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portal hypertension Flashcards

1
Q

most complications of cirrhosis result from

A

portal hypertension

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2
Q

why is there an increased resistance in cirrhosis in the sinusoid space?

A

stellate cell in the space of disse deposits fibrous tissue that leads to constriction of these spaces

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3
Q

portal hypertension can result from (2)

A
  1. increase resistance in the portal flow

2. increase in portal venous inflow

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4
Q

pressure in the venous system is determined by 2 variables

A
  1. increased flow and constant resistance

or

  1. constant flow and increased resistance
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5
Q

in cirrhosis what is the initial mechanism that leads to portal hypertension

A

an increase in intrahepatic vascular resistance

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6
Q

why is there increase intrahepatic vascular resistance?

A

distorted sinusoidal architecture leads to increased resistance

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7
Q

small increases in portal flow in a person without cirrhosis is ok because

A

there is a dilation of the veins and thus there is no increase in portal pressure

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8
Q

in portal hypertension, splanchnic vasodilation results from an increase in

A

nitric oxide

elevated portal pressure leads to an increase in shear stress in the splanchnic vasculature and thus gives rise to an upregulation of endothelial isoform of NO synthase and increasing its production

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9
Q

in more advanced cirrhosis (when ascites are present) there is a further increase in NO production… why?

A

increase in translocation of bacteria from the gut

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10
Q

backward theory of portan HTN

A

intrahepatic vascular tree distorted by fibrosis; portal HTN is solely a consequence of increased vascular resistance

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11
Q

forward theory of portal HTN

A

portal HTN maintained by increased splanchnic flow despite collaterals

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12
Q

portal hypertension is the result of increases in both ______ to portal flow and in portal venous _____

A

resistance and inflow

  • backward and forward theories apply
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13
Q

with measurement of wedged and free pressures is the simplest, safest, most reproducible and most widely used method to indirectly measure portal pressure.

A

Hepatic vein catheterization

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14
Q

The FHVP acts as an internal zero to correct for

A

extravascular, intraabdominal pressure increases

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15
Q

The hepatic venous pressure gradient (HVPG) is obtained by subtracting the

A

free hepatic venous pressure (FHVP) from the wedged hepatic venous pressure (WHVP):

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16
Q

The normal HVPG ranges from

A

3 to 5 mmHg

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17
Q

In sinusoidal PHT, intersinusoidal communications are blocked by fibrous tissue. Dissipation of pressure in the wedged vessels is insignificant and the WHVP is then as elevated as the portal pressure. The FHVP is normal and therefore the HVPG is _____

A

elevated

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18
Q

The normal liver can withstand significant increases in flow, without resulting in increases in portal pressure. The normal portal venous system is a low-pressure system and vessels draining the intraabdominal organs, such as the coronary vein, drain into it.

A

yep

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19
Q

three major catergories of the causes of portal HTN

A
  1. pre-hepatic
  2. intra-hepatic
  3. pots-hepatic
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20
Q

prehaptic causes

A
  1. thrombosis of the portal or splenic vein

2. fistula of spanchnic arteriovenous

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21
Q

intrahepatic causes

A
  1. presinusoidal
  2. sinusoidal
  3. postsinusioidal
22
Q

posthepatic causes

A
  1. budd-chiary syndrome
  2. constrictive pericarditis
  3. right heart failure
23
Q

pre-sinusoidal portal HTN

A

affects the portal venules in the portal triads

  • shistosomiasis- S. mansoni eggs
24
Q

The most common cause of sinusoidal portal hypertension is hypertension.

A

cirrhosis where fibrous tissue deposition, active vasoconstriction and nodule formation obstruct the sinusoids and the intersinusoidal communications leading to sinusoidal and portal

25
Q

post-sinusoidal Portal HTN

A

Any disease that affects the terminal hepatic venules (central-based) will lead to post-sinusoidal portal hypertension. A typical example is veno-occlusive disease where fibrosis occludes the central veins.

26
Q

varices is a progressive disease?

A

yep, they increase in a diameter fashion

27
Q

why does the progression of portal HTN leads to variceal growth and rupture?

A

flow increases through the gastroesophageal varices due to either the increase in resistance to portal flow or increase in portal pressure

28
Q

treatment of acute variceal bleeding 3

A
  1. pharmacologic therapy to reduce portal pressure
  2. sengstaken-blakemore tube to apply pressure to pen wound
  3. endoscopic therapy to obstruct blood flow
29
Q

somatostatin/octreotide

A

they are non-specific beta-blockers that reduces portal pressure and used for acute variceal bleeding

30
Q

Peripheral vasodilation occurs as the result of decreased hepatic clearance of vasodilators such as

A

glucagon and NO

31
Q

The body compensates for the perceived drop in circulating blood volume in two ways:

A
  1. increased cardiac output (Q)

2. activation of the renin-angiotensin system resulting in increased renal retention of sodium and free water

32
Q

Best test for classifying ascites into portal hypertensive (SAAG >1.1 g/dL) and non–portal hypertensive (SAAG <1.1 g/dL) causes.

A

serum ascites albumin gradient (SAAG)

33
Q

A diagnostic paracentesis should be performed in every patient who develops new ascites. It should also be routinely performed if and when a cirrhotic patient is hospitalized, because up to half the episodes of spontaneous bacterial peritonitis are community-acquired and may be asymptomatic.

A

yep

34
Q

Diagnostic paracentesis is essential in patients with signs and symptoms of abdominal or systemic infections (fever, abdominal pain) or in those with renal dysfunction or encephalopathy as these may be the only evidence of spontaneous bacterial peritonitis

A

also yep

35
Q

management of ascites?

A
  1. dietary measures
  2. diuretics like spironolactone
  3. large volume paracentesis
  4. TIPS
  5. peritoneovenous shunt
  6. liver transplantation
36
Q

The hepatorenal syndrome (HRS) occurs in

A

patients with advanced cirrhosis. 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.

37
Q

what is activated in hepatorenal syndrome?

A

neurohumoral systems such as renin and aldosterone

38
Q

The HRS has been divided in 2 types based on clinical characteristics and prognosis.

A

Type 1 HRS is a rapidly progressive renal failure, in which a doubling of serum creatinine (or halving of creatinine clearance) occurs within a 2–week period.

Type 2 HRS is more slowly progressive and is associated with refractory ascites.

39
Q

SURVIVAL IN THE DIFFERENT TYPES OF HEPATORENAL SYNDROME (HRS)

A

Although survival is poor in all patients with HRS, the cumulative probability of survival is significantly worse in patients with HRS type 1 than in those with HRS type 2.

40
Q

THERE ARE MANY CONDITIONS OTHER THAN HEPATORENAL SYNDROME THAT CAN LEAD TO RENAL FAILURE IN PATIENTS WITH CIRRHOSIS

HEPATORENAL SYNDROME (HRS) IS A DIAGNOSIS OF EXCLUSION

A

yep

41
Q

Major Criteria in the Diagnosis of Hepatorenal Syndrome

  1. Advanced _________ and portal hypertension
  2. Creatinine > ___ mg/dL or creatinine clearance < 40 ml/min
  3. Absence of ________
  4. Absence of excessive _______
  5. No improvement in renal function after ______
  6. Urinary protein < _____ mg/dL and normal renal ultrasound
A
  1. Advanced hepatic failure and portal hypertension
  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 100g of IV albumin x 2 days
  6. Urinary protein < 500 mg/dL and normal renal ultrasound
42
Q

ASCITES, HEPATORENAL SYNDROME AND DILUTIONAL HYPONATREMIA IN CIRRHOSIS HAVE A COMMON PATHOGENESIS

A

yep

Cirrhosis and portal hypertension leads to arteriolar vasodilation and activation of neurohumoral systems. This activation leads to sodium retention (and ascites formation), to renal vasoconstriction (and hepatorenal syndrome) and to an impaired free water excretion (and dilutional hyponatremia), therefore it is not rare that the three conditions coexist in advanced cirrhosis

43
Q

Hepatic encephalopathy is defined as the

A

neuropsychiatric manifestations of cirrhosis of the liver.

44
Q

what is the pathophysiology of hepatic encephalopathy

A

the decrease in ammonia clearance by the kidney leads to ammonia crossing the BBB resulting in the upregulation of astrocytic peripheral-type benzodiazepine receptors which lead to neurosteroid production which are major modulators of GABA, which finally resutls in cortical depressio and hepatic encephalopathy

45
Q

clinical stages of hepatic encephalopathy depend on

A

the mental state and neurological signs.

46
Q

Precipitating factors for hepatic encephalopathy include

A

a high protein load, gastrointestinal bleeding or constipation, as well as infection and overdiuresis (leading to azotemia and hypokalemia).

47
Q

Treatment of hepatic encephalopathy involves

A

1) identifying and treating the precipitating factor, and 2) using lactulose adjusted to produce 2-3 bowel movements per day.
3) Rifaximin

Protein restriction is carried out typically when patients have stage 4 hepatic encephalopathy, but may not be necessary. Long-term protein restriction is not required. A vegetable protein diet is better tolerated than an animal protein diet.

48
Q

actions 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.

49
Q

liver transplant survival odds?

A

high!!!

50
Q

liver allocation policy for liver transplants?

A

the higher the score in MELD-Na+, the more the chance they will die in the next three months and thus they are placed first on the list

GI (26 decks)

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