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Nutrition and Digestion > Pathophysiology of Liver Disease > Flashcards

Pathophysiology of Liver Disease Flashcards

1
Q

most common cause of fatty liver and second most common

A

alcohol first
NAFLD second

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2
Q

is alcohol a primary or secondary cause of fatty liver

A

secondary

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3
Q

name causes of fatty liver

A

NAFLD
alcohol
malnutrition and low protein diet
rapid weight loss
hepatitis C
HIV
Wilson’s disease

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4
Q

where is ethanol metabolised

A

in the liver

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5
Q

how does chronic alcohol intake cause fatty liver

A

a product of alcohol acetalhydrate causes NADH production
NADH increases lipogenesis and decreases fatty acid oxidation which leads to a fatty liver

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6
Q

how much alcohol intake is required to cause fatty liver

A

> 60g per day

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7
Q

are males or females more susceptible to alcoholic fatty liver

A

females

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8
Q

what does alcohol do to fat in the body

A

breaks down fat elsewhere in the body
this increases free lipids in the body
alcohol draws fat to the liver and causes it to esterify and stay in the liver

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9
Q

what histological features is diagnostic of alcoholic fatty liver

A

mallory’s hyaline bodies

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10
Q

what syndrome do almost all of those with a BMI > 35 have

A

the metabolic syndrome

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11
Q

what is the criteria for the metabolic syndrome

A

3 or more of the following:

abdominal obesity
- waist >102cm for men, >88cm for women

serum triglycerides >150mg/dl

HDL < 40 mg/dl for men, <50 for women

BP >130/85

Insulin resistance
- fasting blood glucose > 110mg/dl (6.1mmol/l)
- 2h >140mg/dl (7.8mmol/l)

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12
Q

risk factors for NAFLD

A

obese people
type 2 diabetes
genetic (small subgroup)

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13
Q

what can NAFLD progress to

A

non alcoholic steatohepatitis (NASH)
cirrhosis
hepatocellular cancer

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14
Q

what does NASH stand for

A

nonalcoholic steatohepatitis

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15
Q

what is steatosis

A

abnormal accumulation of fat in the liver

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16
Q

what changes in the liver characterise NASH

A

steatosis (fatty deposit)
inflammation
ballooning
+/- mallory hyaline
+/- fibrosis

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17
Q

what features characterise cirrhosis

A

inflammation
fibrosis stage 4
+/- steatosis

18
Q

presentation of NAFLD and signs on investigation

A

asymptomatic
abnormal LFTs
right upper quadrant pain
fatigue
hepatomegaly
acathosis nigricans

19
Q

who get acathosis nigricans and what is it

A

pigment on the neck
morbidly obese children

20
Q

clinical features of NAFLD

A

obesity
hepatomegaly
stigmata of CLD

21
Q

lab features of NAFLD

A

raised:

ALT
AST
GGT
glucose
HOMA-IR
total cholesterol
triglycerides
ferratin
transferrin

22
Q

histological features of NAFLD

A

steatosis (fat accumulation)
inflammation
ballooning
necrosis
fibrosis

23
Q

what is HOMA-IR

A

homeostasis model assessment of insulin resistance

24
Q

equation for HOMA-IR

A

(fasting glucose x fasting insulin)/22.5

25
Q

when in HOMA-IR important

A

in non diabetics
shows insulin resistance

26
Q

what HOMA-IR shows severe insulin resistance

A

> 3

27
Q

what is found within adipose tissue

A

it is a resevoir for hormones and cytokines

28
Q

characteristic of acquired fat

A

it is proinflammatory

29
Q

NAFLD treatment

A

gradual weight reduction
diet
exercise
anti-obesity agents
bariatric surgery
metformin
vitamin E

30
Q

weight reduction rate in NAFLD

A

1.5kg per week

31
Q

diet recommendations in NAFLD

A

low in carbohydrate and saturated fat
rich in polunsaturated fat, fibre, vit E and C

32
Q

pathophysiology of cirrhosis

A
  1. fibrosis disrupts hepatic architecture
  2. disorganised regeneration of hepatocytes
33
Q

complications of cirrhosis

A

portal hypertension
variceal bleeding
ascites
encephalopathy
liver failure

34
Q

albumin, PT, urea and ammonia levels in cirrhosis

A

low albumin (liver can’t produce)
prolonged PT (no/less clotting factors)
low urea (can’t be metabolised from ammonia)
high ammonia (liver can’t clear(

35
Q

albumin, PT, urea and ammonia levels in cirrhosis

A

low albumin (liver can’t produce)
prolonged PT (no/less clotting factors)
low urea (can’t be metabolised from ammonia)
high ammonia (liver can’t clear)

36
Q

what vein is used instead of the route through the liver to get to the IVC and where is this found

A

coronary vein on cardia of stomach

37
Q

definition of acute liver failure

A

loss of liver function that occurs quickly in days or weeks in a person with no pre-existing liver disease

38
Q

causes of acute liver failure

A

paracetamol (staggered or intentional)
hep A and B
drug reactions

39
Q

early presentation of acute liver failure

A

early presentation:
malaise
nausea
vomiting
abdominal pains
dehydration

40
Q

late presentation of acute liver failure

A

late presentation:
acidosis
hypoglycaemia
coagulopathy
encephalopathy
renal failure
multi organ failure

Nutrition and Digestion (30 decks)

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