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Metabolism Flashcards

0
Q

List the 6 essential components of the diet and 1 non essential.

A

Carbohydrates, lipids, protein, vitamins, minerals, water, and fibre.

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1
Q

Describe the condition of diabetes mellitus.(1)

A

When blood glucose is too high, hyperglycaemia, over years and leads to damage to small and large blood vessels.

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2
Q

What is the main store of glycogen?

A

Liver,

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3
Q

Why are lipids an essential part of the diet? And what percentage of our energy intake should they be?

A

30% of our daily energy intake should be from fats.
Necessary for absorption of fat soluble vitamins A, D, E, K.
Structural components of cell membranes.

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4
Q

What part of the diet facilitates metabolic reactions?

A

Vitamins and minerals

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5
Q

Why are amino acids essential? What do they produce? List 3 compounds.

A

Used to synthesise nitrogen containing compounds.

Purines, pyridamines and haem groups.

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6
Q

How is the nitrogen balance altered in starvation and in pregnancy?

A

Normal: N2 intake = N2 loss
Starvation/ muscle wastage: n2< n2 loss
Pregnancy/growth: n2>n2 loss

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7
Q

Why is the nitrogen balance effected by pregnancy or growth?

A

Nitrogen released in the continuous breakdown of tissue protein. These are mostly reused. Excess is secreted in urea.
During growth there is more n2 than loss though.

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8
Q

Name the disorder caused by a low protein, high carbohydrate diet.
That causes symptoms of odema, anaemia, distended abdomen, lethargy and anorexia.
Affects hair and skin.

A

Kwashiorkor.

E.g. A young child displaced from breast feeding and going on to a diet of cassava and carbohydrate.

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9
Q

What condition can occur when a child is nutrient deficient and in particular, low in protein? Leads to no odema?

A

Marasmus

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10
Q

Describe an exergonic chemical reaction

A

When energy input is greater than the energy released

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11
Q

What is the equation for calculating BMI?

A

= weight (kg) /

Height2 (m)

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12
Q

Is energy from fuel released by oxidation or reduction?

A

Oxidation.

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13
Q

There are three components to our daily energy expenditure

A

Basal metabolic rate: energy to required to maintain life. The functioning of the body and physical digestive and emotional rest.
Energy for voluntary physical activities
Energy require to process the food we eat. Diet induced thermogenesis.

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14
Q

How do we estimate BMR? And what are the major tissues contributing to it (4).

A 
Body weight(kg) x 100.
If not obese
Skeletal muscle, 30%
CNS
Liver
Heart
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15
Q

How would you calculate a rough estimate of the total daily energy required for a person who does 2 hrs excercise a day?

A

BMR + 60/70%

+30 sedentary
+100 several hours a day

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16
Q

How much energy is required to process food?

A

10%

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17
Q

BMI values. State ranges.

Normal is 18.5-24.9

A 
Underweight is below 18.5
Overweight is 25-29.9
Obese 30-34.5
Severely obese 35+
Waist to hip more accurate
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18
Q

Define homeostasis and state it’s importance

A

The internal environment of the body. It must remain stable.
It counteracts changes in the internal environment.
Failure - disease

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19
Q

Define cell metabolism and state it’s importance

A

The physical and chemical processes occurring within a living cell necessary for maintenence of life.
derive energy and raw materials from food stuffs and use them in the tissues of the body.
Support the growth, constant repair, and activity of tissues.

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20
Q

Describe anabolic and catabolic metabolism

A

Catabolism is the break down of molecules to release energy. It provides reducing power as it is an oxidation reaction.
Anabolism. Uses reducing power and raw materials to make molecules for growth and maintenance. Uses energy, mostly hydrolysis of ATP

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21
Q

Name 4 catabolic pathways.

A

Glycolysis, lipolysis, fatty acid oxidation, glycosylation, fa syntheis,

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22
Q

Give 4 examples of pathways and reactions that build up molecules.

A

Gluconeogenesis, pentose phosphate pathway, e acceptors other than oxygen

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23
Q

Why do cells need a continuous supply of energy?

A

The supply the cells and ensure that they undergo their normal reactions. Without energy many cells cannot function.

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24
Q

How to we generate heat metabolically?

A

By using coupling reactions to convert the energy released in exergonic reactions to heat production

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25
Q

Where do we get cell nutrients from?

A

They circulate in the blood from the diet,
synthesis in body tissues from precursors
and released from storage in body tissues.
Some is lost as waste in the faeces or via the kidney and lungs

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26
Q

How do we utilise cell nutrients?

A

Degradation to release energy, all tissues
Synthesis of cell components, all tissues
Storage, liver, adipose tissue, skeletal
Inter conversion to other nutrients, liver, adipose, kidney cortex
Excretion, liver, kidney, lungs

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27
Q

Why do we metabolise nutrients?

A

Energy as atp for cell function
Building block molecules
Organic precursor molecules, e.g. Acetlyl coa
Bio synthetic reducing power e.g. NADPH

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28
Q

What type of metabolic reaction is oxidative, releases large amounts of free energy (incl some ATP) and produce intermediary metabolites?

A

Catabolism

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29
Q

Does the total concentration of carrier molecules in cells remain constant? And why, why not?

A

Yes, they cycle between oxidised and reduced forms, so cell function is maintained.

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30
Q

Describe what happens in a reduction reaction?

A

Remove O2

Or add e or H atoms (h+ e-)

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31
Q

Give 2 examples of oxidation reactions

A

Pyruvate oxidation to acetyl coa

Using NAD reduction to NADH and pyruvate dehydrogenase

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32
Q

What kind of reaction occurs spontaneously? Which drives energy requiring reactions?

A

Exergonic

Negative enthalpy change (^H is -ve)

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33
Q

Hydrolysis bond are high or low energy

A

High

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34
Q

Define free energy change (^G)

A

The energy released in an exergonic reaction that is available to do work

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35
Q

How is ATP used and how does it relate to free energy

A

It’s a high energy molecule
It can’t store energy very long
Therfore must be rapidly resynthesised from ADP from free energy from catabolism
Therefore ATP turnover is very high.

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36
Q

What does a high energy signal signal. And give 4 examples

A

That there is enough energy to meet the cells immediate needs
NADH, NADPH, FAD2H, reduced in anabolic reactions

LOW ENERGY: NAD+, NADP+, FAD, oxidised in catabolic reactions

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37
Q

Explain the role of creatine phosphate in muscle cells

A

Creatine phosphate acts as a immediate store of free energy in the muscle cells. Very important in the first few seconds of vigorous excercise.

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38
Q

How is creatine phosphate syntheised?

A

Creatine and ATP to creatine phosphate and ADP. Using creatine kinase
REVERSIBLE

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39
Q

How is creatine used as an indicator of muscle mass?

A

It is measured in the urine as creatine is a waste product.
The rate of production of creatinine is proportional to the concentration of creatine in muscle and therfore related to skeletal muscle mass

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40
Q

How can we measure kidney function

A

Kidneys normally effective at removing creatinine from the blood.
High blood creatinine and low urine creatine conc indicates reduced kidney function

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41
Q

What is the main function of the parathyroid glands?

A

To secret parathyroid hormone which is essential in maintaining serum calcium levels

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42
Q

Where are the parathyroid glands located?

A

In the neck, normally on the posterior surface of the thyroid gland. But may be located elsewhere.
Normally 4

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43
Q

Five main polypeptide hormones released from endocrine pancreas and what cells

A 
Insulin, B cells
Glucagon alpha cells
Somatostatin delta cells (regulates islet cell secretions)
Pancreatic polypeptide 
Ghrelin
44
Q

What is the function of the exocrine pancreas

A

Release digestive enzymes through duodenum

45
Q

How does the ultra structure of a B cell relate to synthesis and storage of Insukin

A 
Mitochondria
RER
Golgi
Storage vesicles
To make new proteins and provide energy for protein synthesis, secretion of the hormones.
46
Q

Describe how insulin is synthesised

A

1) insulin mRNA translated on RER and forms pre pro insulin
2) transported to ER and sorted and modified to pro insulin (A,C,B)
3) to Golgi: C peptide cleaved off. And 2 disulphide bonds connect the A & B peptides.
4) packaged into storage granules
5) released by exocytosis into the blood stream

47
Q

Describe the structure of insulin

A

Big polypeptide
2 polypeptide chains , aloha and beta chains ith insulin rceptors on cell surfaces
Linked by 2 disulphide bonds to connect the cysteine residues
3rd disulphide bond in the aloha chain
Short half life

48
Q

How is insulin secretion controlled?

A

By its metabolites, glucose, amino acids, and fatty acids
Gastrim secretion from the GI tract
Neurotransmitters adrenaline and noradrenalin and acetyl choline inhibits insulin secretion

49
Q

How does insulin resistance occur?

A

B cells try to compensate by increasing insulin production
Eventually unable to maintain and respond effectively which leads to impaired tolerance
Finally B cell dysfunction causes relative insulin deficiency leading to type 2 diabetes

50
Q

How is cortisol released

A

Controlled by acth
ACTH release controlled by corticotrophin releasing factor
Controlled by hypothalamus in response to stress
Negative feedback on pituary and hypothalamus from glucocorticoids
Transported In blood by CBG corticosteroid binding globulin

51
Q

Where is the pituary gland located and what is it connected to?

A

Base of brain suspended from hypothalamus

Connected to anterior pituary

52
Q

Where are the adrenal glands located?

Brief description

A

Pair of multifunctional endocrine glands
Cap upper poles of kidneys
2 regions, adrenal cortex and the medulla

53
Q

Describe the adrenal cortex and what it secretesw

A

Capsule
Zona glomerulosa: secretes mineralocorticoids. E.g. Aldosterone, regulates Ions e.g. Na and k levels
Zona fasiculata, secretes glucocorticoids, e.g. Cortisol and costicosterone. Regulates carbohydrate metabolism increases serum sugars
Zona reticularis: adrenal androgens, adrenaline noradrenaline dopamine,

54
Q

Describe ACTH

A

39aa polypeptide
POMP is its precursor and also produces B endorphins and alpha msh (melanocytes)
Means that higher levels of acth increases above (darker skin)
Short half life so released in pulses
Can interact with other zones receptors

55
Q

What does ACTH bind to to stimulate cortisol release

A

Uses cAMP as a messenger

Receptor used is MC2

56
Q

How does cortisol interact with target cells?

A 
Cross membrane as a steroid,
Bind to cytoplasmic receptors
Bonds to dna in the nucleus
Changes transcription rate
STARVED STATE Causes an increase in gluconeogenesis, lipolysis and proteolysis
57
Q

Describe to role of the hypothalamus in control of pituitary function

A 
Releases inhibiting or releasing hormones
Travel via hypophyseal portal vessels
TRH
CRH
SRH
somatostatin
58
Q

Name the TROPHIC hormones that are released from pituitary gland and what they effect. Also what stimulates their release

A

Thyrotrophin releasing hormone (TRH) stimualtes TSH release affects thyroid gland
Corticotrophin releasing hormone (CRh) Stimulates ACTH release which affects adrenal gland (cortisol)
Somatostatin releasing hormone (SRH). Stimulates GH release (somatotropin) affects liver production of somatomedins
Somatostatin inhibits
LH (ovary and testis hormone production)
FSH (affects ovary and testis function)

59
Q

How would you test for cushings disease/syndrome?

A

Dexamethasone test.
Suppresses secretion of ACTH
Therfore can identify if the high cortisol levels are caused by
An excess secretion of ACTH in pituitary gland, (disease)
An ectopic ACTH secretion caused by a tumour (syndrome)

60
Q

How would you identify and test for addinsons disease

A

Low glucocorticoids, e.g, cortisol
Tired, weak and dehydrated. Fluid loss due to Na imbalances. Pigmentation
Low blood pressure
Hypoglycaemic
Test using synacthin. Similar to acth
Supposed to increase cortisol levels by acting on cortisol receptors

61
Q

Describe the three hormones secreted from the thyroid gland and from which cells

A

Thyroxine (T3) from follicular cells. The active form
Tri iodthyronine (T4) also produced in the follicular fells and is the stable form. Much more released
Calcitonin produced in parafollicular cells and is involved in calcium metabolism

62
Q

How are t3 and T4 synthesised and released into the blood stream (7 steps)

A

1) thyroglobulin synthesised in the follicular cells and stored in the colloid in the lumen of the follicular cell
2) Iodine and sodium imported into cells
3) iodine transported into the lumen
4) oxidisation of iodide
5) attach to tyrosine rings on the thyroglobulin. Either 1 (MIT) or 2 (DIT) iodines attach to each ring.
6) coupling of DIT and MIT to form t3 and T4 in ratio 1:10. Still attached to the thyroglobulin
7) whole molecule transported back into the follicular cell where the thyroglobulin is removed
8) t3&4 then transported out of the cell into the capillaries

63
Q

How is thyroid activity controlled

A

Hypothalamus releases TRH, by stress/cold/
Travels down the hypothalamic pituitary portal system in blood
Anterior pituitary in Thyrotrophs release TSH
stims follicular cells to release t3&4

64
Q

Effects of thyroid hormones on the body

A

Increase metabolic rate of tissues, slowly, increase O2 uptake
Increases BMR, heat production (increased UCP)
Increased mobilisation of fatty acids, proteins etc
Affects growth and development
Increased heart muscle,
Increases nerve cell function, (absence leads to cretinism)
(Stimulates production of nt and hormone receptors (tachycardia)
FSH and lh

65
Q

How does t3 affect target cells

A

Within target cells affecting nucleus as binds to protein receptors
Increases rate of transcription of specific genes which makes specific proteins
Increases cell activity so increased energy use
Needs to be active 3. Therfore remove 5’ iodine from t4

66
Q

What are the roles of calcium in the body

A

Nerve conduction
Muscle contraction
Hormone secretion
Messengers inside cell

67
Q

How is calcium tied with phosphate

A

Form hydroxyapatite crystals to be used in bone

Regulated by PTH and calcitrol

68
Q

How is serum calcium levels regulated.

A

Parathyroid hormone. Decreases urinary loss, increases release and reabsorbtion from bone, increases calcium abosobtion in small intestine
Vitamin d. Activated to calcitrol in kidney. Increases ca uptake from gut
Calcitonin (lowers)in animals.

69
Q

How is PTHrP produced and what problems can it cause?

A

Produced by tumours
Leads to hypercalcaemia
Because increases release of calcium from bone, reduces excretion and reduces reabsorbtion

70
Q

Kidney damage, (stones) constipation, dehydration, tired, depressed, abdominal pain (moans and groans) renal calucci.
Indicated what disorder?

A

Chronic hypocalcaemia
Caused by low calcium levels
In children rickets can occur as bones are broken down
Also more calcium is abosobed in kidney and more take. From the gut by calcitrol
Thin sry hair and skin
Hoarse voice

71
Q

Give signs and symptoms of hypercalcaemia

A 
Hyper excitability of nervous muscular junctions
Pins and needles
Find it hard to sit still
Muscle spasms (tetany)
Paralysis 
Weight loss
72
Q

Describe the metabolic changes in pregnancy

A

First 20 weeks, increased nutrient stores, increase insulin ratio
Then metabolism adapts to increased demands from foetus
Release fatty acids from maternal stores
Reduced disposal of nutrients after meals

73
Q

In pregnancy what can altered metabolism lead to

A

Gestational diabetes.
Due to needing more insulin to promote storage of nutrients
Increased rate of insulin synthesis, B cell hypertrophy and hyperplasia
Can’t release enough insulin leads to gestational diabetes as pancreas can’t cope

74
Q

Explain how glycogen and tag stores differ and their limits

A

Glycogen
Quick release of glucose in muscles, lots of branching. Glycogen phosphorylase
Liver stores used to replenish blood glucos
Not affected by blood supply unlike plasma glucose

Tags: lipolysis is slow and limited by albumin availability to transport
Therfore fatty acid uptake is slow to muscle cells and mitochondria
More oxygen and atp is needed than in glycogen metabolism

75
Q

Describe the metabolic response to sprinting and anaerobic respiration

A

Controlled by noradrenaline (nervous system) and adrenaline (endocrine)
Creatine phosphate converted to creatine and ATP
Muscle glycogen to glucose 6 phosphate
G 6 P metabolised in glycolysis to ATP
Anaerobic glycolysis
Lactate and H ion build up
Fatigue

76
Q

Describe energy utilisation during marathon or aerobic exercise

A

Hormonal control (low insulin and high adrenaline GH glucagon and cortisol) and some noradrenaline
Muscle glycogen stores used for 60 mins
Use blood glucose. Remain constant due to gluconeogenesis and liver glycogen
Fatty acid oxidation

77
Q

What is the first line of defence against super oxide radicals

A

Superoxide dismutase, transfers it to hydrogen peroxide and then catalase oxidises it to water and oxygen :)
If not enough then radicals oxidise proteins, lipid and dna - damage as highly reactive

78
Q

How are ROS formed

A

In mitochondria

By protein carriers prematurely reducing oxygen to O2- ions

79
Q

Name two other radicals? How formed? How eliminateD?

A

Hydroxyl radicals, ‘OH

  • x Rays, gamma rays, uv light
  • damage cell membranes, alter haemolysis in RBC, damage dna, can’t be eliminated by an enzyme system

NO’
From arginine to NO’
Oxidised to form ONOO- peroxynitrate :( inflammation

Oxidising agents e,g antimalarials

80
Q

How do we eliminate ROS

A

Cellular defence
NADPH (from pentose phosphate pathway). Reducing agent
Glutathione (GSH) antioxidant and acts as a reducing agent: front line defence as abundant
Antioxidants C E A
Flavenoids, coloured fruit and veg
Minerals: selenium and zinc

81
Q

What can oxidative stress lead to? Which three areas are damaged? What diseases can it cause? How does stress occur?

A

Damage dna, lipids in cell membrane (plaque formation), proteins

Occurs if too many ROS or antioxidant levels too low
Leads to: atherosclerosis, Parkinson’s, Alzheimer’s, inflammatory reaction

82
Q

Describe oxidative burst

A

When a neutrophils or monocytes produces a massive restlessness of ROS - destroys cell and the bacteria or fungus
Produced by NADPH oxidase

83
Q

List the main lipid classes

A 
Cholesterol
Cholesterol esters
Phospholipids
Tags
Fatty acids
84
Q

Describe cholesterol and its uses

A

Found in membranes
Precursor to bile salts, steroid hormones,
Syntheised in the liver and also from the diet

85
Q

How are lipids transported

A

In carrier proteins
Fatty acids in albumin (limited)
Others in lipoprotein particles
Outside membrane, cholesterol, phospholipids, apoproteins
Insoluble inside: tags, cholesterol esters,

86
Q

Describe chylomicrons.
Where synthesised, what do they transport, how do they release their load and when should you expect to see them in the blood?

A

Low density
Transport dietary tags from the intestines to tissues
They are syntheised in enterocytes lining the intestine
They release the tags at the capillary endothelial cells.
Lipase breaks them down (cleaves) releasing tags
Glycerol released into circulation for glycolysis
Fatty acids used for b oxidation
Appear 4-6 hrs after meal

87
Q

Describe VLDL

Where synthesised, what do they transport, how do they release their load.

A

Carry tags synthesised in the liver to adipose tissue for storage
VLDL syntheised in the liver
Capillary endothelium binds the VLDL, cleaves the VLDL releasing TAGs
Broken down to fatty acids and glycerol
Some VLDL remnants used in HDL formation

88
Q

Describe LDL

Where synthesised, what do they transport, how do they release their load.

A 
Syntheised in liver
Transport liver cholesterol to tissues.
Apo B100 used to transport
High lol high risk of atherosclerosis 
Cells have LDL receptors.
Bind lol, and release by endocytosis 
Cholesterol ester released and cleaved to cholesterol and fatty acids
Controlled by cholesterol concentration in the cell
89
Q

Describe HDL

Where synthesised, what do they transport, how do they release their load.

A

Syntheised in tissues
Transports excess cholesterol to the liver for disposal as bile salts :)
Cholesterol delivered via the capillaries to the HDL particles

90
Q

Describe Hyperlipoproteinaemia

A

Raised levels of lipoprotein
Most types leads to increased risk of coronary artery diseases
Caused by over production or under removal, due to defective enzymes (lipase), receptors, or apoproteins
Genetic or caused by lifestyle and diet

91
Q

Describe the pharmokinetics of a drug. What the body does to the drug, and their metabolites in the body

A

Absorption
Distribution
Metabolism
Elimination

92
Q

Why can’t we just excrete drugs

A

Most are lipid soluble so get reabsorbed in kidney tubule

Therfore alter them so that they are soluble in water

93
Q

What is a prodrug and give an example

A

A drug that is activated by the body
E.g, codeine to morphine

Normally drugs are deactivated by metabolism in the body

94
Q

Describe the drug metabolism pathways

A

Phase 1: expose reactive groups so it can be eliminated rapid,y , some skip this step. Occurs in liver microsomes, GI tract, kidney for e.g
Uses an enzyme system: cytochrome p450 and NADPH as a cofactor

Phase 2: conjugation in the liver using cytosolic enzymes. The altered drug combines with water soluble group e.g. Glucuronic acid

95
Q

How can environmental factors affect enzyme inhibition and induction

A

Grapefruit and cranberry juice and cimetidine can inhibit metabolism of other drugs- poly therapy problems
Enzyme induction: metabolism of one agent induces enzymes in liver. And increases metabolism of other drugs. E.g. Alcohol

96
Q

Describe the metabolic response to alcohol.

A

Alcohol oxidised to acetyl aldehyde in liver using NAD+ to NADH and acetyl dehydrogenase
Further oxidised to acetate (can form acetic acid) in liver using aldehyde dehydrogenase and producing NADH.
Then to acetyl coa to generate energy.

97
Q

How can we treat alcoholism

A

Disulfiram: inhibits aldehyde dehydrogenase
Causes build up of acetyl aldehyde
Causes a very bad hangover. Controlled conditions

98
Q

Describe metabolism of paracetamol

A

Metabolised by phase 2 conjugation

Normal dose: phase 2, glucuronidation (add glucuronide sulphate) or sulphation

Toxic dose: saturate pathway so use alternative pathway
Phase 1: NAPQI toxic metabolite
Phase 2: conjugation with glutathione (used in antioxidants, depleted=liver failure from ROS damage)
Treatment: rapidly with n-acetyl cysteine antioxidant

99
Q

Describe the metabolic effects of alcohol abuse. Direct and indirect

A

Leads to build up of NADH which means that there is not enough NAD for glycolysis .
Excess NADH used for:
-pyruvate to lactate shift
- lipid synthesis: glycerol or fatty acids
- electron transport chain: therfore inhibiting normal oxidation of fats in B oxidation or the citric acid cycle therfore they build up and can produce ketone bodies.
Excess fats also secreted into the blood stream: atherosclerosis

Build up of acetyl aldehyde can lead to cirrhosis and hepatitis: liver damage.
Damages cells in GI tract- loss of appetite, diahorrea, low folic acid (anaemia)
Non direct: poor diet, vitamin and mineral deficient, low carb and protein intake

100
Q

What is the function of glucagon?

A

Opposes insulin
Promotes increased glucose levels in blood
Increases proteolysis, gluconeogenesis from amino acids, glycogen lysis, ketogenesis,
Controlled by adrenaline and noradrenaline

101
Q

How do steroid, thyroid and lipid hormones affect target cells?

A

Cross cell membranes
To nucleus, bind to dna and stimulate or inhibit protein synthesis
Produce mRNA

102
Q

How do peptide, amine and water soluble hormones affect target cells

A

Can’t cross cell membranes so bind to receptor
Activate a messenger pathway
Exerts a metabolic response

103
Q

Describe the control of appetite

A

Appetite centre: arcuate nucleus of the hypothalamus
Primary neurones sense metabolites in the blood( FA and glucose) and respond
Excitory pathway- stimulate appetite
Inhibitory pathway - reward system or suppress appetite

104
Q

Describe the excitory pathway in appetite control

A

Neurotransmitter control: release neuro peptide Y
Agouti related peptide (AgRP)
Stimulates appetite

105
Q

Describe the inhibitory pathways in appetite control

A

POMC cleaved
Produces B endorphins: reward system activates
And alpha melanocytes stimulating hormone: suppress appetite

106
Q

Describe ghrelin and its effect

A

Feedback from gut to hypothalamus when stomach empty
Stimulates primary neurones to release neurotransmitters
Stimulates excitory pathway: stimulate apetite

107
Q

Describe the hormones that stimulate the apetite inhibitory pathway

A

Leptin: released from adipocytes. If deficient then severe overeating. Induces uncoupling in mitochondria- heat produced instead of atp
Insulin: suppress
Amylin: form B cells in pancreas, inhibits the excitory response.

My ESA1 (4 decks)

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