Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Life Maintenance > Liver physiology > Flashcards

Liver physiology Flashcards

1
Q

What are the main types of cells in the liver?

A

Hepatocytes, Kupffer cells, endothelial cells, stellate (Ito) cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the function of the stellate cells and where are they located?

A

Perisinusoidal cells, located specifically in the Space of Disse.
Functions: store vitamin A, fat and collagen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the functional unit of the liver?

A

The hepatic lobule: hexagonal plates around a central hepatic portal vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What does a portal triad contain?

A

Portal vein, hepatic artery, bile duct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are Kupffer cells?

A

fixed tissue macrophages, which filter blood coming from the small intestine via the hepatic portal vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

In which direction does bile flow in the liver? In what?

A

Bile flows in canniculae (sit between hepatocytes). Flows in a retrograde manner from the common vein to the portal triad.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the main components of bile?

A

cholesterol, phospholipids, bilirubin, bile acids, water, electrolytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What do hepatocytes do in bile secretion?

A

secrete bile acids, cholesterol and other organic components into the cannaliculae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the second stage of bile acid secretion facilitated by endothelial cells in bile ducts?

A

Addition of water to the bile salts etc, plus electrolytes (inc: Na+ and HCO3-)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the hormonal control of bile acid synthesis and release from the liver?

A

Secretin is released from S cells in response to gastric acid in the duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How much bile does the gall bladder store on average?

A

30-50ml

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the hormonal control for release of bile from the gall bladder?

A

Release of cholecystokinin (CCK) from I cells in response to fat in the duodenum.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Cholesterol is immediately broken into which 2 acids?

A

cholic acid + chenodeoxycholic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Why are bile salts conjugated with amino acids (e.g. taurine or glycine)?

A

AA-conjugation makes the bile salts water-soluble

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are primary bile salts?

A

Refers to the species occurring as Na+-salts, secreted from the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are secondary bile salts?

A

Formation of deoxycholic acid and Lithocholic acid following bacterial fermentation in the small intestine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How are secondary bile salts transported back to the liver?

A

Transported from the terminal ileum via enterohepatic circulation back to the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are 2 main types of gall stones?

A

Cholesterol (80%), pigment (20%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the main risk factors for gall stones?

A

HFD, gall bladder mucosal inflammation, F>M, excess oestrogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the function of bile?

A

To emulsify fats, enabling lipase-mediated digestion and aiding absorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is bilirubin?

A

Breakdown product of RBC degradation, yellow pigment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What helps to neutralise the HCL in gastric acid?

A

Bile + pancreatic juices

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What reaction is bilirubin generated from?

A

Haem -> (iron +) porphyrin -> bilirubin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the intermediate formed before bilirubin that can cause a greenish jaundice

A

biliverdin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Which cell type catalyses the breakdown of haem into bilirubin? Where does this occur?

A

Kupffer cells (macrophages) in the sinusoids of lobules

26
Q

How is unconjugated bilirubin carried in the blood (during physiology)?

A

It is conjugated to albumin, thus making it water-soluble?

27
Q

What are the 3 methods of paracetamol conjugation in the liver?

A

Sulfonation, n-hydroxylation, glucoronidation

28
Q

What is free bilirubin conjugated to in the liver?

A

Glucuronic acid

29
Q

How is conjugated bilirubin then excreted?

A

It leaves the liver with bile, and is then either excreted renally (as urobilin) or in faeces (as stercobilin)

30
Q

What is jaundice? Why does it happen?

A

yellowish tinge to skin, mucosa or sclera (eyes).

Caused by accumulation of unconjugated/free bilirubin in the plasma

31
Q

At what [bilirubin] is jaundice likely to be present?

A

> 1.5mg/dL

32
Q

How does conjugated bilirubin in the bile get excreted in faeces?

A

conjugated bilirubin is metabolised by intestinal microbiota, redox reactions promote the formation of stercobilin. This colours and is excreted in faeces

33
Q

A mutation in what causes the rare green jaundice (biliverdin)?
What can exacerbate this?

A

mutation in biliverdin reductase
prevents conversion of biliverdin to bilirubin
Can be aggravated by EtOH cirrhosis

34
Q

What can be used to treat jaundice in low-income countries, particularly in infants?
How do they work?

A

Sunlight canopies
Filters so that only blue light gets through
Therefore reduced UV-mediated damage

35
Q

What are the 2 main processes by which glucose is generated in the liver?

A

gluconeogenesis

glycogenolysis

36
Q

Through which process is Glucose-6-phosphate converted to pyruvate?

A

Glycolysis

37
Q

Which enzyme catalyses the breakdown of glycogen to glu-1-P?

What is the name of this reaction?

A

Glycogen phosphorylase

Glycogenolysis

38
Q

Which transporter is used for uptake of Glu into the hepatocyte?

A

Glut2

39
Q

Which hormones stimulate glycogenolysis?

A

Glucagon (GCG)

Adrenaline

40
Q

Which hormones stimulate glycogenesis?

A

insulin

41
Q

What are the 4 methods of fat metabolism in the liver?

A

Adipose storage
Oxidation of TGs to ATP (OXPHOS)
Lipoprotein synthesis
cholesterol and phospholipid synthesis

42
Q

What are the 4 methods of protein metabolism in the liver?

A

transamination/deamination of AAs
synthesis of non-essential AAs
synthesis of plasma proteins (e.g. albumin)
urea synthesis (excretion of ammonia)

43
Q

How is glutamine (AA) removed by the liver?

A

Conversion to NH3 and then excretion via the urea cycle

44
Q

Why is glutamine (accumulation) toxic?

A

Glutamine interferes with GABA and dopamine receptors and can cause hepatic encephalopathy

45
Q

What clinical feature is indicative of excess/toxic oestrogen? How many is considered to be concerning?

A

Spider angiomas

>5

46
Q

What are the broad phases of liver metabolism/detoxification? What do they involve?

A 
Phase 1 (redox)
Phase 2 (conjugation)
Phase 3 (excretion)
47
Q

Why is an OD more likely with paracetamol?

A

It has a narrow therapeutic window

48
Q

What is the toxic metabolite generated through breakdown of paracetamol? Through which phase I reaction does it occur?

A

NAPQI

Generated through n-hydroxylation and dehydration of paracetetamol

49
Q

What are the toxic effects of NAPQI?

A

Liver necrosis and renal failure

50
Q

Why is there an accumulation of NAPQI in paracetamol during OD?

A

NAPQI should be conjugated to GSH, but this gets depleted and it is then left to circulate a free species in the plasma

51
Q

What is the antidote for paracetamol OD? How does it work?

A

N-acetyl cysteine (NAC), IV infusion
NAC is the precursor to GSH, it enables restoration of the GSH stores and therefore allows conjugation and excretion of NAPQI

52
Q

How is EtOH metabolised?

A

EtOH -> acetaldehyde -> conjugate acid

53
Q

Which enzymes catalyse the metabolism of EtoH?

A 
alcohol dehydrogenase (EtOH -> acetylaldehyde)
acetylaldehyde dehydrogenase (-> conjugate acid)
54
Q

Consequences of chronic EtOH abuse (>10yr)

A

fatty liver disease
cirrhosis
alcoholic hepatitis

55
Q

What kind of cells are hepatocytes?

A

stable cells: will only regenerate in response to injury or trauma. Otherwise cells are quiescent (G0)

56
Q

What is an example of a labile cell?

A

Skin

57
Q

What are the 2 main pathways of liver generation?

A

growth factor mediated

cytokine dependent

58
Q

How does chronic EtOH dependence affect liver regeneration?

A

reduced ability for liver to regenerate

59
Q

Activation of liver regeneration can occur via non-parenchymal cells. Which cells are these?

A

stellate (Ito)

Kupffer

60
Q

Which LFT is an indicator of bile flow obstruction? Which other marker may be indicated?

A

elevated ALP

elevated GGT

61
Q

Hypoalbuminaemia indicates:

A

malnutrition or chronic liver disease

Life Maintenance (25 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions