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

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

24
Q

when are phase II metaoblised drugs affected

A

late (these are preferred)

25
paracetamol toxicity
not enough glutathione to counteract highly reactive intermediate
26
paracetamol in liver disease
reduced glutathione stores longer half life increased P450 2E1 in alcoholics toxicity with normal doses
27
Hy's rule
ALT/AST > 5 x ULN and bilirubin >3
28
what does frusemide cause
diuretic causes reduced intra-vascular volume, hypokalaemia, hypomagnesaemia
29
what does thiazide cause
hypokalaemia, hypomagnesaemia
30
what does spironolactone cause
best drug with fluid restriction aim at 1kg/day weight loss
31
superior mesenteric + splenic vein + gastric + part from inferior mesenteric = ?
portal vein
32
portal vein carries outflow from what organs (5)
``` spleen oesophagul stomach pancreas small/large intestine ```
33
what are the four collateral pathways
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
what are the pre-hepatic causes of portal hypertension
blockage of the portal vein before the liver; due to portal vein thrombosis or occlusion secondary to congenital portal venous abnormalities
35
what are the intrahepatic causes of portal hypertension
due to distortion of the liver architecture, either presinusoidal or post sinusoidal