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Metabolism 2 > Microanatomy 2 > Flashcards

Microanatomy 2 Flashcards

1
Q

list the major functions of the liver

A

Detoxification of metabolic waste products.

Destruction of used red blood cells and reclamation of their constituents.

Synthesis and secretion of bile which facilitates the absorption of fats and is essential for the absorption of fat-soluble vitamins. The addition of pigments to bile is a mechanism whereby the liver eliminates some waste products of spent red blood cells.

Synthesis of plasma lipoproteins.

Metabolic functions, e.g. glycogen synthesis, gluconeogenesis and storage of glycogen, some vitamins, iron and lipid.

Detoxification of various drugs and toxins, e.g. alcohol.

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2
Q

what is the blood supply of the liver

A
  • the liver has both arterial and venous blood supplies
  • absorbed food products pass directly from the gut to the liver via the hepatic portal vein
  • oxygen required for liver metabolism is supplied through the hepatic artery
  • venous drainage occurs by the way of the hepatic vein
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3
Q

what are hepatocytes

A

These are parenchymal cells that form plates. They are the main functional cells of the liver.

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4
Q

what are sinusoids

A

These are the wide vascular channels that separate the plates of hepatocytes.

The majority of cells lining the sinusoids are endothelial cells.

However, scattered among these cells are specific macrophage type cells termed Kupffer cells. These are part of the liver’s defence system.

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5
Q

what are bile ducts

A

These carry bile from the hepatocytes eventually into the duodenum.

Bile is produced in hepatocytes and is secreted into a network of minute bile canaliculi (no discrete structure of their own) positioned between plasma membranes of adjacent hepatocytes.

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6
Q

what are portal tracts

A

These are islands of connective tissue containing branches of the portal vein and hepatic artery, running side by side, that bring blood to the sinusoids.

They also contain bile ducts, which carry bile in the opposite direction to the blood flow.

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7
Q

where is bile produced in

A

produced from the hepatocytes and secreted into a network of minute bile canaliculi

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8
Q

what is good about sinusoids

A
  • as blood passes through sinusoids it is in intimate contact with the hepatocytes so it can exchange nutrients and metabolic products
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9
Q

what is hepatic acinus

A
  • it is now through that the blood flow and function of the liver are more accurately defined by the unit structure known as the hepatic acinus
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10
Q

describe the hepatic lobule concept

A
  • the lobule is roughly hexagonal in shape
  • centred on a terminal hepatic venue
  • portal tracts are positioned at the angles of the hexagon
  • blood from the portal vein and hepatic artery in the portal tract flow to the central vein
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11
Q

describe the hepatic acinus concept

A
  • more accurate functionally then the hepatic lobule concept
  • more difficult to define histologically
  • berry shaped unit of liver parenchyma centred on a portal tract
  • lies between two or more terminal hepatic venues and the blood flows from the portal tracts through the sinusoids to the venues
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12
Q

what are the zones of the acinus

A
  • divided into 3 zones
    zone 1
    zone 2
    zone 3
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13
Q

describe the three zones of the acinus

A

zone 1
- most central and closest to the terminal distributing branches of the portal venue and hepatic arteriole
- receives oxygen, hormones, and nutrients from the bloodstream and is the site of the most glycogen and plasma protein synthesis
zone 2
- receives slightly less oxygenated blood
zone 3
is furthest away, receiving the least amount of oxygenated blood
- first to show ischemic necrosis and fat accumulation if metabolism is altered and the site of most drug detoxification

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14
Q

what zone in the hepatic acinus is susceptible to ischaemic injury

A

zone 3 as it receives the least amount of oxygenated blood

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15
Q

describe the grouping of hepatic acinus

A
  • Simple acini are grouped into complex acini and they are grouped into acinar agglomerates.
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16
Q

why is the connective tissue (storm) of the liver important

A
  • maintains the ordered architecture of the liver and the close relationship between the hepatocytes, vasculature and the bile ducts
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17
Q

what happens in cirrhosis

A
  • the normal architecture is disrupted by excess fibrocollagenous tissue resulting in impaired liver function
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18
Q

what are the 3 distinctive ways in which the liver deals with damage

A

Necrosis of hepatocytes
Fibrosis
Regeneration.

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19
Q

what is the region called in which the larger vascular and billiard components travel

A

Portal tract

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20
Q

name three major components that are located in the portal tract

A

Hepatic artery, portal vein and bile duct

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21
Q

where is the central vein

A

In the centre of the lobule

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22
Q

what is found between the cords of hepatocytes

A

hepatic sinusoids

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23
Q

what causes haematemesis

A
  • varices have very thin fragile walls so if there is any trauma such as vomiting they can rupture and this can cause haematemsis
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24
Q

How does the liver respond to injury

A
  • hepatocyte degeneration and intracellular accumulations
  • hepatocyte necrosis and apoptosis
  • inflammation
  • regeneration
  • fibrosis
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25
Q

what are zonal necrosis

A
  • this is when cells die from toxic insult or as a result of cardiac failure or other alteration in venous drainage
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26
Q

what is interface hepatitis due to

A
  • due to a number of chronic conditions

- results in hepatocyte death around the portal tracts

27
Q

what is bridging necrosis

A
  • this is within zone 3 of the acinus
  • feature of severe hepatitis
  • in apoptotic forms typical of acute viral hepatitis, single cell die
28
Q

what follows chronic liver disease

A
  • may follow an episode of acute liver injury or develop insidiously over an extended time course
29
Q

how is the severity of liver cell damage graded

A
  • extent of interface hepatitis
  • the degree of bridging or confluent necrosis
  • the frequency of interlobular apoptotic hepatocytes
  • the density of the inflammatory infiltrate in portal tracts
30
Q

what are the stages of severity of liver cell damage

A
  • staging relates to architectural disturbance and ranges from normal architecture, fibrous enlargement of portal tracts, bridging fibrosis to cirrhosis
31
Q

the greater the disturbance to liver cells ….

A
  • the greater the disturbance the less likely that it is reversible once the inflammatory activity has subsided
32
Q

what happens in primary billiard cirrhosis

A
  • this is when there is chronic destructive inflammatory disease centres on the bile ducts
33
Q

in primary billiary cirrhosis what do the larger bile duct show

A
  • they show early change including inflammatory infiltration of their walls and surrounding tissues by lymphocytes, macrophages, plasma cells and occasional eosinophils
  • characterstically there is formation of granulomas near damaged bile ducts
34
Q

what is a cirrhosis

A
  • not a disease itself but an end result of chronic liver injury caused by a variety of different diseases
35
Q

what are the three complications of cirrhosis

A
  • liver failure
  • portal hypertension
  • hepatocellular carcinoma
36
Q

what are Stellate cells

A
  • normal connective tissue cells, much like fibroblasts, responsible for the production fo the reticular tissue that supports the sinusoidal capillaries and hepatocytes in the “space of disse”
37
Q

what do stellate cells do

A
  • help produce extracellular matrix
  • storage of vitamin A
  • act as capillary pericytes regulating interlobular blood flow and aid hepatic regeneration
38
Q

what does hepatic fibrosis do to stellate cells

A
  • the main mechanism of hepatic fibrosis involves the activation of these cells to induce their proliferation and differentiation into highly fibrogenic “myofibroblast cells”
39
Q

what causes stellate cells to become active

A
  1. factors released during chronic inflammation from Kupffer cells and lymphocytes
  2. cytokines and chemokine from Kupffer cells, endothelial cells, ductal epithelium, and hepatocytes in response to disruption of the extracellular matrix
  3. toxins acting directly on the stellate cells
40
Q

what is cirrhosis classified according to

A

morphology of regeneration nodules
- based on the average size of regeneration nodules, cirrhosis can be classed as macro nodular (greater than 3mm) or micro nodular(less than 3mm)

also by
- aetiology - this can be often deduced from clinical, biochemical, immunological or biopsy findings

41
Q

what is the most common causes of micro nodular cirrhosis

A
  • alcoholic liver disease
42
Q

what causes complication of macro nodular cirrhosis

A

macro nodular cirrhosis has a greater risk of complication by hepatic cell carcinoma

43
Q

what are the causes of cirrhosis

A
  • viral hepatitis
  • alcohol haemochromatosis
  • autoimmune liver disease
  • recurrent biliary obstruction
  • Wilsons disease
44
Q

what is used to obtain liver

A
  • needle biopsy

- this is used to obtain liver tissue for histopathological analysis during diagnosis and to monitor the disease state

45
Q

what is the mechanism of jaundice in hepatobillary diseases

A

failure of mechanism to excrete bile

46
Q

what is the mechanism of bleeding in hepatobillary diseases

A

failure of hepatic synthesis of clotting factors

47
Q

what is the mechanism of oedema in hepatobillary diseases

A

failure of hepatic synthesis of albumin resulting in decreased plasma oncotic pressure

48
Q

what is the mechanism of ascites in hepatobillary diseases

A

low serum in albumin and portal hypertension

49
Q

what is the mechanism of gynaecomastia in hepatobillary diseases

A

failure to detoxify endogenous oestrogen’s

50
Q

what is the mechanism of encephalopathy in hepatobillary diseases

A

failure to detoxify ammonia and break down amino acid products

51
Q

what is the mechanism of haematonesis in hepatobillary diseases

A

bleeding from oesophageal varicose and rectum varicoses owing to portal hypertension

52
Q

most malignant neoplasms in the liver are metastases…

A

form a primary tumour in another organ

53
Q

what are aetiological factors associated with primary hepatocellular carcinoma

A
  • HBV, HBC, aflatoxins, and cirrhosis
54
Q

what are aflatoxins

A
  • these are carcinogenic mycotoxins which are found in food stored in humid conditions
55
Q

what type of growth is consistent with heptacellular carcinoma

A
  • dysplastic hepatocyte

growth

56
Q

what is the region called in which the large vascular and biliary components travel

A

portal tract

57
Q

name the three major components that are located in the portal tract

A

Hepatic artery 􏰀
Portal vein
Bile duct

58
Q

where is the central vein

A
  • located in the centre of the lobule
59
Q

what type of collagen is stained black

A

collagen type III this is also known as reticulin

60
Q

what is found between the cords of hepatocytes

A

hepatic sinusoids

61
Q

In which direction does the blood flow in the liver

A

blood flows from the portal tract into the sinusoids

62
Q

in which direct does bile flow int he liver

A

flows from the hepatocytes in the bile duct towards the duodenum

63
Q

what do you get haematomesis

A
  • vascular dynamics become distorted
  • this leads to hypertension
  • results in gastro-oesophageal varies, ascites and other vascular disturbances
  • varices tend to rupture due to their thin wall
  • results in haematemesis

Metabolism 2 (40 decks)

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