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Baz Y2 Semester 2 > Week 4 Nutrition and Digestion Overview > Flashcards

Week 4 Nutrition and Digestion Overview Flashcards

1
Q

Main vessels entering and leaving the liver

A
  • Hepatic vein
  • Portal veins
  • Hepatic artery
  • Lymphatics
  • Hepatic ducts
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2
Q

Blood supply to liver?

A
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3
Q

What is a liver lobule and what is it’s shape?

A

It is the functional unit of the liver.

Approx 50’000-100’000 lobules

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4
Q

What does the portal triad consist of?

A
  1. Branch of hepatic artery
  2. Branch of portal vein
  3. Bile duct
  4. Lymph vessal (not included in the triad naming)
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5
Q

Try to draw out a lobule

A
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6
Q

What is a sinusoid?

A

It is a drainage channel where mixed oxygenated and nutrient rich blood from the portal triad can pass through the gaps in the endothelial lining to enter the space of disse and be taken up by the hepatocytes.

Further down towards the center of the hepatocyte blood containing stuff released by the hepatocytes drain back into the sinusoid form the space of disse where it drain into the central vein

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7
Q

What is a kupfer cell?

A

These are macrophages which gaurd the gaps between the sinusoid and the space of disse

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8
Q

What drains the other way out of the space of disse and back to the periphery (portal tracts)?

A

Lymph

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9
Q

What is produced by hepatocytes but drain back into the portal triad and not into the central vein?

A

Bile

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10
Q

What is the liver acinus?

A

As well as the classic lobule model some blood will perfuse from the edges of the hexagon (peripheral veins) of the lobule.

The liver acinus centers itself around one of these edges.

It is a way to divide up the hepatocytes in a lobule based on how much perfusion of blood from the portal triad they recieve.

Zone 1 gets the most perfusion and hence would become the most damaged from toxic substances in the blood.

Zone 3 gets the least perfusion and hence would suffer the most if the blood didn’t have enough oxygen.

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11
Q

What are the two types of faces on a hepatocyte?

A
  • Sinusoidal face - faces the sinusoid, takes in nutrients and toxin, releases other stuff
  • Lateral faces - faces other hepatocytes, some are modified to form the bile canaliculi
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12
Q

What are the bile channels within a lobule called?

What do they come together to form before the bile duct?

A

Bile caniliculi

Canal of hering

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13
Q

How is the lymph in a lobule formed?

A

By the filtration of plasma into the space of disse

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14
Q

Which three major vessels make up the portal vein?

A
  • Inferior mesenteric vein - from colon (large intestine)
  • Superior mesenteric vein - from small intestine
  • Splenic vein - from the spleen

Hint: inferior mesenteric comes formt he colon because the colon lies at the end (bottom) of the intestinal tract

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15
Q

Where does the hepatic artery come from and what is the other vessal that comes from the bifurcation?

A

It comes from the celiac trunk which forms both the hepatic artery and the splenic artery

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16
Q

Describe the glucagon-insulin cycle

A
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17
Q

What is bilirubin?

A

It is formed form the breakdown of haemoglobin at the end of a RBCs lifecycle

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18
Q

Describe the bilirubin cycle

A

Unconjugated bilirubin is toxic and must be removed from the blood.

This is done by the liver which turns it into conjugated bilirubin and excretes it into the biliary system. Conjugated bilirubin is then excreted directly in the faeces (brown colour) or converted into urobilinogen where it goes back through the liver and to the kidneys and excreted in urine

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19
Q

How does bile exit the liver?

A

Through the common bile duct where it combines witht eh pancreas’ bile and enter into the duodenum.

At the entrance to the duodenum there is a valve. If this shuts then refluxed bile goes to the gallbladder and is stored.

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20
Q

What are the general steps to liver detoxification?

A
  1. Fat soluable toxins enter liver
  2. Liver processes them using various vitamins and nutrients
  3. Water soluable toxins leave the liver
  4. Exit via bile and then to the bowel or to the kidney and urine
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21
Q

What is jaundice and what is it a sign of?

A

This is where the skin becomes yellow due to a build up of billirubin. It is a sign of liver damage or bile duct blockages

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22
Q

What would elevated bilirubin in a blood test signify?

A

Liver cirrhosis and/or choleostasis

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23
Q

What acid is stomach acid?

A

Hydrochloric acid

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24
Q

What are the sphincters that prevent stomach acid from leaving the stomach?

A

Osophageal sphincter and Duodenal sphincter

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25
What protects the stomach from acid?
Mucosa
26
What cells make stomach acid?
Parietal cells
27
What cells in the stomach make gastrin
G Cells
28
What cells in the stomach make somatostatin
D Cells
29
What cells in the stomach make histamine?
Enterochromaffin cells
30
What is gastrin?
Gastrin is a hormone primarily responsible for enhancing gastric mucosal growth, gastric motility (movement of food) and secretion of hydrochloric acid (HCl) into the stomach
31
What cells int he stomach make mucus?
Mucus cells
32
What cells in the stomach make pepsinogen (becomes pepsin which breaks down proteins in food)
Cheif cells
33
What does amylase do and where is it made?
34
What are proteases and what are the three main proteases?
35
What are lipases?
36
What are bile salts?
The emulsify fats and allow lipases to act
37
Describe the process of B12 absorption?
B12 is liberated from proteins by acid and pepsin int he stomach Then binds to R-factors Complex released by pancreatic proteases in the duodenum where it is bound to intrinsic factor (made by parietal cells) It is then IF-B12 and can be absorbed in the terminal ileum
38
What is the name of B-12 which can be absorbed?
IF-B12 intrinsic factor bound B12
39
Main causes of B12 deficiency
* Poor dietary intake * Small bowel disease (crohn's / post surgery) * Pernicious anaemia (antibodies ot parietal cells)
40
What disorder does S have and what is going on?
Pernicious anaemia It is where you have antibodies to parietal cells therefore they don't make intrinsic factor and you can't absorb B12 reuslting in anaemia This is overcoming by directly injecting B12 hence you can bypass the absorbtion issues
41
Two types of dietary iron. Where is each one found and which is better at being absorbed
* Fe2+ - ferrous - found in heme from meats - well absorbed * Fe3+ - ferric - from vegetables - not well absorbed
42
Stomach acid's role and vit C in iron absorbtion?
Stomach acid and vit c can help reduce Fe3+ to Fe2+
43
What is hepcidin and what is it's role in ron metabolism?
It blocks iron absorbtion by degrading ferroportin (a way iron is stored before entering the blood) High circulating iron is toxic so if iron in the blood plasma is high then hepcidin becomes high which impaires further iron absorbtion. Hepcidin lasts for 48h therefor there is an argument to give iron supplimentation every 48h for optimum absorbtion
44
What is the metabolic role of ATP (what does it achieve?)
45
What is the metabolic role of NADPH? (what does it achieve?)
46
What does the word "anabolic" refer to?
Tissue building or the sythesising of complex molecules from simple molecules
47
What does the word catabolic refer to?
The breakdown of complex molecules into simple ones
48
How do the roles of ATP and NADPH differ?
ATP is pure energy and can be used directly or for synthesis of complex molecules. NADPH is a reducing agent and is used in sythesis only
49
Efficiency of glycolysis (anaerobic) vs TCA cycle and oxidative phosphorylation (aerobic)
2 ATP per glucose for anaerobic vs 30 ATP per glucose for aerobic
50
What is Leptin and what is the effect of congenital Leptin deficiency
Leptin is a peptide hormone that is released by adipocytes. Its circulating levels therefore correspond with body fat. It's effects are the suppression of appetite and increasing metabolism. It is essentially a weight regulating hormone. If someone is deficient in Leptin then they are particularly susceptible to obesity.
51
What are gallstones and what is a common cause?
What causes gallstones? Gallstones are thought to develop because of an imbalance in the chemical make-up of bile inside the gallbladder. In most cases the levels of cholesterol in bile become too high and the excess cholesterol forms into stones.
52
What is a common effect of pancreatitis
When the pancreas becomes damaged, pancreatic enzymes are not produced, and malabsorption results.
53
Three main types of enzymes?
* Lipases * Amylase * Proteases
54
What do bile salts have to do with diarrhoea?
Bile salts are recyled from the small intestine into the liver and back into bile If they make their way to the large intestine they cause diarrhoea therefore diarrhoea can be a sign that somthing is up with the liver and bile salt recycling
55
Fill this baddy in
When oxygen is high it supports oxygen intensive processes such as gluconeogenesis. As oxygen depletes it favours anaerobic processes such as glycolysis Again xenobiotic metabolism doesn't require large oxygen levels so here you get a concentration of cytochrome P450 (CYP450) enzymes
56
What is xenobiotic metabolism?
The breaking down of drugs and toxins not normally produced by the body. Biotransformation typically occurs through a series of enzymatic reactions involving the cytochrome P450 system.
57
Draw out paracetamol metabolism
58
What is the toxic intermediary produced in paracetamol metabolism?
NAPQI Hint: Key to the forever nap
59
What can you give to negate the liver damage in a paracetamol overdose?
Acetylcysteine (NAC) This is a precursor to glutathione and replenishes stores of glutathione allowing the continued breakdown of NAPQI
60
Lead causes of acute liver failure UK
**Paracetamol (leading cause in the UK)** **viral (Hep B, A ), Non-A-E** Other viruses (EB, CMV) Wilson’s disease **Drug reactions** Budd-Chiari Autoimmune hepatitis Amanita falloides mushrooms Reye’s syndrome
61
Fill in the signs, symptoms and effects of acute live disease as more hepatocytes are lost
HE is hepatic encephalopathy
62
What is hepatic encephalopathy?
A neurological complication that arises when the liver is unable to remove toxins from the blood, causing them to build up and affect brain function
63
Overview of bilirubin metabolism
Bilirubin is formed by the breakdown of haemaglobin Unconjugated BR is not water soluable and bound to albumin therefore isn't present in urine normally. Bilirubin is the conjugated by the liver where is is excreted into the bowels via bile or excreted by urine. Conjugated bilirubin is further metabolised by gut flora into urobilinogen where some is resorbed and recycled. The rest is ecreted and this is what makes faeces brown and pee dark.
64
What happens with bilirubin in choleostasis?
Conjugated bilirubin gets backed up and builds up in the blood and body. Lots of conjugated bilirubin is then excreted in the urine. The result is yellow skin, pale stool, dark urine.
65
What happens with bilirubin in liver failure?
Liver becomes worse at conjugating bilirubin therefore it builds up in the blood and body. However the build up will be mostly unconjugated bilirubin. Stool is fairly unchanged as enough conjugated bilirubin is geting excreted. Urine can still get dark but due to bile and urobilinogen. (don't quite get last part)
66
Describe the pathophysiology of liver cirrhosis (how hepatocytes get damaged and liver looks like what it does)
Stellate cells seal fenestrations (gaps in hepatocytes) with collogen in response to danger (useful in acute danger as it effectively quarantines the area) This however causes hepatocytes to become ischeamic. When these die more danger signals are released and more collogen is deposited. The hepatocytes do regenerate but in a disorganised state.
67
What are stellate cells?
These are liver cells which normally are inactive and store vitamin A. When activated in response to danger they lay down collagen which is part of the process leading to cirrhosis
68
How do we get from portal hypertension to the symptoms?
Osophageal varices: This is due to the viens in the oesophagus acting as an anastomosis between the portal vien and the IVC. Also get gastric and umbilical varices. Ascites: Splenic viens become dialated -> Reduced effective arterial circulation -> Activation of RAAS -> Oedema
69
How do we end up with AFLD?
Alcohol increases hepatic glycerol 3-phosphate (3-GP) due to NADH/NAD (product of alcohol metabolism) **Large amount of alcohol enhances lipolysis and release of free fatty acids** Increased 3-GP enhances **esterification of fatty acids** Alcohol is associated with increased **ROS which lead to mitochondrial dysfunction** Oxidation of fatty acids is inhibited by alcohol Triglyceride production is increased in the liver and VLDL are released in the blood The end result is steatosis (macrovesicular with large droplets of fat accumulating within the hepatocyte) Stellate cells activated etc....
70
Describe alcohol metabolism
71
What is Acetaldehyde?
Is a toxic intermediary in alcohol metabolism responsible for many of the negative effects of a hangover.
72
What does MASLD stand for?
Metabolic acsociated liver disease
73
What is one of the pre-requisits for MASLD?
Diabetes
74
What are the diagnostic criteria for MASLD?
3 of the following: Abdominal fat High lipids Low HDL High BP Diabetes
75
What is the progression of MASLD?
MASLD -> MASH -> Cirrhosis + Fibrosis ->
76
What is MASH?
Metabolic ascosciated steatohepatitis (inflamation due to fat build up)
77
What is the pathophysiology of MASLD?
Takeway: Diabetes and obesity -> mitochondrial dysfunction -> activation of stellate cells
78
Clinical features of MASLD?
* Asymptomatic * Abnormal liver biochemistry on routine check up * RUQ abdo pain, fatigue * Hepatomegaly * Acanthosis nigricans (children)
79
What is Acanthosis nigricans?
Acanthosis nigricans is a condition that causes areas of dark, thick velvety skin in body folds and creases.
80
What's more dangerous for metabolic disease, visceral fat or subcataneous fat?
Visceral fat is store of hormones and cytokines which can be dangerous for metabolic disease (but some are protective). Take away is it is a storer of hormones and cytokines.
81
What is the cystic duct?
This is the duct leading from the bile duct to the galbladder
82
How do you test for malnutritian?
MUST score (remember from HCA days)
83
What MUST scores count as risky?
84
How do you calculate units of alcohol?
Volume(in L) x Percentage 1 unit = 10ml pure alcohol
85
What is the effect of abstinance in relation to ALD?
Many features may reverse or improve with abstinence

Baz Y2 Semester 2 (20 decks)

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