05b: Cirrhosis Flashcards
Normal portal pressure is (X) mmHg. Clinical manifestations of portal HTN is seen at/over (Y) mmHg.
X = 2-6 Y = 12
Two mechanisms that cause portal HTN.
- Increased resistance to portal flow (mechanical obstruction)
- Secondary increase in portal blood flow
Portal flow can be measured by which clinical tool?
Doppler ultrasound
About 60% of cirrhosis cases are caused by which two etiologies?
HCV and EtOH (either separately or in combo)
Most common cause of portal HTN worldwide is (X). And in the US is (Y).
X = schistosomiasis Y = cirrhosis
Portal HTN: Calculating the (X) gradient has been shown to have prognostic value in patients with cirrhosis. If below (Y) value, there’s significantly lower risk of bleeding from varices.
X = HVPG (Hepatic venous pressure gradient);
Y = 12 mmHg
Most forms of cirrhosis are (pre-hepatic/hepatic/post-hepatic).
Hepatic (sinusoidal)
Splenic/portal vein thrombosis is example of (pre-hepatic/hepatic/post-hepatic) cirrhosis.
Pre-hepatic
CHF can lead to (pre-hepatic/hepatic/post-hepatic) cirrhosis.
Post-hepatic
Schistosomiasis is example of (pre-hepatic/hepatic/post-hepatic) cirrhosis.
Hepatic (pre-sinusoidal)
Budd-Chiari Syndrome caused by (X) and is example of (pre-hepatic/hepatic/post-hepatic) cirrhosis.
X = Hepatic v thrombosis
Post-hepatic
Of all the clinical signs in decompensated cirrhosis, (X) is the most dramatic and cause of death in up to (Y) of all patients with cirrhosis.
X = esophageal varices bleeding Y = 1/3
List the 5 main parameters used in “Child” criteria to assess severity/mortality with bleeding varices in cirrhosis.
Acronym: ABCPE
Albumin, BR, asCites, PT, Encephelopathy
Patient actively bleeding from esophageal varices requires emergent:
- Endoscopy (variceal ligation)
2. Resuscitation (IV fluids, blood)
Which drugs used for Rx in acute esophageal variceal bleeding?
Octreotide (long-acting somatostatin analog)
Cirrhosis: (X) cells are responsible for the ECM deposition and fibrosis.
X = hepatic stellate cells (which act as myofibroblasts)
Cirrhotic liver pathophysiology: sinusoidal fenestrations are (normal/wider/narrower).
Narrower (lost!) - hence increased resistance to blood flow within sinusoid lumen
(High/low) platelets may be marker of portal HTN. Why?
Low;
Blood backs up to spleen (splenomegaly) and platelets sequestered there
Increased intrahepatic resistance in cirrhosis is caused by both architectural and functional alterations. What are examples of functional alterations?
Active contraction of stellate/myofibroblast and vascular smooth muscle cells (modifiable by drugs)
Octreotide used in cirrhosis patients for treatment of (X) complication. What are the mechanisms by which it does this?
X = esophageal varices bleeding (somatostatin analog)
- Decrease post-prandial hyperemia (by inhibiting glucagon release)
- Direct vasoconstriction of splanchnic arteriolar muscle (decrease collateral flow)
Screening followed by primary prophylaxis for variceal bleeding includes (X) drugs/procedure.
X = non-selective beta-blockers OR endoscopic band ligation (EBL)
Esophageal variceal bleeding prophylaxis: (selective/non-selective) beta blockers used only for which effects?
Non-selective;
B1: decreases CO and splanchnic blood flow
B2: Allows unopposed alpha1 splanchnic vasoconstriction
T/F: Part of treating active variceal bleed is to give antibiotic prophylaxis.
True
All patients with ascites should undergo (X) diagnostic procedure.
X = paracentesis (of 50cc fluid)
