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Health And Disease In Populations > Metabolism > Flashcards

Metabolism Flashcards

1
Q

What are the classifications for BMI weights

A
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2
Q

What is malnutrition

A

a condition caused by imbalance in what an individual eats and what is required

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3
Q

what is malabsorption

A

a condition caused by the failure to absorb nutrient properly

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4
Q

What is undernutrition

A

a condition caused by an eating disorder

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5
Q

what is homeostasis

A

the maintenance of a constant internal environment within limits of a dynamic equilibrium

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6
Q

How do you calculate the BMI

A

BMI = Weight (kg) / Height ^ 2 (meters)

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7
Q

what is metabolism

A

the chemical reactions that happen in organisms to sustain life

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8
Q

What enzyme turns HMG acid into Cholesterol

A

HMG Co enzyme A reductase

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9
Q

In metabolism of Acetyl Co-A, what regulates the production of ketone bodies or cholesterol

A

Ketone Bodies are increased in response to Glucagon

Cholesterol is increased in response to Insulin

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10
Q

What is the intermediate between Acetyl Co-A and Ketone Bodies or Cholesterol?

A

Hydroxylmethyly Glutaric Acid

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11
Q

What is the level of ketone bodies in the blood that suggest diabetes?

A

More than 10mM

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12
Q

What are the products of Beta Oxidation of fatty acids

A

Acetyl Co-A, NADH, FADH2

No ATP

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13
Q

What are the three ketone bodies and their properties

A

Acetone, acetoacetate and beta-hydroxybutyrate. water soluble and can enter the tri-carboxycylic acid chain.

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14
Q

Which parts of the body requires glucose for energy exclusively

A

Cornea of the eye, medulla of the kidney, testes, RBC, CNS preferentially

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15
Q

Name 3 different classes of lipids and 2 examples of each

A

Fatty Acids - triacylglycerols, phospholipids, fatty acids
Hydroxy Methyl Glutaric acid derivatives - Ketone Bodies and Cholesterol
Vitamins - A, D, E, K

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16
Q

Where are ketone bodies and cholesterol synthesised

A

liver

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17
Q

Where are fatty acids metabolised

A

Most tissues in the body with mitochondria, except CNS as difficulty in crossing the blood brain barrier.

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18
Q

where is glycogen stored

A

liver and muscles

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19
Q

what are the advantages of glycogen

A

stable, large surface area for rapid access, osmotically neutral

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20
Q

What is glycogenesis

A

Creation of glycogen, using hydrolysis -

Glucose - glucose 1 phosphate - glucose 6 phosphate + UTP - UDP glucose + glycogen

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21
Q

What enzymes are used in glycogenesis

A

1, Hexokinase = glucose - glucose 6 phosphate

2, Phosphoglucomutase = glucose 6 phosphate - glucose 1 phosphate

3, Glycogen synthase and Branching Enzyme - UDP glucose + glycogen

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22
Q

What is gycogenlysis

A

Degradation of glycogen, phosphorylation reaction

glycogen - glucose 1 phosphate - glucose 6 phosphate - glucose

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23
Q

What are the enzymes in glycogenlysis

A

1, Debranching enzyme & amp; Glycogen phosphorylase = Glycogen - glucose 1 phospate

2, Phosphoglucomutase = glucose 1 phospate - glucose 6 phosphate

3, Glucose 6 phosphatase = glucose 6 phosphate - glucose

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24
Q

What effect does glucagon have on glycogen

A

Activates glycogenlysis - phophorlyation of glycogen synthase decreasing activity and phosphorylation of glycogen phosphorylase increasing activity

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25
Q

What effect does insulin have on the glycogen

A

Glycogenesis - dephosphorylation of glycose synthase leading to activation, dephosphorylation of glycogen phosphorylase leading to inhibition

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26
Q

Give two examples of glycogen storage diseases and the enzymes they effect

A

Von grieke disease - glucose 6 phosphatase, cannot convert glucose 6 phosphate to glucose in the liver

McArdle disease - glycogen phosphorylase cannot breakdown glycogen in liver or muslce

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27
Q

What are the advantages of lipid storage

A

bulk, energy rich, anhydrous, highly calorific - stoerd as triacyglycerol in adipose tissue.

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28
Q

What effect does glucagon and insulin have on fat stores

A

Glucagon - phosphorylates Hormone sensitive lipase activation

Insulin - dephosphorylates Hormone sensitive lipase deactivation

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29
Q

Name three energy storing molecules apart from ATP

A

Phosphoenolpyruvate

1,3 - Bisphosphoglyerate

Creatine Phosphate

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30
Q

Where is Creatine Phosphate, what does it do and how is it made

A

Creatine is transformed into creatine phosphate with the enzyme creatine kinase, this requires energy of ATP.

Creatine Phophate is a more stable form of energy than ATP but only lasts a short time and is produed in muscles when there are high concentrations of ATP

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31
Q

What is creatinine

A

Creatinine is formed spntaneously from the breakdown of creatine or creatine phosphate. High levels in urine suggest muscle wasting.

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32
Q

What are the characteristics of monosaccharides and give examples

A

Partially oxidised, hydrophilic - glucose, fructose, galactose, ribose, glyceraldehyde

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33
Q

What is the first step in glycolysis

A

glucose to glucose 6 phosphate

enzyme - hexokinase or glucokinase in liver

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34
Q

What is the commiting step in gycolysis

A

Fructose 6 phosphate - fructose 1,6, bisphosphate

Phosphofructokinase

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35
Q

What is the second step in glycolysis

A

glucose 6 phosphate - fructose 6 phosphate

Isomerase

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36
Q

Which two steps require ATP in glycolysis

A

Step 1 creation of glucose 6 phosphate

Step 3 creation of fructose 1,6 bisphosphate

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37
Q

What are the net products of gycolysis

A

2 x (pyruvate + 2ATP + NADH + H + H20)

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38
Q

What are the two products of step 4 in glycolysis

A

Dihydroxyacetone phosphate - that can become glycerol phosphate making phospholipids and TAG

Glyceraldehyde - 3 - phosphate

Enzyme is Aldolase

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39
Q

What is substrate level phosphorylation

A

direct creation of ATP from carbohyrates, rather than indirectly from ATP synthase in the electron transport chain

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40
Q

What are the advantages of glycolysis

A

Many small steps makes, Little energy lost, can be controlled by multiple enzyes, versatility to connect with other metabolic pathways

Anaerobic

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41
Q

Name an enzyme that breaksdown polysaccharides and disaccharides

A

Amylase - polysaccharides in the mouth a1,4 glycosidic bonds
Sucrase - glucose/fructose
lactase - galactose/glucose
Maltase - glucose/glucose

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42
Q

Absorption of Glucose

A

In gut - sodium dependent glucose transporter SGLT
GLUT 1- RBC
GLUT 2 - both ways - liver, basolateral surface of epithelia, kidneys
GLUT 3 - nerurons
GLUT 4 - insulin dependent muscle / adipose tissue

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43
Q

Name 2 alternative products of glycolysis

A

2,3 Bisphosphoglycerate (2,3BPG) - from 1,3, BPG in step 6. uses enzyme bisphosphoglycerate mutase

Glycerol phosphate - from dihydroxyacetone phosphate in step 4, used in producing lipids

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44
Q

How is glycolysis regulated

A

Product inhibiton - high NADH leads to inhibition of Step 6

Allosteric inhibition - Phosphofructokinase in Step 3 activated by ATP inhibitied by AMP

Dephosphorylation - Glucagon activates protein Kinase A, which phosphorylates Pyruvate Kinase in step 10 of glycolysis

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45
Q

What is the purpose of the lactate pathway

A

To generate oxidised NAD+ to be used in RBC for glycolysis

Cannot be retrieved from stage 4 of carbohydrate metabolism in electron transfer chain

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46
Q

When does lactate pathway happen

A

In RBC to generate NAD+, in muscle when insufficient oxygen

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47
Q

What is the process of lactate pathway

A

NADH + H + pyruvate — lactate + NAD+

lactate dehydrogenase is the enzyme, reversibly

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48
Q

Which tissues can use lactate

A

Cardiac muscle converts it back to pyruvate

Liver can convert it back to glucose / glycogen

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49
Q

What are the consequences of high lactate

A

Lactic acidosis >5mM

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50
Q

Fructose pathway involves which steps

A

Fructose - Fructose 1 phosphate - 2x Glyceraldehyde-3-phosphate - glycolysis

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51
Q

What are the consequences of difunctional enzymes in the fructose pathway

A

Fructokinase - no problem, fructose excreted in urine

Aldose - fructose 1 phosphate builds up in the liver causing toxic damage

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52
Q

What is the galactose pathway

A

Galactose - Galactose 1 phosphate - Glucose 1 phosphate - Glucose 6 phosphate - Glycolysis

Enzymes - galactokinase and galactose 1-P uridyl transferase

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53
Q

What are the consequences of enzyme deficiencies in the galactose pathway

A

galactokinase - increase in galactose which is forced into the galactitol pathway

glactose 1-P-uridyl transferase - galactose 1 phosphate builds up in liver causing disease and build up of galactose

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54
Q

What are the consequences of increased galactose

A

galactose converted into galactitol. Using NADPH in NADP+. By aldose reductase

NADPH is important in creating reduced glutathione, which prevents formation of inappropriate disulphide briges. So without it can cause cataracts in the eye

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55
Q

At what stage in glycolysis can the pentose pathway begin? what is the purpose of the pentose pathway?

A

Stage 1 - glucose 6 phosphate to C5 sugar?

Produces reducing power NADPH required for lipogenesis and glutathione reduction

Produces C5 sugars for nucleotides

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56
Q

What enzyme works on the pentose 5 pathway

A

glucose 6 phosphate dehydrogenase

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57
Q

What are the products of each rotation of the Kreb’s cycle

A

3 NADH, 1 FADH2, 1 GTP, oxoacetate, 2 CO2

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58
Q

What are the 2 irreversible steps in the Kreb’s cycle and the enzymes that regulate them

A

Isocitrate - ketoglutarate & amp & CO2 = isocitrate dehydrogenase

Ketoglutarate - Succinyl CoA = keoglutarate dehydrogenase

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59
Q

What effects the rate of reaction in the Kreb’s cycle

A

ADP - activates isocitrate dehydrogenase

ATP/ NADH - inhibit isocitrate dehydrogenase and ketoglutarate dehydrogenase

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60
Q

What are the products of the Kreb’s cycle used for

A

citrate = fatty acids

ketoglutatrate / malate = amino acids

FADH NADH2 = carriers of reducing power in electron transport chain

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61
Q

Where does glycolysis, Kreb’s cycle, and Electron Transport Chain take place

A

cytoplasm, matrix of mitochondria, inner membrane of mitochondria

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62
Q

Where does the fructose, galactose and pentose 5 sugar metabolism take place in the cell.

A

liver, liver, all cells but mostly liver - all take place in cytoplasm

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63
Q

What enzyme converts pyruvate to acetyl CoA, where is it found and what does it produce

A

pyruvate dehydrogenase, takes pyruvate into the mitochondria, produces CO2 and NADH + H

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64
Q

Pyruvate dehydrogenase is activated and inhibited by what products

A

Activated by - ADP, NAD+, Insulin, Pyruvate

Inibited by - ATP, NADH, Glucagon, Acetly CoA

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65
Q

What is the difference between substrate and oxidative phosphorylation

A

substrate - direct transfer of phosphate group to ADP or GDP, happens in cytoplasm, not oxygen dependent, produces less ATP

oxidative - happens on inner membrane of mitochondria, using energy from electrons to generation a proton motive force that activate ATP synthase, requires oxygen, produces more ATP

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66
Q

How many ATP molecules do the reducing agents create

A

NADH - 2.5 ATP

FADH2 - 1.5 ATP

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67
Q

What is the molecule that transports protons across the inner membrane of the mitochondria

A

proton translocating complext - 3 types

ATP synthase - inward bound

The inner membrane of the mitochondria is highly impermeable to protons.

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68
Q

What regulates the proton transport chain

A

Build up of ATP, lowers ADP, meaning less H+ can re-enter the matrix build up of H+ on intermembrane space is such that hydrogen pumping trhrough proton translocating membrane ceases

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69
Q

What inihibits the oxidative phosphorylation

A

cyanide - blocks one of the proton translocating complexes preventing the passage of electrons to oxygen.
CO - blocks provision of oxygen

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70
Q

What are uncouplers and give examples

A

They separate the proton translocating complex from the ATP synthase. By increasing the permeability of the inner mitochondial membrane.

Thermogenin, UCP 1, dinitrophenol

Common in brown adipose tissue and hibernating animals to produce heat

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71
Q

What are the essential amino acids

A

Isoleucine, leucine, threonine, histidine, lysine, methionine, phenylalanine, tryptophan, valine

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72
Q

What is transamination

A

Exchange of and amino group between an amino acid and keto acid, creating a different amino acid. Uses an aminotransferase enzyme - example alanine transaminase, aspartate transaminase

Alpha ketoglutarate - glutamate
Oxaloacetate - aspartate

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73
Q

What is deamination, and give example

A

Removal of amino group from amino acids for excretion

Glutamine - Glutamate - ketoglutarate

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74
Q

GIve two examples of amino acid clinical problems

A

Phenylketonuria: Phenylalanine - tyrosine, using phenylalnine hydroxylase. High phenylalanine causes mental retardation by inhibitin mitochondrial metabolism. Detected in urine, or heel prick of new borns.

Homocystinuria: Homocysteine - Cystathionine, by cystathionine beta synthase. High homosysteine damages connective tissue, CNS, muscle.

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75
Q

What are the two ways of processing ammonia and transporting it in the blood

A

Glutamate + ammonia = glutamine in tissues safe to transport in blood, used in liver to convert to urea or excreted in kidneys

Pyruvate + ammonia = alanine

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76
Q

What are the advantages of urea?

A

Non toxic, metabolically inert, high nitrogen content, soluble, chemically inert

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77
Q

What is the urea cycle inputs

A

glutamate and aspartate

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78
Q

what are the dangers of ammonia

A

extremely toxic to brain, readily dissolvable, alters pH, effects Kreb’s cycle, metabolism

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79
Q

What is refeeding syndrome

A

When patients are severly malnourished, they have insufficient protein and exnzymes to process amino acids into safe urine. Consequently ammonia levels increase severely. This can cause death, BMI

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80
Q

Give uses for 5 amino acids

A 
Histidine - histimine
Cystein - glutathione
Arginine - nitric acid
Glycine - hae
Tyrosine - Thyroid hormones
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81
Q

What are apoproteins

A

They are proteins that provide structural support to phospholipid bilayers, and idenitify the vessicles and act as cofactors.

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82
Q

What are lipoproteins

A

Phospholipid vesicles, with apoprotein structural units containing a hydrophobic lipid core

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83
Q

Where are lipoprotein lipases found and what interacts with them

A

On capillary walls, interact with apo C on chylomicrons, VLDL, IDLs

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84
Q

How is artherosclerosis caused

A

LDLs, lack Apo E and Apo C, they are not effectively cleared by the cells in the body. The cholesterol contents can get oxidised, as they hang in the blood for so long. The LDLs are then consumed by macrophages, which turn into foam cells, causing a fatty streak in the intima of blood vessels, this can narrow the lumen, or burst and cause a MI/ stroke

85
Q

What Apoproteins do HDL have and what are their purpose

A

ATP Binding Cassete Protein (ABCA1) needed on tissues to form and HDL with cholesteroll and it will transport the cholesterol to the liver for processing. Deliver to liver for use in producing bile, or steroidal cells producing hormones

86
Q

Give two examples of hyperlipoproteinaemias

A

Type 1 - High chylomicrons, defective LPL
Type 2 - Defective LPL, high chance of artherosclerosis
Type 3 - High IDL and chylomicrons, defective Apo E

87
Q

Give three symptoms of hypocholerstolaemia and three treatments

A

Xanthelasma - yellow eyelid blotches
Tendon Xanthoma - nodules on tendons
Corneal Arcus - white rings around iris

diet, exercise, cholesterol sequestration in diet, statins target HMG-CoA reductase

88
Q

What disease are aused by oxidative stress

A

Mulitple Sclerosis, CVD, Parkinson’s,, Arthritis, Alzheimers

89
Q

What is a free radical and give examples

A

an atom with an inpaired electron - hydroxyl radical (most damaging), superoxide, nitric oxide

90
Q

What damage can free radicals cause

A

DNA - misspairing of nucleotides, strand breaks, damage to the backbone
Protein - change structure, gain or loss - eg. create cysteine and inappropriate disulphide bonds
Lipids - bind ot unsaturated fatty acids creating lipid radicals - eg. lipid peroxyl radical. Last a long time in the blood

91
Q

Soures of biological oxidation

A

Endogenous - electron transport chain, nitric oxide synthase, NADPH oxidase
Exogenous - radiation, pollutants, tobacco, toxins

92
Q

What is a respiratoy burst

A

A release of free radicals by a phagocyte to destroy pathogens - typically using NADPH oxidase, Nitric oxide, and hydrogen peroxide

93
Q

Name 4 different defences against free radicals in the body

A

Glutathione - in reduced from can accept free radicals to form a disulphide bridge between two cystein amino acids
Catalase - Catalase - hydorogen peroxide to water and oxygen
Vitamin E - prevents lipid peroxidation with the help of vit C
Superoxide dismutase converts super oxide to hydrogen peroxide and oxygen.

94
Q

Two diseases that increase free radival vulnerability

A

Galactosaemia - causes Galactose to be converted to Glactitol by the enzyme aldose reductase. Using NADPH and preventing any for regenerating Glutathione
Glucose 6 posphate dehydrogenase non function - cannot produce pentose sugars from gluose 6 phosphate, so not creating NADPH.

Consequences Heinz bodies and anaemia from RBC, cataracts

95
Q

What are the consequences of Paracetamol

A

Excess paracetamol creates NAPQI - depletes gluthione and causes oxidative damage to the liver.

Antidote is acetylcysteine - regenerates the glutatione

96
Q

give three examples of positive feedback in the body

A

ovulation, lactation, blood clotting

97
Q

What is a zeitgeber

A

environmental stimuli - light, temperature, activity, diet

98
Q

what is a suprachiasmatic nucleus

A

collection of neurons in the brain

99
Q

What is an osmole

A

the amount of substance required to dissociate in water to form one mole of osmotically active particles

100
Q

What is osmolality

A

the number of osmoles per kilogram of solution

101
Q

How many litres of water in a 70kg man

A

42 L - 28L intracellular, 9.4L extracellular, 4.6L blood,

102
Q

Give examples of 5 hormones produced by organs not glands

A 
stomach - ghrelin, gastrin
Liver - IGF1
Adipose - Leptin
Kidney - Renin Calcitrol
Heart - ANP / BNP
103
Q

What type of hormone are insulin and glucagon

A

small polypepetide, soluble hormones

104
Q

What are examples and characteristics of amino acid hormones

A

adrenaline, noradrenaline, thyroid - former water soluble latter lipid soluble.

105
Q

Give examples of glycoprotein hormones and their character

A

Large, water soluble - Lutenizing hormone, Follicle stimulating hormone, thyroid stimulating hormone

106
Q

What are the advantages of binding proteins to non-soluble hormones

A

Increase solubility, half life and accessability.

107
Q

What are the differences between the water soluble hormones and lipid soluble hormones

A

Cannot cross the plasma membrane for water soluble hormones, require carrier protein. Eg. G-protein for adrenaline and Insulin for Tyrosine Kinase

108
Q

What is the region of the skull that holds the pituitary gland

A

sella turcica

109
Q

What does the hypothalmic / pituitary axis control

A

growth, lactation, reproduction, adrenal gland, thyroid gland, water , puberty

110
Q

Where does the pituitary develop from

A

anterior pituitary - ectoderm

posterior pituitary - nervous system

111
Q

What are tropic hormones and their examples

A

They effect the release of other hormones. Released from anterior pituitary gland, following neurosecretory stimulation from the hypothalamus.

thyrotropin releasing hormone - thyroid stimulating hormone
cortiotropin releasing hormone - adenocorticotropic hormone
prolacti releasing hormone - prolactin

112
Q

what is diabetes

A

chronic hyperglycaemia

113
Q

List the main differences between Type 1 and Type 2 diabetes

A

Type 1 - in young people, rapid onset, destruction of beta cells, treated with insulin

Type 2 - generally occurs in middle age, gradual onset, simultaneous loss of beta cells and tissue resistance to insulin, initially untreatable with insulin

114
Q

What are the genetic markers for diabetes type 1 and symptoms and diagnostic

A

polydipsia, polyuria, weight loss - HLA DR3 and HLA DR4

115
Q

what are the symptoms of ketonacidosis

A

hyperventilation, prostration, nausea, vomiting, dehydration

116
Q

what are the symptoms of type 2 diabetes

A

polydipsia, polyuria, weight loss

tiredness, lethargy, persistent infections, infected feet.

117
Q

what are the diagnostic blood tests for diagnosing diabetes

A

> 7mMol fasting

>11.1mMol/L random

118
Q

Name two medicines for type 2 diabetes and their function

A

Metformin - decrease insulin resistance and decrease gluconeogenesis
Sulphonureas - increase insulin release from pancreas cells

119
Q

what level of HBA1c suggests hyperglycaemia

A

> 10% glycated HBA1c

120
Q

what are the consequences of hyperglycaemia

A

high glucose creates sorbitol via aldose reductase, using NADPH, which can no longer be used for reducing glutathione and protecting against disulphide bridges.

Macrovascular - stroke, MI, poor circulation
Microvascular -
retinopathy weak vessels burst,
glaucoma (change in osmotic pressure of the eye),
nephropathy (decrease blood vessel diameter and infection), neuropathy (change in micro blod vessels for neurons)
diabetic feet (poor blood supply)

121
Q

What is the structure of insulin and how is it produced and released

A

alpha and beta chain, 3 disulphide brides, 110amino acids long.
preproinsulin chain in ER
proinsulin in Golgi apparatus
storage granules Insulin and c peptide

secretion - high glucose, absorbed through GLUT2, increase ATP, open ATP sensitive K+channels, depolarsing cell releasing Ca2+, releasing granules.

122
Q

At what stage in glycolysis can the pentose pathway begin? what is the purpose of the pentose pathway?

A

Stage 1 - glucose 6 phosphate to C5 sugar?

Produces reducing power NADPH required for lipogenesis and glutathione reduction
Produces C5 sugars for nucleotides

123
Q

What enzyme works on the pentose 5 pathway

A

glucose 6 phosphate dehydrogenase

124
Q

What are the products of each rotation of the Kreb’s cycle

A

3 NADH, 1 FADH2, 1 GTP, oxoacetate, 2 CO2

125
Q

What are the 2 irreversible steps in the Kreb’s cycle and the enzymes that regulate them

A

isocitrate - ketoglutarate & CO2 = isocitrate dehydrogenase
ketoglutarate - Succinyl CoA = keoglutarate dehydrogenase

126
Q

What effects the rate of reaction in the Kreb’s cycle

A

ADP - activates isocitrate dehydrogenase

ATP/ NADH - inhibit isocitrate dehydrogenase and ketoglutarate dehydrogenase

127
Q

What are the products of the Kreb’s cycle used for

A

citrate = fatty acids
ketoglutatrate / malate = amino acids
FADH NADH2 = carriers of reducing power

128
Q

Where does glycolysis, Kreb’s cycle, and Electron Transport Chain take place

A

cytoplasm, matrix of mitochondria, inner membrane of mitochondria

129
Q

Where does the fructose, galactose and pentose 5 sugar metabolism take place in the cell.

A

liver, liver, all cells but mostly liver - all take place in cytoplasm

130
Q

What enzyme converts pyruvate to actyl CoA, where is it found and what does it produce

A

pyruvate dehydrogenase, takes pyruvate into the mitochondria, produces CO2 and NADH + H

131
Q

Pyruvate dehydrogenase is activated ad inhibited y what products

A

Activated by - ADP, NAD+, Insulin, Pyruvate

Inibited by - ATP, NADH, Glucagon, Acetly CoA

132
Q

What is the difference between substrate and oxidative phosphorylation

A

substrate - direct transfer of phosphate group to ADP or GDP, happens in cytoplasm, not oxygen dependent, produces less ATP
oxidative - happens on inner membrane of mitochondria, using energy from electrons to generation a proton motive force that activate ATP synthase, requires oxygen, produces more ATP

133
Q

How many ATP molecules do the reducing agents create

A

NADH - 2.5 ATP

FADH2 - 1.5 ATP

134
Q

What is the molecule that transports protons across the inner membrane of the mitochondria

A

proton translocating complext - 3 types
ATP synthase - inward bound
The inner membrane of the mitochondria is highly impermeable to protons.

135
Q

What regulates the proton transport chain

A

Build up of ATP, lowers ADP, meaning less H+ can reenter the matrix build up of H+ on intermembrane space is such that hydrogen pumping trhrough proton translocating membrane ceases

136
Q

What inihibits the oxidative phosphorylation

A

cyanide - blocks one of the proton translocating complexes preventing the passage of electrons to oxygen.
CO - blocks provision of oxygen

137
Q

What are uncouplers and give examples

A

They separate the proton translocating complex from the ATP synthase. By increasing the permeability of the inner mitochondial membrane.

Thermogenin, UCP 1, dinitrophenol

Common in brown adipose tissue and hibernating animals to produce heat

138
Q

What are the essential amino acids

A

Isoleucine, leucine, threonine, histidine, lysine, methionine, phenylalanine, tryptophan, valine

139
Q

What is transamination

A

Exchange of and amino group between an amino acid and keto acid, creating a different amino acid. Uses an aminotransferase enzym - example alanine transaminase, aspartate transaminase

Alpha ketoglutarate - glutamate
Oxaloacetate - aspartate

140
Q

What is deamination, and give example

A

Removal of amino group from amino acids for excretion

Glutamine - Glutamate - ketoglutarate

141
Q

GIve two examples of amino acid clinical problems

A

Phenylketonuria: Phenylalanine - tyrosine, using phenylalnine hydroxylase. High phenylalanine causes mental retardation by inhibitin mitochondrial metabolism. Detected in urine, or heel prick of new borns.

Homocystinuria: Homocysteine - Cystathionine, by cystathionine beta synthase. High homosysteine ddamages connective tissue, CNS, muscle.

142
Q

What are the two ways of processing ammonia and transporting it in the blood

A

Glutamate + ammonia = glutamine in tissues safe to transport in blood, used in liver to convert to urea or excreted in kidneys

Pyruvate + ammonia = alanine

143
Q

What are the advantages of urea?

A

Non toxic, metabolically inert, high nitrogen content, soluble, chemically inert

144
Q

What is the urea cycle inputs

A

glutamate and aspartate

145
Q

what are the dangers of ammonia

A

extremely toxic to brain, readily dissolvable, alters pH, effects Kreb’s cycle, metabolism

146
Q

What is refeeding syndrome

A

When patients are severly malnourished, they have insufficient protein and exnzymes to process amino acids into safe urine. Consequently ammonia levels increase severely. This can cause death, BMI

147
Q

Give uses for 5 amino acids

A 
Histidine - histimine
Cystein - glutathione
Arginine - nitric acid
Glycine - hae
Tyrosine - Thyroid hormones
148
Q

describe glucagon and its effects

A

29 amino acids in length, produced by alpha cells in the pancrease, no dsulphde bridges, amino acid hormone

increases glycogenlysis, gluconeogenesis, ketogenesis, lipolysis
inhibits lipogenesis

149
Q

What are the three regions of the adrenal cortex and their products

A

zona glomerulosa - mineralcorticcoids - salts Na+/K+, aldosterone
zona fasciculata - glucocorticcoids - sugars, cortisol
zona resticularis - androgens - glucocorticoids testosterone

150
Q

Describe the adrenal cortex axis

A

1- hypothalamus detects pain, heat, emotion releases CRF corticotropin releasing factor
2- anterior pituitary responds by releasing 29 aa Adrenocorticotropic Hormone (from POMC)
3 - ACTH reacts with receptors on zona fasiculata and reticularis of the the adrenal gland
4, stimulates cholesterol esterase, producing cortisol

151
Q

What are the effects of cortisol

A

increase proteolysis, glycogenlysis, gluconeogenesis, lipolysis
decrease glucose absorption in blood by blocking GLUT4

Stress hormone, increases metabolites

152
Q

What are the catecholamines

A

adrenal hormones from the medulla, a modified symptathetic ganglion

153
Q

What are the effects of adrenaline and where is it synthesised from

A

increase CNS, cardiovascular, glycogenlysis, lipolysis

Origin is tyrosine

154
Q

What is Addion’s disease

A

low cortisol - lethargy, postural hypotension, low glucose, low

In some case ACTH may be expressed at high level without stimulating cortisol but causing pigmentation of the skin. Melanocyte Stimulating Hormone MSH, is part of the ACTH

155
Q

What is Cushing’s disease

A

Chronic high coritsol - moon face, buffalo hump, hypertension, striae, muscle wasting in the limbs, mood swings. Cortisol causes redistribution of fat in body.

caused excess ACTH, cortisol or external steroid influence

156
Q

What is exogenous cushing’s and an example of a causative

A

A source of steroid that mimics the effects of elevated cortisol taken. Often anti-inflammatory drugs fro arthritis, asthma, inflammatory bowel disease
eg. dexamethasone /Prednisolone

157
Q

How do you diagnose Cushing’s

A

Look at natural ACTH and cortisol cycle. Test reaction to anacthen (ACTH analogue) and dexamethosone (cortisol analogue)

158
Q

What are the two types of cells in the thyroid

A

follicular cells - T3/T4

parafollicular cells - calcitonin

159
Q

How is T3 and T4 created

A

Tysoine is taken into follicular cells
Converted into thyroglobulin
Thyroglobulin is sereted into the colloid of the cell
Iodinating species are also concentrated in the colloid
Iodination of thyroglobulin creates Mono iodotyrosine or Di-iodotyrosine (MIT and DIT). Form together to make T3 and T4

160
Q

How is coritsol spread around the body

A

transcortin, overcomes hydrophobic nature of crotisol. Cortisol crosses cell membrane and enters the nucleus

161
Q

What stimulus produces T3 and T4

A

stress and temperature, causes hypo to release thyrotropin releasing hormone TRH, which stimulates ant pit to release thyroid stimulating hormone TSH

162
Q

What are the characteristics of TRH and TSH

A

TRH is a tri-peptide hormone

TSH is a glycoprotein, 2 sub-units

163
Q

How are T3 and T4 transported

A

thyronine binding globulin, albumin, pre-albumin. When bound to the carrier, it is not biologically active.

164
Q

What are the metabolic effects of T3 and T4

A

General increase in metabolism across the body. Increase BMR, glucose uptake, lypolysis, protein metabolism, heat production, bone production

165
Q

How do T3 and T4 work

A

Directly effect the DNA of the cell, receptos have a greater affinity for T3 than T4. Ratio of 1:10. Generally increase metabolism

166
Q

Describe Hashimoto’s Disease

A

1% of population - destruction of thyroid follicular cells, espcially TSH receptors. Symptoms - lethargy, mood swings, cold intolerance, constipation, brittle skin, ataxia

167
Q

Describe consequences of low thyroid hormone in childhood

A

Cretinism - lack of thryoid hormone, leads to large tongue, pronounce brown, poor eyes, short stature and mental retardation. Effects neural development in children

168
Q

Causes of hypothyroidism

A

destruction of thyroid gland, congenital defect, lack of TSH, lack of iodine

169
Q

Describe Hyper thyroidism

A

Grave’s disease - 1% population, autoimmune disease, antibody constantly stimulates TSH receptor. Thyroid stimulating immunoglobulin. Syptoms- high heat, bulging eyes, tachycardia, rapid bowel movements, weight loss.

170
Q

What is the treatment of hyperthyroidism

A

carbimazole inhibits thyroglobulin, radioactive iodine obliterates thyroid, surgical removal of the thyroid

171
Q

What are the functions of the parathyroid gland

A

Regulate calcium serum levels closely between 1-1.3mol / L

172
Q

What regulates serum calcium levels

A

parathyroid hormone PTH, vitamin D, calcitonin

173
Q

What are the symptoms of hypocalaemia

A

Hyperexcitability, tetany, paralysis, convulsions

174
Q

What are the symptoms of Hypercalcaemia

A

kidney stones, constipation, depression, tiredness

175
Q

How can tumours effect calcium levels

A

Common breast and pancreatic tumours release PTHrP - parathyroid hormone related peptide

176
Q

What are the differences between PTH and Vitamin D (calcitrol) effects on calcium.

A

Both increase osteoclasts to release calcium from bone hydroxy apatite

PTH stimulates Vit D to increase Ca uptake in the gut

PTH increases reabsoption of Ca in kidneys, Vit D increases reabsorption of Ca and K in kidneys.

PTH increases blood Ca, Vit D increases serum Ca and K

177
Q

What is Ricket’s

A

A deficiency in dietary Ca leading to Ca serum levels maintained at the expens of bone. Symptoms - bony necklace, bow legs, soft kull, lumpy joints

178
Q

Where is Ca absorbed

A

In the gut, jejunum and ileum mainly, chaperoned across gut epithelia by the Vit D

179
Q

What are the three regions of the adrenal cortex and their products

A

zona glomerulosa - mineralcorticcoids - salts Na+/K+, aldosterone
zona fasciculata - glucocorticcoids - sugars, cortisol
zona resticularis - androgens - glucocorticoids testosterone

180
Q

Describe the adrenal cortex axis

A

1- hypothalamus detects pain, heat, emotion releases CRF corticotropin releasing factor
2- anterior pituitary responds by releasing 29 aa Adrenocorticotropic Hormone (from POMC)
3 - ACTH reacts with receptors on zona fasiculata and reticularis of the the adrenal gland
4, stimulates cholesterol esterase, producing cortisol

181
Q

What are the effects of cortisol

A

increase proteolysis, glycogenlysis, gluconeogenesis, lipolysis
decrease glucose absorption in blood by blocking GLUT4

Stress hormone, increases metabolites

182
Q

What are the catecholamines

A

adrenal hormones from the medulla, a modified symptathetic ganglion

183
Q

What are the effects of adrenaline and where is it synthesised from

A

increase CNS, cardiovascular, glycogenlysis, lipolysis

Origin is tyrosine

184
Q

What is Addion’s disease

A

low cortisol - lethargy, postural hypotension, low glucose, low

In some case ACTH may be expressed at high level without stimulating cortisol but causing pigmentation of the skin. Melanocyte Stimulating Hormone MSH, is part of the ACTH

185
Q

What is Cushing’s disease

A

Chronic high coritsol - moon face, buffalo hump, hypertension, striae, muscle wasting in the limbs, mood swings. Cortisol causes redistribution of fat in body.

caused excess ACTH, cortisol or external steroid influence

186
Q

What is exogenous cushing’s and an example of a causative

A

A source of steroid that mimics the effects of elevated cortisol taken. Often anti-inflammatory drugs fro arthritis, asthma, inflammatory bowel disease
eg. dexamethasone /Prednisolone

187
Q

How do you diagnose Cushing’s

A

Look at natural ACTH and cortisol cycle. Test reaction to anacthen (ACTH analogue) and dexamethosone (cortisol analogue)

188
Q

What are the two types of cells in the thyroid

A

follicular cells - T3/T4

parafollicular cells - calcitonin

189
Q

How is T3 and T4 created

A

Tysoine is taken into follicular cells
Converted into thyroglobulin
Thyroglobulin is sereted into the colloid of the cell
Iodinating species are also concentrated in the colloid
Iodination of thyroglobulin creates Mono iodotyrosine or Di-iodotyrosine (MIT and DIT). Form together to make T3 and T4

190
Q

How is coritsol spread around the body

A

transcortin, overcomes hydrophobic nature of crotisol. Cortisol crosses cell membrane and enters the nucleus

191
Q

What stimulus produces T3 and T4

A

stress and temperature, causes hypo to release thyrotropin releasing hormone TRH, which stimulates ant pit to release thyroid stimulating hormone TSH

192
Q

What are the characteristics of TRH and TSH

A

TRH is a tri-peptide hormone

TSH is a glycoprotein, 2 sub-units

193
Q

How are T3 and T4 transported

A

thyronine binding globulin, albumin, pre-albumin. When bound to the carrier, it is not biologically active.

194
Q

What are the metabolic effects of T3 and T4

A

General increase in metabolism across the body. Increase BMR, glucose uptake, lypolysis, protein metabolism, heat production, bone production

195
Q

How do T3 and T4 work

A

Directly effect the DNA of the cell, receptos have a greater affinity for T3 than T4. Ratio of 1:10. Generally increase metabolism

196
Q

Describe Hashimoto’s Disease

A

1% of population - destruction of thyroid follicular cells, espcially TSH receptors. Symptoms - lethargy, mood swings, cold intolerance, constipation, brittle skin, ataxia

197
Q

Describe consequences of low thyroid hormone in childhood

A

Cretinism - lack of thryoid hormone, leads to large tongue, pronounce brown, poor eyes, short stature and mental retardation. Effects neural development in children

198
Q

Causes of hypothyroidism

A

destruction of thyroid gland, congenital defect, lack of TSH, lack of iodine

199
Q

Describe Hyper thyroidism

A

Grave’s disease - 1% population, autoimmune disease, antibody constantly stimulates TSH receptor. Thyroid stimulating immunoglobulin. Syptoms- high heat, bulging eyes, tachycardia, rapid bowel movements, weight loss.

200
Q

What is the treatment of hyperthyroidism

A

carbimazole inhibits thyroglobulin, radioactive iodine obliterates thyroid, surgical removal of the thyroid

201
Q

What are the functions of the parathyroid gland

A

Regulate calcium serum levels closely between 1-1.3mol / L

202
Q

What regulates serum calcium levels

A

parathyroid hormone PTH, vitamin D, calcitonin

203
Q

What are the symptoms of hypocalaemia

A

Hyperexcitability, tetany, paralysis, convulsions

204
Q

What are the symptoms of Hypercalcaemia

A

kidney stones, constipation, depression, tiredness

205
Q

How can tumours effect calcium levels

A

Common breast and pancreatic tumours release PTHrP - parathyroid hormone related peptide

206
Q

What are the differences between PTH and Vitamin D (calcitrol) effects on calcium.

A

Both increase osteoclasts to release calcium from bone hydroxy apatite

PTH stimulates Vit D to increase Ca uptake in the gut

PTH increases reabsoption of Ca in kidneys, Vit D increases reabsorption of Ca and K in kidneys.

PTH increases blood Ca, Vit D increases serum Ca and K

207
Q

What is Ricket’s

A

A deficiency in dietary Ca leading to Ca serum levels maintained at the expens of bone. Symptoms - bony necklace, bow legs, soft kull, lumpy joints

208
Q

Where is Ca absorbed

A

In the gut, jejunum and ileum mainly, chaperoned across gut epithelia by the Vit D

Health And Disease In Populations (2 decks)

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