics and sedatives

70
Q

hepatic encephalopathy treatment

A

Lactulase (decreases ammonia producing bacteria and excretes ammonia in stool), antibiotics (reduce ammonia production by bacteria in gut), change protein to vegetable source. Ornithine aspartate and benzoate increase ammonia fixation in liver

DEMS I (28 decks)

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