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Nutrition and Digestion > Introduction to Liver Cirrhosis > Flashcards

Introduction to Liver Cirrhosis Flashcards

1
Q

what ligaments divides the right and left lobes

A

falciform ligament

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2
Q

5 functions of the liver

A

detoxification
synthesis of digestive enzymes
protein production
storage of nutrients
metabolism

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3
Q

functions of periportal zone

A

gluconeogenesis
bile salt formation

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4
Q

functions of perivenous/pericentral zone

A

glycolysis
lipolysis
glucuronidation

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5
Q

what is the cholangiole

A

the bile channels/bile cannaliculi

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6
Q

what % of the liver is hepatocytes

A

80%

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7
Q

what are pit cells

A

natural killer cells of the liver

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8
Q

what cell types are found in the perisinuosoidal space

A

stellate cells
dendritic cells

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9
Q

what substances can be used to make glucose in gluconeogenesis

A

lactate
pyruvate
glucogenic amino acids
glycerol

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10
Q

describe the steps of lipid metabolism

A
  1. bile digests lipids in the gut
  2. chylomicrons are formed
  3. these travel in the lymphatic system to the liver
  4. chylomicrons are metabolised by lipoprotein lipase to cholesterol, phospholipids, triglycerides and free fatty acids
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11
Q

how does the liver metabolise proteins

A

via the citric acid cycle

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12
Q

function of vitamin k

A

required for post translational modification of many of the clotting factors

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13
Q

key protein made in the liver

A

albumin

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14
Q

what is a cause of brain damage in liver disease

A

the blood is diverted past the liver due to cirrhosis
which means ammonia is not removed from the blood
the ammonia damages the astrocytes in the brain

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15
Q

what is ammonia a waste product of

A

protein metabolism

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16
Q

what does the liver do to ammonia

A

detoxifies it by converting it to urea in the urea cycle

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17
Q

what are the three phases of drug metabolism

A
  1. oxidation, reduction and hydrolysis
  2. conjugation in cytoplasm of hepatocytes
  3. secretion into the bile
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18
Q

what enzymes control phase 1 (oxidation, reduction and hydrolysis) of drug metabolism and where are these found

A

CYP450
in endoplasmic reticulum of the liver

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19
Q

what control excretion of metabolised drugs into bile

A

ATP

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20
Q

how much bile is made in a day

A

1-2L

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21
Q

what are the constituents of bile

A

bile acids
phospholipids
cholesterol
conjugated drugs
electrolytes (Na+, Cl-, HCO3-, Cu)
bilirubin

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22
Q

what’s the difference between primary and secondary bile acids

A

primary - made in liver
secondary - absorbed

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23
Q

what contributes to the brown colour of stool

A

stercobilin
a form of urobilinigon

24
Q

where is heme broken down into unconjugated bilirubin

A

spleen

25
Q

what vitamin are stored in the liver

A

A
D
B12
K

26
Q

what minerals are stored in the liver

A

copper
iron (as ferritin and haemosiderin)

27
Q

how much vitamin K is stored in the liver and how quickly does it deplete with decreased dietary intake

A

small
quickly

28
Q

what does the liver do to vitamin D

A

metabolises from inactive form (cholecalciferol vitamin D3) to active form (25-hydroxyl vitamin D)

29
Q

what mechanisms does the liver have for immune regulation

A

filters all blood from gut
kupffer cells phagocytose pathogens from gut
supply chemokines
prime T cell responses

30
Q

what chemokines are supplied by the liver

A

interleukins
tumour necrosis factor

31
Q

what mediates resolution from early fibrosis back to normal liver

A

macrophages

32
Q

cirrhosis without treatment leads to

A

hepatocellular carcinoma

33
Q

what two proteins/peptides are released when hepatocytes are damaged

A

TGF alpha
IGF1

34
Q

what follows stellate cell activation in hepatocyte injury

A

cells transform into myofibroblast like cells
this causes increased collagen and proinflammatory factors

35
Q

what follows stellate cell activation in hepatocyte injury

A

cells transform into myofibroblast like cells
this causes increased collagen and proinflammatory factors
an autocrine loop is formed where stellate cells activate themselves

36
Q

steps of liver cirrhosis

A
  1. stellate cells transform into myofibroblasts and increase collagen production
  2. metabolite and oxygen exchange decrease across the space of disse
  3. hepatocytes disfunction
  4. new blood vessels are formed and sinusoid is remodelled
  5. sinusoidal resistance increases causing portal hypertension
37
Q

what metabolic diseases can cause cirrhosis

A

haemochromatosis
wilson disease

38
Q

why is sodium and water retention a feature of liver cirrhosis

A

portal hypertension causes splanchnic (abdominal) vessels to vasodilate
which causes hypotension in the rest of the body
so the RAAS is activated
which causes vasocontriction and Na+ and water retention

39
Q

difference between compensated and decompensated stage of liver disease

A

compensated - asymptomatic
decompensated - symptomatic

40
Q

median survival of compensated liver disease

A

12 years

41
Q

median survival of decompensated liver disease

A

2 years

42
Q

what signs can be seen on the hands of someone with liver cirrhosis

A

xanthoma
duputren’s contracture
clubbing
liver palms

43
Q

symptoms of decompensated liver cirrhosis

A

neurological (disorientation, drowsy, coma)
hepatic flap
variceal bleeding
jaundice
ascites
oedema
caput medusae

44
Q

how does albumin change in liver cirrhosis

A

decreased in end stage due to decreased function

45
Q

how does prothrombin time change in liver cirrhosis

A

increases due to decreased synthesis of clotting factors

46
Q

what PT time is an indicator of liver dysfunction

A

> 12s

47
Q

how does bilirubin change in liver cirrhosis

A

increase due to decreased clearance

48
Q

how does platelets change in liver cirrhosis

A

decreased
increased consumption due to splenomegaly

49
Q

investigations to diagnose fibrosis and cirrhosis

A

liver biopsy
serum markers
transient elastography (fibroscan)

50
Q

advantages of liver biopsy

A

quantitative
can detect cause of cirrhosis

51
Q

disadvantages of liver biopsy

A

prone to sampling error
risk of bleeding and others

52
Q

advantages of serum markers

A

cheap
widely available

53
Q

disadvantages of serum markers

A

nonspecific
grey zone for intermediate fibrosis

54
Q

advantages of transient elastography

A

non invasive
quick

55
Q

disadvantages of transient elastography

A

machine cost
user and patient experience

56
Q

what does the fibroscan detect

A

liver stiffness and (some machines) fat

57
Q

what score can be used for prognosis of liver disease

A

child-pugh score

Nutrition and Digestion (30 decks)

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