cirrhosis Flashcards

1
Q

three main factors of cirrhosis

A

reduced liver blood flow
reduced metabolic function
reduced plasma proteins

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2
Q

cirrhosis

A

small hard liver

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3
Q

why is there portal hypertension

A

harder to pass through the liver

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4
Q

portal hypertension give you __

A

varices veins in oesophagus

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5
Q

caput medusae

A

the appearance of distended and engorged superficial epigastric veins, which are seen radiating from the umbilicus across the abdomen.

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6
Q

what creates ascites

A

high portal pressure and low albumin

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7
Q

first pass metabolism

A

The first pass effect is a phenomenon of drug metabolism whereby the concentration of a drug, specifically when administered orally, is greatly reduced before it reaches the systemic circulation.

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8
Q

oral dose > IV dose

A

first pass

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9
Q

first order metabolism

A

as plasma conc increases, metabolism increases

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10
Q

zero-order metabolism

A

Zero-order kinetics is described when a constant amount of drug is eliminated per unit time but the rate is independent of the concentration of the drug.

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11
Q

low albumin senses

A

low plasma volume

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12
Q

what is renin secretion from the kindeys stimulated by?

A

low albumin

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13
Q

what does a cirrhosed liver produce instead of aldosterone

A

secondary aldosteronism

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14
Q

what hormones have an effect on cirrhosis

A

endothelia and oesotrogen

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15
Q

angiotensin II

A

important vasoconstrictor

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16
Q

what hormones cause sodium retention

A

angiotensin II, aldosterone, SNS

17
Q

aldosterone promotes

A

potassium loss

18
Q

what does ADH do

A

vasoconstrictor and promotes reabsorption of free water
effect: pull in more free water and dilutes blood = hyponatremia, increase sodium retention but more free water resteion = hypokalaemia

19
Q

water retention occurs with

A

ADH

20
Q

consequences of cirrhosis

A

gut oedema (poor absorption)
liver and kidney congestion (reduced function)
gross oedema and ascites
CHF

21
Q

what happens when liver is given NSAID

A

real PGE synthesis decrease (worst renal impairment, further sodium retention, risk of hepato-renal syndrome, worsening of CHF)
cirrhosis peptic ulcers increase (risk of GI bleed or perforation)

22
Q

NSAID or COX-2 inhibitor should always be co-prescribed with a ____ because it is ____

A

PPI, more cost effective

23
Q

when are phase I metabolised drugs affected

A

early

24
Q

when are phase II metaoblised drugs affected

A

late (these are preferred)

25
Q

paracetamol toxicity

A

not enough glutathione to counteract highly reactive intermediate

26
Q

paracetamol in liver disease

A

reduced glutathione stores
longer half life
increased P450 2E1 in alcoholics
toxicity with normal doses

27
Q

Hy’s rule

A

ALT/AST > 5 x ULN and bilirubin >3

28
Q

what does frusemide cause

A

diuretic causes reduced intra-vascular volume, hypokalaemia, hypomagnesaemia

29
Q

what does thiazide cause

A

hypokalaemia, hypomagnesaemia

30
Q

what does spironolactone cause

A

best drug
with fluid restriction
aim at 1kg/day weight loss

31
Q

superior mesenteric + splenic vein + gastric + part from inferior mesenteric = ?

A

portal vein

32
Q

portal vein carries outflow from what organs (5)

A
spleen
oesophagul
stomach
pancreas
small/large intestine
33
Q

what are the four collateral pathways

A

oesophageal and gastric venous plexus

umbilical vein from the left portal vein to the epigastric venous system

retroperitoneal collateral vessels

the haemorrhoids venous plexus

34
Q

what are the pre-hepatic causes of portal hypertension

A

blockage of the portal vein before the liver; due to portal vein thrombosis or occlusion secondary to congenital portal venous abnormalities

35
Q

what are the intrahepatic causes of portal hypertension

A

due to distortion of the liver architecture, either presinusoidal or post sinusoidal