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YEAR 1 - Biochemistry and Medical Genetics (Anton) > 2. Cellular Metabolism (TT) > Flashcards

2. Cellular Metabolism (TT) Flashcards

(115 cards)

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1
Q

Draw a summary of all of the functions of the liver.

A
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2
Q

What are micronutrients? What are the main types?

A

Things that we get from our diets that we only need small amounts of:

  • Vitamins
  • Trace elements
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3
Q

What are vitamins?

A
  • Organic molecules that are an essential micronutrient which an organism needs in small quantities for the proper functioning of its metabolism.
  • Precursors of enzyme cofactors, anti-oxidants.
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4
Q

What functions do trace elements perform?

A
  • Enzyme cofactors
  • Components of hormones/proteins
  • Redox reactions
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5
Q

What are the main members of the vitamin B group you need to know about?

A
  • Niacin
  • Riboflavin
  • Pyridoxine
  • Thiamine
  • Cobalamin
  • Folic acid
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6
Q

What are the B vitamin names for these:

  • Niacin
  • Riboflavin
  • Pyridoxine
  • Thiamine
  • Cobalamin
  • Folic acid
A
  • Niacin -> B3
  • Riboflavin -> B2
  • Pyridoxine -> B6
  • Thiamine -> B1
  • Cobalamin -> B12
  • Folic acid -> B9
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7
Q

Which B vitamin is niacin?

A

B3

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8
Q

What is the role of niacin?

A
  • Precursor of nicotinamide, which is the primary constituent of the coenzymes nicotinamide adenine dinucleotide (NAD+, NADP+)
  • NAD+ and NADP+ are involved in many dehydrogenase reactions and many catabolic reactions: Glycolysis, fatty acid synthesis and respiration
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9
Q

How can niacin be synthesised?

A

It can be synthesised from tryptophan.

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10
Q

What does a deficiency of niacin (vit B3) result in? What causes this deficiency?

A
  • Pellagra:
    • Dermatitis (inflamed skin/rash)
    • Diarrhoea
    • Delirium
  • Associated with low protein-corn based diets.
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11
Q

For niacin, summarise:

  • Which B vitamin is it
  • What its role is
  • How it is synthesised
  • What a deficiency results in
A
  • Vitamin B3 (a.k.a. nicotinic acid)
  • Used to synthesise nicotinamide, which is used to produce NAD+ and NADP+
  • Synthesised from tryptophan
  • Deficiency results in pelegra (caused by low-protein corn-based diets)
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12
Q

Which B vitamin is riboflavin?

A

B2

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13
Q

What is the role of riboflavin?

A
  • Precursor of FAD and FMN -> These are the redox components of dehydrogenases
  • FAD and FMN are involved in the action of very many enzymes, including the electron transport chain, monoamine oxidases and NADH-cytochrome P450 reductase
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14
Q

How can riboflavin be taken up?

A

It can be taken up via a sodium-dependent active process into enterocytes.

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15
Q

What does a deficiency of riboflavin result in?

A

Relatively minor symptoms if you consider the huge range of enzymes FAD and FMN play a role in:

  • Angular stomatitis + Cheilosis (inflammation of the mouth)
  • Atrophy of papillae of tongue
  • Anaemia
  • May also be important for vision
  • Interferes with the metabolism of other nutrients, especially other B vitamins
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16
Q

For riboflavin, summarise:

  • Which B vitamin is it
  • What its role is
  • How it is absorbed
  • What a deficiency results in
A
  • Vitamin B2
  • Used to synthesise FAD and FMN
  • Absorbed into enterocytes by a sodium-dependewnt active process
  • Deficiency results in inflammation of the mouth, atrophy of papillae of the tongue, anaemia and problems with metabolism of other B vitamins.
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17
Q

How can you convert from riboflavin to FAD and FMN?

A
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18
Q

Which B vitamin is pyridoxine?

A

B6

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19
Q

What is the role of pyridoxine?

A
  • Component of pyridoxal phosphate -> A co-enzyme important to the metabolism of amino acids or any substrate containing nitrogen (transaminase reactions).
  • Synthesis of GABA, serotonin, dopamine, norepinephrine and epinephrine.
  • Important to the synthesis of haeme protein.
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20
Q

How can pyridoxine be absorbed?

A
  • The three forms of pyroxidine can passively diffuse into enterocytes
  • They are then trapped within the cell by phosphorylation by a kinase protein
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21
Q

What does a deficiency of pyridoxine result in?

A
  • Seizures -> Can be quickly remedies by infusion of vitamin B6 (pyridoxine)
  • Anaemia -> Due tecreased amino acid catabolism, especially the conversion of tryptophan to niacin
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22
Q

For pyridoxine, summarise:

  • Which B vitamin is it
  • What its role is
  • How it is absorbed
  • What a deficiency results in
A
  • Vitamin B6
  • Used to synthesise pyroxidal phosphate
  • Absorbed into enterocytes by a passive process, then trapped by phosphorylation
  • Deficiency results in seizures and anaemia
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23
Q

What are the 3 main forms of pyridoxine?

A
  • Pyridoxine
  • Pyridoxal
  • Pyridoxamine
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24
Q

Draw the importance of pyridoxine in the synthesis of neurotransmitters.

A

Pyridoxal phosphate helps catalyse some of the reactions.

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25
Draw the importance of pyridoxine in the synthesis of haem.
26
Which B vitamin is thiamine?
B1
27
What is the role of thiamine?
Precursor for thiamine pyrophosphate -\> Cofactor in α-ketoacid dehydrogenases and transketolase
28
What does a deficiency of thiamine result in?
Beriberi
29
What are the two types of beriberi? What are the symptoms of each?
* Wet beriberi: * Affects the cardiovascular system * Fast heart rate, shortness of breath, and leg swelling * Dry beriberi: * Affects the nervous system * Numbness of the hands and feet, confusion, trouble moving the legs, and pain. * A form with loss of appetite and constipation may also occur.
30
For thiamine, summarise: * Which B vitamin is it * What its role is * What a deficiency results in
* Vitamin B1 * Used to synthesise thiamine pyrophosphate * Deficiency results in beriberi
31
Draw a diagram to show the formation of thiamine pyrophosphate.
32
Which B vitamin is folic acid?
B9
33
What is the role of folic acid?
It is used in one carbon transfer reactions -\> e.g. In purine and pyrimidine biosynthesis.
34
What does a deficiency of folic acid result in?
Dietary deficit is rare -\> Usually only secondary to pregnancy, alcoholism, etc: * Megaloblastic anaemia * In pregnancy -\> Neural tube defects (i.e. spina bifida)
35
For folic acid, summarise: * Which B vitamin it is * What its role is * What a deficiency results in
* Vitamin B9 * Important to one carbon transfer as in purine and prymidine synthesis * Deficiency leads to megaloblastic anaemia and during pregnancy results in neural tube defects (i.e. spina bifida)
36
How is folic acid targetted clinically? [EXTRA]
* Dihydrofolate reductase is the enzyme that converts folic acid into its active form * Dihydrofolate reductase inhibitors (such as methotrexate) are used: * In anti-cancer treatment * As antibiotics * As anti-malarials * In rheumatoid arthritis
37
Which enzyme converts folic acid into its active form? What is the active form?
* Dihydrofolate reductase * Produces dihydrofolate
38
Draw an equation to show how folic acid is important in purine and pyrimidine synthesis.
* Folic acid (in its active forms) is involved in transfers of one carbon between molecules * This creates pyrimidines and purines * For example, in this reaction, N5,N10-methylene-THF donates a carbon to dUMP, producing a trinucleotide and dihydrofolate
39
Deficiencies in what vitamin can lead to neural tube defects?
Folic acid (B9)
40
What is megaloblastic anaemia, what are the causes and what are the symptoms?
* An anemia (of macrocytic classification) that results from inhibition of DNA synthesis during red blood cell production. * This occurs due to vitamin B12 or folic acid deficiency, since these are involved in DNA synthesis * Symptoms: * Fatigue and lethargy * Breathlessness + Feeling faint * Headaches * Pale skin * And a wide range of other symptoms
41
What is the recommended intake of folic acid, for normal people and for those pregnant? Why?
* Normal people -\> 0.2 mg/day * Decreases risk of cardiovascular disease and megaloblastic anaemia * Around conception -\> 0.4 mg/day * Decreases risk of neural tube defects * Late pregnancy -\> 0.4 mg/day * Decreases risk of megaloblastic anaemia
42
What is the B vitamin name for cobalamin?
B12
43
What is at the centre of cobalamin molecules?
Cobalt
44
What are the two forms of cobalamin and what is the role of each?
* Methylcobalamin * Cofactor for the cytosolic methionine synthase -\> Involved in methionine synthesis * Adenosylcobalamin * Cofactor for mitochondrial methylmalonyl-CoA mutase -\> Involved in oxidation of odd-chain fatty acids
45
How is cobalamin involved in odd-chain fatty acid metabolism?
One of the two main forms of cobalamin, adenosylcobalamin, is involved:
46
What are the symptoms of cobalamin deficiency?
* Pernicious anaemia * Megaloblastic anaemia -\> Due to inability to synthesise RBC DNA * Gastrointestinal symptoms * Neurological symptoms -\> Sensory and motor deficiencies, plus degradation of spinal cord * Numbness of peripheral nerves * High levels of odd chain fatty acids in tissues methylmalonic aciduria
47
What is the main methyl donor in folate and vitamin B12 reactions?
SAM (S-adenosylmethionine) (Check what this is!)
48
Draw the important reaction that methylcobalamin is involved in.
49
Remember to revise the absorption of vitamin B12.
In P&P -\> Binding to IF
50
For cobalamin, summarise: * Which B vitamin it is * What its role is * What a deficiency results in
* B12 * Cofactor for methionine synthesis and for oxidation of odd-chain fatty acids * Deficiency results in pernicious anaemia (megaloblastic anaemia, GI symptoms, neurological symptoms), Numbness of peripheral nerves, High levels of odd chain fatty acids in tissues
51
What are the three trace metals you need to know about?
* Copper * Zinc * Iron
52
What are the biological roles of zinc in the body?
* Essential to the function of over 70 enzymes * Important to activity of DNA and RNA polymerase * Zinc finger proteins needed for gene expression
53
What are the biological roles of copper in the body?
Cofactor for a variety of enzymes involved in: * Iron use * Collagen synthesis * Electron transport chain * Antioxidants
54
What are the biological roles of iron in the body?
* Haemoglobin synthesis * Cytochrome activity * Urea cycle activity * Lipogenesis * Cholesterogenesis
55
Explain the importance of trace metal interactions.
* Trace metals have different oxidation states and can interfere with each other to alter the oxidation state. * This oxidation state determines the absorption and use of the trace metal.
56
How many oxidation states does zinc have and what are they?
Just Zn2+
57
Draw a diagram to show the flux of zinc in the body, as well as its distribution.
Zinc is present in all organs, tissues, fluids, and secretions in the body, but the majority of zinc (83%) is present in skeletal muscle and bone.
58
What is zinc bound to in the blood?
Albumin
59
How much of zinc is absorbed from the diet (as opposed to excreted)? Why?
* Only 10-40% of dietary zinc is absorbed * This is due to phytates (a major form of phosphate in plants), which promote excretion instead
60
What is the typical daily intake of zinc?
4 - 15 mg/day
61
How much zinc is typically found in tissue stores?
1.5 - 2.5g
62
Describe the intestinal absorption of zinc. What proteins are involved?
Zinc is taken up both actively and passively: * Active absorption involves: * Multiple carrier proteins (metallothionine) * Cysteine-rich proteins (CRIP) * Non-specific binding proteins (NSBP) * In the plasma, it then binds to albumin
63
What can cause zinc deficiencies?
* Unleavened bread with high phytate levels * Rare autosomal recessive disease characterised by the inability to absorb zinc intestinally
64
Describe how much copper is found in the body and where.
100mg -\> Mostly in skin, muscle, bone marrow, liver and brain.
65
What is blood copper concentration and what is it bound to?
* 15 µmol/L * Bound to a protein called caeruloplasmin
66
Name two enzymes that copper is involved in the function of.
* Cytochrome oxidase (in the ETC) * Superoxide dismutase (antioxidant role)
67
Aside from transport of copper in the blood, what is another function of caeruloplasmin?
Involved in Fe homeostasis: * Has ferroxidase activity * This forms Fe3+ for mobilisation of Fe in transferrin
68
Describe the absorption and excretion of copper.
* Actively absorbed from stomach and duodenum * Excreted by the GI tract, and to a lesser extent in urine and from the skin
69
Is copper deficiency common?
No, it is rare.
70
What are the symptoms of copper deficiency?
* Anaemia * Hypothermia * Neurological symptoms * Aneurysms * Skeletal demineralisation
71
Draw a diagram to show the absorption of iron from the diet.
See P&P flashcards for more details.
72
In what forms can iron be absorbed from the diet?
In both haem and non-haem forms.
73
What is iron bound to in the blood?
Transferritin
74
Is there a way for the body to dispose of excess iron?
Only bleeding.
75
How much iron is there in the body?
3 - 4g
76
Where in the body is iron found?
* Mostly in haemoglobin, myoglobin and cytochromes * Rest is found stored as soluble form ferritin or as insoluble aggregate haemosiderin -\> In liver, muscle and bone marrow
77
What hormone is involved in iron homeostasis and what does it do?
* Hepcidin * Levels increase when there is high iron in circulation * It prevents uptake through enterocytes
78
Describe the cycling of iron in the body.
* Bone marrow synthesises RBCs using iron in the plasma * These RBCs can be broken down by macrophages * Excess iron can be stored in the liver * Some of the plasma iron (bound to transferrin) also goes to other tissues, including muscle and the brain
79
Describe the concept of cellular iron homeostasis.
* Iron can be in two forms (Fe+ and Fe2+) -\> Fe+ is safer and less toxic, so it must be kept this way * In the blood, iron is bound to transferrin * It is taken up into the cell via transferring receptor receptor * Iron is taken off transferrin by STEAP and instead binds to ferritin * Ferritin levels can be regulated (via levels of iron) * When iron high, more ferritin is produced to sequester the iron * Iron is exported by ferroportin 1
80
What are the causes, symptoms and treatments of iron overload?
Causes: * Primary genetic * Alcoholic cirrhosis * Chronic pancreatitis * Excessive blood transfusion Symptoms: * Skin pigmentation * Hepatic haemosiderosis (iron overload) + cirrhosis * Pancreatic fibrosis, diabetes * Hypogonadism * Cardiac disease * Arthropathy Treatment: * Iron chelation with desferrioxamine * Ascorbic acid
81
What are some causes of iron deficiency? [EXTRA]
* Loss of blood in the GI tract * Kidney disease -\> Elevated hepcidin * Cancer -\> Tumours that sequester iron * Alzheimer’s disease -\> Impaired Hb synthesis * Osteoporosis/infections/obesity
82
What are the two forms of anaemia and what are the biomarkers of each?
* Iron defecient anaemia (IDA) * Decreased ferritin * Increased transferrin * Anaemia of chronic inflammation (ACI) * Increased ferritin * Decreased transferrin
83
Add a couple of flashcards summarising iron, zinc and copper.
Do it.
84
What cofactor is important for transaminase and aminotransferase enzymes? Which vitamin is this derived from?
* Pyridoxal phosphate * Derived from vitamin B6
85
Where is ammonia produced by amino acid breakdown handled?
In the liver and kidneys.
86
How is ammonia (produced by amino acid breakdown) transported from peripheral tissues to the liver and kidneys? Which enzymes are involved?
* Ammonia transported as glutamine, which is produced by glutamine synthetase: * NH3 + Glutamate -\> Glutamine. * It occurs in nearly all tissues of the body. * Ammonia is unloaded via glutaminase: * Glutamine -\> NH3 + Glutamate. * It occurs in the kidneys and liver.
87
What ammonia acid is most abundant in the blood? Why?
Glutamine, because this is how ammonia is transported to the liver.
88
What is the blood ammonia and blood glutamine concentration?
* Blood ammonia -\> 10-20µM * Blood glutamine -\> 400-600µM
89
In what form do the kidneys and liver excrete ammonia?
* Liver -\> Urea * Kidneys -\> Ammonium ions
90
Which part of the brain is ammonia toxic to?
Brain
91
Add one flashcard about the urea cycle step by step.
Do it.
92
Aside from the liver, where else is glutamine produced by muscles metabolised? [IMPORTANT]
* Intestines * Renal cortex
93
Remember to add flashcards about metabolism of glutamine in the small intestine and kidneys. [IMPORTANT]
Do it!
94
Describe step 1 of the urea cycle, including enzymes and where it takes place.
* In the mitochondria * CO2 + NH3 → Carbamoyl phosphate * Catalysed by carbamoyl phosphate synthetase I This is the rate-limiting step and requires ATP.
95
Describe step 2 of the urea cycle, including enzymes and where it takes place.
* In the mitochondria * Carbamoyl phosphate + Ornithine -\> Citrulline * Catalysed by ornithine transcarbamoylase (OTC)
96
How is ornithine (produced by step 2 of the urea cycle) transported out from mitochondria into the cytosol?
Ornithine translocase
97
Describe step 3 of the urea cycle, including enzymes and where it takes place.
* In the cytosol * Citrulline + Aspartate -\> Arginosuccinate * Catalysed by argininosuccinate synthetase (ASS1) This requires ATP.
98
Describe step 4 of the urea cycle, including enzymes and where it takes place.
* In the cytosol * Arginosuccinate -\> Arginine + Fumarate * Catalysed by argininosuccinate lyase
99
Describe step 5 of the urea cycle, including enzymes and where it takes place.
* In the cytosol * Arginine + H2O -\> Urea + Ornithine * Catalysed by arginase
100
What are some factors that can increase the load on the urea cycle?
* Increased protein intake * Deficiency of an essential amino acid(s) from the diet * General starvation * Catabolic states -\> Trauma, surgery
101
Can ammonia cross the blood-brain barrier?
Yes
102
What are the two cell types in the brain that are affected by ammonia?
* Astrocytes * Neurons
103
Does the brain produce ammonia?
Yes, both the astrocytes and neurons produce NH3.
104
What is the role of the astrocytes in the brain?
They protect the neurons from ammonia, glutamine and glutamate.
105
What is the mechanism for ammonia's neurotoxicity?
* Effects on cell membrane: * Ammonia acts like K+ * Increases resting potential * Decreases threshold * Reduces amplitude of action potential * The result is depolarisation block * Effects on neurotransmitters: * Diversion of carbon skeleton to glutamine. * Decreased levels of glutamate and aspartate * Excitatory neurotransmitters -\> Altered binding of GABA Add details on this?
106
What are the symptoms of the toxicity of ammonia?
General symptoms: * Lethargy * Poor feeding * Hypothermia * Vomiting * Hyperventilation * Respiratory distress * Seizures * Unresponsiveness, coma, death Cerebral pathology: * Acute: * Cerebral oedema * Swollen astrocytes in cortex * Chronic: * Cerebral atrophy * Neuronal loss in cortex * Gliosis
107
How do high levels of ammonia affect metabolism? Why?
Symptoms: * Increased lactate * Reduced phosphocreatine * Decreased ATP + Increased ADP and AMP Explanations: * Glycolysis stimulated as ammonia is allosteric activator of phosphofructokinase * Aerobic oxidation is inhibited as ammonia inhibits isocitrate dehydrogenase and α-ketoglutarate dehydrogenase in TCA cycle * Malate-aspartate shuttle inhibited by decreased glutamate. Increased cytoplasmic NADH results in increased lactate production.
108
Read up on the case study presented in the hepatic ammonia handling lecture. [EXTRA?]
Do it.
109
What are ammonia scavengers?
* Mainstay drugs for by-passing the urea cycle -\> Used to treat high levels of ammonia: * Conjugation of benzoate with glycine generates hippurate * Conjugation of phenylacetate (phenylbutyrateis its precursor) with glutamine generates phenylacetylglutamine * Conjugates are excreted in urine
110
What is the simplest treatment for hyperammonaemia?
Low-protein diet
111
How does ammonia affect IQ in the long-term?
It frequently results in lowered IQ.
112
Add a flashcard on the size of the dietary intake of iron.
Do it. One source said that men and women only need under 2mg/day.
113
What is the role of the ER and Golgi apparatus in biochemistry?
* Biosynthesis of lipids, complex carbohydrates and glycoproteins * Detoxification -\> Cytochrome P450s are in the ER (and mitochondria)
114
What is the role of peroxisomes in biochemistry?
Play a key role in the oxidation of specific biomolecules.
115

YEAR 1 - Biochemistry and Medical Genetics (Anton) (8 decks)

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