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Medicine Semester 1 > Metabolism > Flashcards

Metabolism Flashcards

0
Q

What is metabolism?

A

The process that derives energy and raw materials from food stuffs to use to support REPAIR, GROWTH and ACTIVITY of the tissues of the body.

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1
Q

What is catabolic metabolism?

A
  • The break down of molecules to release energy.

- Reducing power

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2
Q

What’s anabolic metabolism?

A

The use of energy to make molecules for growth and repair.

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3
Q

What does exergonic mean?

A

Energy released > Energy used

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4
Q

What does endergonic mean?

A

Energy used > Energy released

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5
Q

What are the key components of the diet?

A
  • Protein
  • Carbohydrates
  • Fat
  • Water
  • Fibre
  • Vitamins and minerals
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6
Q

For the key components of the diet name what their roles are:
(Protein, carb, water, fibre, fat, nutrients and minerals)

A
  • energy and amino acids
  • energy
  • hydration
  • GI function
  • energy and fatty acids
  • essential
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7
Q

Name the essential nutrients and minerals.

A

Minerals: Na, K, Ca, Mg, Cu
Nutrients:
- A,K,D,E (fat soluble)
- B and C (water soluble)

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8
Q

The nutrients in the blood are taken to tissues for what uses?

A
  • Utilisation
  • Storage
  • inter-conversion
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9
Q

What materials do cells produce for the blood?

A

Clotting proteins

Waste products to excrete (e.g. Respiration)

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10
Q

Why may some products vary in concentration in the blood?

A
  • Variable usage depending on situation.

- Supply from nutrients vary

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11
Q

What are the nutrients and waste products in the blood plasma?

A
  • Glucose
  • Amino acids
  • Fatty acids
  • Triacylglycerides
  • Cholesterol
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12
Q

What are the factors affecting basal metabolic rate?

A 
Surface area
Gender
Environmental temp
Body temp (e.g. Fever)
Endocrine (thyroid/reproductive hormones)
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13
Q

Calculate the BMI of a 90kg person of height 6’1”

And what does it mean?

A

Mass/height^2
90/1.825^2 = 27
Which means he is overweight (27>25)

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14
Q

What are the co-morbidities associated with obesity?

A
  • Type 2 diabetes
  • hypertension
  • Cancer
  • Gall bladder disease
  • CVS disease
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15
Q

What are the potential problems with malnutrition?

A
  • Nutrient deficiency diseases
  • Low energy intake damage
  • Low protein levels: changes osmotic pressure of the blood.
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16
Q

How does a low protein intake effect the cardiovascular system?

A

Low protein means there’s a higher water potential inside the capillaries, so less water is absorbed back so oedemas form due to the excess water content of the interstitial fluid.

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17
Q

What is homeostasis?

A

The maintenance of the internal environment.

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18
Q

If homeostasis were to fail what would it lead to?

A

Disease

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19
Q

What are the products of catabolic metabolism?

A
  • Organic precursors (e.g. Acetyl CoA)
  • Building block materials
  • Biosynthetic reducing power (NADPH)
  • Energy for cell function
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20
Q

Energy is produced in metabolism, what is it used for?

A
  • Biosynthetic work (synthesis of cellular components)
  • Transport system across membranes
  • Specialised functions.
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21
Q

When a reaction has a delta G value < 0 it is said to be what 2 things?

A

Exergonic and spontaneous.

So the opposite is true…

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22
Q

Name the 3 main H carriers.

A

NAD
NADP
FAD

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23
Q

What are the carriers of reducing power for:

1) ATP synthesis
2) Biosynthesis

A

1) NADH

2) NADPH

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24
Q

Show the reaction of ATP hydrolysis and why does this provide a large amount of energy?

A

ATP —> ADP + Pi

The hydrolysis is a highly exergonic reaction

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25
Q

Why is ATP only a carrier of energy?

A
  • It is only stable enough to carry energy for a few seconds.
  • It is stable in the absence of specific catalysts.
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26
Q

Name the four high energy signals and what do they do?

A
  • ATP
  • NADH
  • NADPH
  • FAD2H
  • They activate the anabolic metabolism pathway.
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27
Q

When cells need a store of energy but still need it immediately, what is used? Outline the reaction.

A

Creatine phosphate (phosphocreatine)

        Creatine kinase Creatine  ----------> Phosphocreatine
          ATP --> ADP
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28
Q

How can Creatine kinase be a marker of MI?

A

Cells undergoing MI release more CK into the blood. So after a few hours the blood concentration of CK is high.

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29
Q

What is the general formula for carbohydrates?

And what types of groups are there?

A

(CH2O)n

Keto and aldehyde group.

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30
Q

Which type of isomer is present when it’s a natural protein?

A

D Isomer

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31
Q

Name two properties of carbohydrates.

A
  • Hydrophilic

- Partially oxidised (needs less oxygen to oxidise)

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32
Q

What is the significance of an enzyme with a beta bond?

A

It can’t be broken down by natural digestive enzymes.

Apart from lactose

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33
Q

Name 3 polysaccharides linked by glycosidic bonds:

A
  • Glycogen (Highly branched)
  • Cellulose (Can’t be digested as beta 1-4 bond can’t be broken)
  • Starch (Mix of amylose and amylopectin)
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34
Q

Name the two methods of absorption of monosaccharides.

A
  • Facilitated diffusion using transport proteins

- Active transport

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35
Q

What does the blood glucose concentration need to be maintained as?

A

~5mMol

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36
Q

Name 4 tissues that absolutely require glucose.

A

RBC, kidney medulla, WBC and lens of the eye.

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37
Q

What is glycolysis’ 3 main functions?

A
  • Oxidise glucose/NADP production
  • Synthesis of ATP
  • C6 and C3 intermediates
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38
Q

Name 3 features of glycolysis.

A
  • Exergonic
  • Oxidative
  • Anaerobic
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39
Q

Write the equation for glycolysis.

A

Glucose + 2Pi + 2ADP + 2NAD
—–>
2Pyruvate + 2ATP + 2NADH + 2H+ + 2H2O

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40
Q

Why is glycolysis made up of multiple, smaller steps?

A
  • Efficient energy conversion
  • Easier
  • Versatility
  • Controllable
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41
Q

What role does glycerol phosphate have in glycolysis?

A
  • Triacylglyceride and phospholipid biosynthesis.
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42
Q

How is glycolysis regulated?

A
  • Allosterically (catalytic and regulatory sites)

- Covalently ((de)phosphorylation)

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43
Q

What would happen if NAD isn’t regenerated from NADH during glycolysis?

A

Product inhibition.

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44
Q

Normally NAD is regenerated in stage 4 of glycolysis, however RBC don’t have this stage, so how do they regenerate NAD, show the equation:

A

Pyruvate + H+ + NADH —–> NAD + lactate

Via the enzyme LDH: lactate dehydrogenase

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45
Q

What 3 things does lactate concentration in the blood depend on?

A
  • Production
  • Utilisation (liver, heart, muscle)
  • Disposal (Kidneys)
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46
Q

When is lactate produced?

A
  • Strenuous exercise

- Psychological situations (shock/congestive heart disease)

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47
Q

How is lactate important?

A
  • Used in heart muscles
  • Gluconeogenesis
  • Impaired liver disease
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48
Q

What are the clinical conditions associated with fructose?

A
  • Fructosuria (Fructose can’t go to F-1-P, absence of fructokinase)
    No symptoms only high levels in urine
  • Fructose intolerance (No aldolase so accumulation of F-1-P)
    Liver damage, treatment = remove fructose from diet.
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49
Q

How does cataracts occur from galactosaemia?

A

Glucose —–> Galactitol
NADPH —> NADP
- So NADPH levels are depleted, structural damage occurs as s-s bonds form, forming cataracts.
Treatment: remove lactose from the diet.

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50
Q

Outline the two stages of the Pentose phosphate pathway.

A

1) oxidative decarboxylation
G-6-P —-> 5C sugar + CO2
NADPH –> NADP

2) Rearrangement to glycolytic intermediates
3,5C sugars —-> glyceraldehyde + 2fructose.

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51
Q

What are the features of the PPP?

A
  • No ATP production
  • Irreversible: loss of CO2
  • Controlled by NADPH/NADP ratio at G-6-P stage
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52
Q

What are the functions of the PPP?

A
  • NADPH production
    (Prevent S-S bonds forming & reducing power)
  • Produces 5C sugars
    (For nucleotides needed in nucleic acid)
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53
Q

How is G6PDH a problem?

A

Decrease is NADPH concentration so proteins are oxidised (s-s bonds form)
So the structure of the proteins change, causing their function to change.
So the PPP keeps proteins reduced.

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54
Q

Outline the reaction to form Acetyl CoA from Pyruvate.

And why is he reaction irreversible?

A

Pyruvate + CoA + NAD = Acetyl CoA + CO2 + NADH + H+

Loss of CO2

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55
Q

What is PDH sensitive to?

A

Vitamin B1 deficiencies.

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56
Q

What’s the TCA reaction equation and where does it occur?

A
  • Acetyl CoA + 3NAD + FAD + 2H2O + Pi + GDP
  • -> 2CO2 + 3NADH + FAD2H + GTP + CoA + 3H+
  • Mitochondria
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57
Q

How is the TCA cycle regulated?

A

Activated by ADP

Inhibited by NADH

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58
Q

What is electron transport?

A

Electrons on NADH and FAD2H are transported by a series of carrier molecules to oxygen.

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59
Q

What is oxidative phosphorylation?

A
  • Electrons transferred from NADH and FAD2H to molecular O2
  • Energy released is used to generate a proton gradient and so PMF
  • Energy from dissipation of PMF is used for the synthesis of ATP from ADP
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60
Q

What is PMF?

A

Proton motive force: the hydrogen concentration across the inner mitochondrial membrane.

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61
Q

What inhibits oxidative phosphorylation?

A

CO and CN, competitively with a high affinity

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62
Q

What’s an uncoupler?

A
  • Increases the permeability of the inner mitochondrial membrane to protons.
  • dissipates the H+ ions so the PMF reduces.
  • No drive for ATP synthesis.
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63
Q

Brown adipose tissue is found where and to what use?

A
  • Newborn infants, to maintain heat around the vital organs.

- Hibernating animals, to generate heat.

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64
Q

What’s the difference between oxidative and substrate phosphorylation?

A

Substrate: soluble enzymes, coupling by high energy hydrolysis, can work in limited O2.

Oxidative: needs membrane associated complexes, coupling by PMF, cannot work without O2.

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65
Q

What are the 4 classes of lipids?

A
  • Ketone bodies
  • Fatty acids
  • Triglycerides
  • Vitamins
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66
Q

Where does FA catabolism occur?

A

Mitochondria

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67
Q

How is FA synthesis activated?

What problem is there with that?

A

Linking to Acyl CoA

Acyl CoA molecule is with Acyl too large to cross membrane.

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68
Q

Name and outline the mechanism that allows for FA to cross inner mitochondrial membranes.

A
  • Carnitine shuttle.
  • Acyl CoA -> CoA which using CAT1 adds Acyl to carnitine.
  • Acyl carnitine can pass through the membrane. The reverse occurs on the other side of the membrane using CAT2.
  • Acyl group has passed through the membrane
  • FA is resynthesied inside the membrane.
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69
Q

Is more energy derived from FA oxidation or glucose oxidation?

A

FA oxidation

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70
Q

What are the three types of ketone bodies?

A
  • Acetoacetate
  • Acetone
  • B-Hydroxybuterate
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71
Q

Where are ketone bodies synthesised and under what chemical conditions?

A
  • Liver

- Low insulin to glucagon ratio (starvation/diabetes)

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72
Q

Fill in:
Acetyl CoA —> X —> W
Insulin (fed state)

Acetly CoA —> X —-> Y
Z (starvation)

A
  • X = HMG CoA
  • W = Cholesterol
  • Y = Ketone bodies
  • Z = Glucagon
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73
Q

What is the blood glucose value?

A

5mM

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74
Q

Why is glycogen a good way of storing glucose?

A
  • Large molecule, so efficient.

- Minimal osmotic effect

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75
Q

What are the 4 equations of glycogenesis?

A
  • Glucose + ATP —> G-6-P + ADP
    Hexokinase
  • G-6-P —–> G-1-P
    Phosphoglucomutase
  • G-1-P + UTP + H2O —> UDP-Glucose + 2Pi
  • Glycogen (n) + UDP-glucose —-> Glycogen (n+1) + UDP
    Glycogen synthase
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76
Q

When does glycogenolysis occur?

A
  • In the skeletal muscles in response to exercise

- In the liver in response to fasting or stress

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77
Q

Outline the 3 steps of glycogenolysis

A

Glycogen —> Glucose-1-P —-> Glucose-6-P —–> Glucose

             1) .                          2).                           3). 1) Glycogen phosphorylase 2) Phosphoglucomutase 3) Glucose-6-Phosphatase
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78
Q

What is 1) Glycogen synthesis regulated by?

2) Glycogen degradation regulated by?

A

1) Glycogen synthase

2) Glycogen phosphorylase

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79
Q

In glycogen regulation what occurs when there’s an excess/diminished amount of glycogen?

A
  • Excess = tissue damage

- Diminished = hypoglycaemia / poor exercise tolerance

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80
Q

What is Gluconeogenesis and where does it occur?

A
  • The production of glucose from non-carbohydrate precursors.
  • Liver & Kidney cortex
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81
Q

When does Gluconeogenesis occur?

A
  • Starvation/fasting
  • Prolonged exercise
  • Stress
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82
Q

What enzymes stimulate/inhibit Gluconeogenesis?

A

Stimulate: High levels of PEPCK and fructose 1,3 bisphosphatase

Inhibit: Low levels of PEPCK and fructose 1,3 bisphosphatase

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83
Q

What is needed in FA synthesis?

Where does is occur?

A
  • NADPH
  • ATP
  • Cytoplasm
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84
Q

How is Acetyl CoA transported into the cytoplasm?

A

Acetyl CoA + oxaloacetate = citrate
Citrate can be transported into the cytoplasm
Citrate -> Acetyl CoA + oxaloacetate

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85
Q

What is the overall equation for lipogenesis?

A

Acetyl CoA + 7ATP + 14NADPH + 6H+ ——-> Triglyceride + 7ADP + 14NADP + 6H2O + 8CoA + 7Pi

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86
Q

For lipogenesis what is the multi-enzyme complex used?

A

Fatty acid synthase

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87
Q

What is the difference between FA oxidation and FA synthesis?

A

Oxidation: mitochondrial, glucagon and adrenaline stimulate, insulin inhibits.

Synthesis: Cytoplasm, glucagon and adrenaline inhibits, insulin stimulates.

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88
Q

What regulates lipolysis?

A
  • Adrenaline and glucagon activates

- Insulin inhibits

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89
Q

When would a positive N balance occur?

A
  • Pregnancy

- Growth

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90
Q

When would a negative N balance occur?

A
  • Tissue wasting disease

- Starvation

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91
Q

What are the 8 essential amino acids?

A
  • Lysine
  • Isoleucine
  • Leucine
  • Threonine
  • Valine
  • Tryptophan
  • Phenylalanine
  • Methionine
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92
Q

Why is -NH2 removed from amino acids?

And by what two processes?

A
  • Potentially toxic
  • Transamination
  • Deamination
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93
Q

What are the 2 possible reactions for Transamination?

A

Alpha ketogluterate + amino acid —> glutamate + Keto acid

Oxaloacetate + amino acid —> aspartate + Keto acid

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94
Q

What are ALT and AST and what do they do?

A

ALT alanine amino transferase (alanine -> glutamate)

AST aspartate amino transferase (glutamate -> aspartate)

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95
Q

How is the NH3 group disposed of?

A
  • Urea

- Glutamine

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96
Q

Name 6 characteristics of urea

A
  • Non toxic
  • Inert
  • Excreted mainly in urine
  • High N content
  • Very water soluble
  • Useful osmotic effect in kidney tubules
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97
Q

Where does the urea cycle occur and how many enzymes does it involve?

A
  • Liver

- 5

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98
Q

What do partial losses in urea related enzymes lead to?

A
  • Hyperammonaemia
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99
Q

What clinical signs are there for urea defects?

A
  • Vomiting
  • Lethargy
  • Irritability
  • Mental retardation
  • Coma
  • Seizures
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100
Q

How are urea defects treated?

A
  • Low protein diet

- amino acids replaced by Keto acids

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101
Q

In which 3 ways is ammonia toxic to cells?

A
  • pH effects.
  • Reduces TCA cycle, so less energy supply to cells.
  • Neurotransmitter synthesis in CNS.
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102
Q

What is the normal level of NH4+?

A

20-40 micro moles.

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103
Q

How is NH3 used during detoxification?

A
  • Synthesising Glutamine

- Then excreted directly or converted to urea.

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104
Q

How is Glutamine synthesised?

A
  • Glutamate + ammonia –> Glutamine (ATP required)
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105
Q

What is phenylketonuria?

A
  • Autosomal recessive genetic disorder
  • disfunction of phenylalanine hydroxylase prevents Tyrosine production and so Noradrenaline/adrenaline/dopamine
  • So more phenylpyruvate produced instead.
  • So excess in urine.
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106
Q

What is homocystinuria?

A
  • Autosomal recessive
  • Fibrillin-1’s protein structure affected
  • No/reduced CBS, so less cystathionine and so cystine produced.
  • More methionine with a B12 catalyst produced.
  • Elevated plasma homocysteine associated with CV disease
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107
Q

What and how are Arginine and Cystine affected by gas signalling molecules?

A
  • Arginine: NO, vasodilator, neurotransmitter, inflammatory mediator
  • Cysteine: H2S, ^,^,^.
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108
Q

What are the 5 different classes of lipids?

A
  • Triacylglycerides
  • Fatty acids
  • Cholesterol
  • Cholesterol esters
  • Phospholipids
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109
Q

What role does cholesterol have in the body?

A
  • Major component of membranes

- Precursors to steroid hormones and bile acids

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110
Q

How is cholesterol made?

A
  • Synthesised in the liver

- Found in diet

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111
Q

What are phospholipids and what role do they play?

A
  • Diacylglycerol with a phosphate group.
  • Major component of membrane
  • Phospholipid bilayer.
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112
Q

How are lipids transported in the bloodstream?

A
  • Proteins: albumin/lipoprotein particles

- Micelles (hydrophilic outer layer with apoproteins and a hydrophobic centre)

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113
Q

Why do different classes of lipids have to have specific apoproteins?

A
  • Function: Activation of enzymes, recognition of cell surface receptors
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114
Q

What are the different classes of lipoprotein particles?

A
  • Chylomicrons
  • VLDL
  • LDL
  • HDL
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115
Q

How are Chylomicrons formed and where?

A
  • By enterocytes lining the intestine.
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116
Q

What are the roles of chylomicrons?

A
  • Reformation of triacylglycerides from food with specific apoproteins
  • Carries lipids from the diet to tissues (especially adipose)
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117
Q

When are chylomicrons found?

A
  • 4-6 hours after a meal
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118
Q

What does VLDL, LDL and HDL stand for?

A
  • VLDL: Very low density lipoproteins
  • LDL : Low density lipoproteins
  • HDL: High density lipoproteins
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119
Q

Where are VLDLs produced and what is its role?

A
  • Liver
  • Storage of energy by combining apoproteins and triacylglycerides.
  • Transport lipids from the liver to tissues when needed.
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120
Q

What is the role of LDLs

A

Transport liver cholesterol and apoproteins to tissues.

121
Q

Why is having a high level of LDLs dangerous to your health?

A
  • Cholesterol rich

- Increases the risk of atherosclerosis.

122
Q

Where are HDLs formed, how and what do they do?

A
  • Formed in tissues
  • Cholesterol from tissues + apoproteins
  • Carries excess cholesterol from tissues to liver.
123
Q

How are triacylglycerides transferred from chylomicrons to VLDL?

A
  • Chylomicrons and VLDL bind
  • Lipase from endothelial cells of capillaries cleaves triglycerides into glycerol (remains in circulation) and FA (goes to tissues for metabolism)
124
Q

After the transfer of triacylglycerides from chylomicrons to VLDL what happens to the VLDL remnants?

A
  • Removed by liver/converted to other types of lipoproteins.
125
Q

How does the transfer of cholesterol from LDLs occur?

A
  • LDL receptors on cells
  • Complex proteins bind to LDL and taken into cells by endocytosis
  • Cholesterol ester released and LDL cleaved into cholesterol and FA
  • Uptake stimulated by need
126
Q

How are HDLs formed?

A
  • Nascent HDL (HDL shells) are synthesised
  • Sources from VLDL remnants and cholesterol in capillaries
  • Mature into HDL particles.
127
Q

Why may Hyperlipoproteinanaemia occur?

A
  • Defective enzymes
  • Defective receptors
  • Defective apoproteins
128
Q

What is Hyperlipoproteinanaemia?

A
  • Raised levels of one or more lipoprotein classes.

- Caused by over production/under removal.

129
Q

How does an atheroma form?

A
  • Oxidation of LDLs -> macrophages produced -> Foam cells -> accumulation in interior of b.v walls -> Fatty streak -> Atheroma
130
Q

What are the treatments for Hyperlipoproteinanaemia?

A
  • Reduce cholesterol and saturated lipids in the diet
  • Increase exercise
  • Stop smoking
  • Statins
131
Q

What do statins do?

A
  • Reduce cholesterol synthesis by inhibition of HMG CoA reductase
  • Increases expression of LDL receptors in hepatocytes
132
Q

What does ROS stand for?

A
  • Reactive oxygen species
133
Q

How are SOR converted into harmless substances?

A

SOR —-> H2O2 —-> H2O + O2

SOD. Catalase

134
Q

How are hydroxyradicals produced?

A
  • UV
  • X-Rays
  • Gamma radiation
  • Are all very damaging to cell membranes, can’t be eliminate by an enzyme system
135
Q

What are the cellular defences against NO?

A
  • Glutathione (GSH) SH groups are an antioxidant.

- Oxidise form has S-S bonds, glutathione disulphide.

136
Q

How is NADPH a cellular defence?

A

Is an oxidising agent. NADPH —> NADP

Works against OH radicals

137
Q

Give examples of antioxidants.

A
  • Vitamin C, E, and A
  • Flavenoids: polyphenols, beta carotine
  • Minerals: selenium, zinc
138
Q

What is oxidative stress?

What can it cause?

A
  • When the antioxidants are lower than the ROS so they are free to damage cells and interfere with DNA, lipids in cell membranes and proteins.
  • Can cause cancer, emphysema, pancreatitis and CV disease.
139
Q

Oxidative stress can lead to lipid peroxidation, what is this?

A
  • ROS reacts with unsaturated lipids to form lipid peroxides
  • Damages cell membranes
140
Q

What is an oxidative burst and how can it be useful?

A
  • Rapid release of superoxide and H2O2 from leukocytes

- Rapid production of ROS kills pathogens in the locality.

141
Q

What is pharmacology? And how is is split?

A
  • ‘The study of how chemical agents affect the function of living systems’
  • Pharmacokinetics
  • Pharmacodynamics
142
Q

What is pharmacodynamics?

A
  • What the drug does to the body
143
Q

What is pharmacokinetics?

What are the stages?

A

The study of the time course of drugs and their metabolites in the body.

  • Absorption
  • Distribution
  • Metabolism
  • Elimination
144
Q

Why is the property of being lipid soluble in drugs a problem?

A
  • Lipid soluble (not water soluble) can’t be excreted by the kidney as they are easily re absorbed into the blood.
145
Q

How does drug metabolism help with excretion of drugs?

A
  • Turns parent drug molecule into a polar, lipid-insoluble, water soluble derivative. (Metabolites)
146
Q

What are the two main roles if drug metabolism?

A
  • Deactivation

- Elimination

147
Q

What happen in Phase 1 of drug metabolism?

A
  • Oxidation, reduction, hydrolysis

- Adds/exposes reactive group.

148
Q

What are the main sites of Phase 1 drug metabolism?

A
  • Liver

- Microsome situated on ER in hepatocytes.

149
Q

What’s the main role for Phase 2 metabolism?

A
  • Conjugation (altered drug molecules combined with a water soluble group.
150
Q

What is the enzyme system used for drug metabolism pathways?

A
  • CYP (Cytochrome P450)
151
Q

For Phase 2 of drug metabolism what are the main sites and what reactions occur there?

A
  • Liver, cytosolic enzymes

- Glucuronidation, sulphate conjugation, glutathione conjugation

152
Q

What is Glucuronidation?

A

Glucuronic acid + UDP —> UDPGA

UDP Glucuronic acid

153
Q

What is polymorphism?

A
  • The individual variation that causes drugs to affect people differently.
154
Q

What is pharmacoepidemiology?

A
  • The study of drug effects in large populations
155
Q

What is pharmacovigilance?

A
  • The reporting of adverse drug reactions post-marketing.
156
Q

What environmental factors have an effect on drug metabolism?

A
  • Enzyme inhibition

- Enzyme induction: metabolism of on agent induces enzymes in the liver which increases the metabolism of other drugs.

157
Q

What occurs to the Phase 2 pathway when a toxic dose of paracetamol has been taken?

A
  • It becomes saturated
158
Q

What happens to the Phase 1 pathway when a toxic dose of Paracetamol has been taken?

A
  • It produces NAPQ1 from the paracetamol which then undergoes phase 2 metabolism = glutathione conjugation
159
Q

What is the treatment for an overdose of paracetamol?

A
  • N Acetyl cysteine (antioxidant)
160
Q

What is the role of alcohol dehydrogenase?

A
  • Converts alcohol to acetaldehyde (toxic metabolite)
  • Ethanol ——> acetaldehyde
    NAD —> NADH + H+
161
Q

What are the recommended alcohol units for men and women?

A
  • Men 21 units (4 units over 5 days)

- Women 14 units (3 over 5 days)

162
Q

What are the effects of chronic alcohol toxicity?

A
  • Excess NADH simulates fat deposition
  • Acetaldehyde damages liver cells —> ‘fatty liver’
  • Alcoholic hepatitis and cirrhosis
163
Q

What is the treatment for chronic alcohol toxicity?

A
  • Disulfiram (aldehyde dehydrogenase inhibitor)
164
Q

What are the different types of communication in control systems?

A
  • Nervous (action potential)
  • Endocrine (hormones)
  • Paracrine (local hormones)
  • Autocrine (many agents)
165
Q

Outline the receptor - effector loop.

A

Stimulus -> Sensor -> Signal AFFERENT pathway -> Control centre -> Signal EFFERENT pathway -> Effector

166
Q

What is a negative feedback loop? And where is it found?

A
  • Effector opposes stimulus

- Most hormonal control systems

167
Q

What is a positive feedback loop and where are they found?

A
  • Stimulus produces an increase in effect
  • ‘Catastrophic change’
  • Ovulation
168
Q

How does the biological clock work?

A
  • Suprachiasmatic nucleus in hypothalamus

- Melatonin is released from pineal gland in the light/dark cycle.

169
Q

What are the total body water percentages in an adult male and female?

A
  • Male 50-60%

- Female 45-50%

170
Q

How many litres of water are there in a 70kg male?
And how many litres of water are there in:
- Intracellular fluid
- Extracellular fluid
- Blood plasma

A
  • 42 Litres
  • 28 Litres
  • 9.4 Litres
  • 4.6 Litres
171
Q

How is the water concentration in the blood plasma maintained?

A
  • Increase in osmolality of blood plasma —> release of anti diuretic hormone (ADH) from posterior pituitary gland —> Increase in Reabsorption of H2O from urine into blood in collecting ducts in the kidney —> Decreased osmolality of blood plasma.
172
Q

How is osmolality and Na+ concentrations monitored?

A
  • Osmoreceptors in hypothalamus
173
Q

Why do endocrine hormones only affect certain cells?

A

The hormones only interact with cells with receptors?

174
Q

How are endocrine hormones released?

A
  • Hypothalamus produces releasing factors
  • Stimulates the anterior pituitary gland (mast gland) to release trophic hormones
  • Endocrine glands are stimulated by the trophic hormones
175
Q

What does HPA stand for in HPA axis?

A
  • Hypothalamic pituitary adrenal.
176
Q

Outline the HPA axis.

A
  • Hypothalamus produces carticotrophin releasing hormone
  • Anterior pituitary detects, releases ACTH (adrenocarticotrophic hormone) via the blood
  • Adrenal cortex detects, releases Cortisol
177
Q

How are hormone secretions controlled?

A
  • By other hormones or itself.
178
Q

What type of hormones are water soluble and which are not?Z

A
  • Water soluble: Peptide and amine

- Not water soluble: steroid and thyroid

179
Q

How are non water soluble hormones transported in the blood?

A
  • Carrier proteins
  • Increase solubility of hormone in plasma
  • Increase in half life
  • Readily accessible reserve
180
Q

When are hormones biologically active?

A
  • When in the free form.
181
Q

What are the different classes of hormones?

A
  • Polypeptide
  • Glycoproteins
  • Amino acid derivatives
  • Steroid hormones
182
Q

Give examples of polypeptide hormones.

A
  • It’s the largest group (20)
  • Growth hormone
  • Insulin
183
Q

Give examples of glycoprotein hormones.

A
  • Thyroid stimulating hormone
  • LH
  • FSH
  • Human chorionic gonadotrophin
184
Q

Examples of amino acid derivatives.

A
  • Tyrosine
  • Thyroid hormones, T4 & T3
  • Adrenaline
  • Histamine from histidine
  • 5-hydroxytryptamine (5-HT) from tryptophan
185
Q

Give examples of steroid hormones and what are they derived from?

A
  • Derived from Cholesterol
  • C27- calciterols
  • C21- corticosteroids
  • C19- Androgens
  • C18- Oestrogen
186
Q

How do hormones act?

A
  • By binding to receptors on/in target cells
187
Q

What does the magnitude of hormone effect depend on?

A
  • Concentration of active hormone
  • Receptor number
  • Affinity of hormone for receptor
  • Degree of signal amplification
188
Q

How does a hormone effect a target cell if it can’t cross the cell membrane?

A
  • Binds to receptor on cell surface
  • Activates 2nd messenger pathway
  • 2nd internal messenger exerts metabolic effects.
189
Q

How can steroid hormones cross cell membranes?

A
  • Lipid soluble (cholesterol derivatives)
190
Q

What part of the hypothalamus controls appetite?

A
  • Appetite/Satiety centre (arcuate nucleus)
191
Q

In the arcuate nucleus what are the roles of the primary and secondary neurones?

A
  • Primary: sense glucose, FA in blood, response to hormones

- Secondary: synthesise input, co-ordinate a response

192
Q

How come primary neurones are able to detect hormones?

A
  • No blood brain barrier.
193
Q

Outline the excitatory pathway from primary neurones for appetite.

A
  • NPY, Neuropeptide Y
  • AgRP, Agouti-related peptide
  • These stimulate appetite.
194
Q

Outline the inhibitory pathway for appetite.

A
  • Pro-opiomelanocortin (POMC)
  • Beta-endorphin leads to a reward system when full.
  • Alpha-melanocyte stimulating hormone. (@-MSH) suppresses appetite.
195
Q

What hormones feedback to the hypothalamus from the gut and what do they do?

A
  • Ghrelin: peptide released from wall of stomach when empty.
    stimulates excitatory neurones in arcuate nucleus
    Filling stomach inhibits Ghrelin
  • PYY: peptide hormone released from wall of small intestine.
    suppresses appetite
196
Q

What hormones are responsible for feedback from the body to the hypothalamus, for appetite?

A
  • Leptin: released from adipocytes
    stimulates inhibitory neurones in arcuate nucleus
    suppresses appetite
    induces expression of uncoupling proteins in mitochondria.
  • Insulin: surprises appetite (same as above, not as important)
  • Amylin: peptide hormone
    secreted from beta cells in pancreas, surpresses appetite
197
Q

What is metabolic syndrome?

A
  • Insulin resistance
  • Dyslipidaemia
  • Impaired glucose tolerance
  • Hypertension
  • 12-25% affected in developed countries.
198
Q

What is foetal programming?

A
  • Foetus adapts to conditions in utero e.g supply of nutrients.
  • Biochemical adaptions become ‘programmed’ in pre-disposing to adult disease conditions.
199
Q

What is epigenetics?

A
  • Inherited phenotype resulting from changes in chromosomes without changes in DNA sequence.
200
Q

Outline some characteristics of Type 1 diabetes and who it commonly affects

A
  • Insulin deficiency
  • Can be autoimmune or non-autoimmune
  • Destruction of beta cells.
  • Younger people (less than 30yrs)
201
Q

Outline some characteristics of Type 2 diabetes and who it commonly effects.

A
  • Insulin deficiency and resistance

- Obese people who are older (normally)

202
Q

What are the common symptoms of diabetes mellitus?

A
  • Polyuria (high glucose conc in urine, needing to go all the time as glucose has an osmotic effect)
  • Polydipsia (thirsty all the time)
  • Blurring of vision
  • Urogenital infections (thrush)
  • Inadequate energy utilisation (tiredness, weakness, lethargy, weight loss)
203
Q

What does the severity of the diabetes depend on?

A
  • Rate of rise of blood glucose

- Absolute levels of glucose.

204
Q

Name 4 types of diabetes diagnosis test and their criteria

A
  • 1) Fasting venous plasma glucose: (>7mmol/l)
  • 2) Random ^ : (>11.1mmol/l)
  • 3) HbA1c: (>6.5%)
  • 4) Oral glucose tolerance test (1&or 2)
205
Q

What are the specific symptoms typical of type 1 diabetes?

A
  • Rapid onset: weight loss, Polyuria, Polydipsia
  • Late presentation: vomiting due to ketoacidosis (only found in type 1)
  • Too late: coma/death
206
Q

What is the diagnostic tool to detect the presence of ketones?

A
  • ketostik

- ketones present signifies absolute lack of insulin.

207
Q

What is the treatment of type 1 diabetes?

A
  • Subcutaneous injection several times per day.
208
Q

What are the specific symptoms of type 2 diabetes?

A
  • Absence of ketones in urine (means not type 1)

- Elevated venous plasma glucose

209
Q

What are the acute complications of diabetes?

A
  • Hyperglycaemia: diabetic ketoacidosis in type 1
    hyperosmolar non-ketotic syndrome in type 2
  • Hypoglycaemia: Coma
    brain needs glucose
210
Q

What are the chronic complications of diabetes?

A
  • Macrovascular: stroke, heart attack, intermittent claudication, gangrene (cerebrovascular, cardiovascular, peripheral vascular disease)
  • Microvascular: Blindness, renal replacement therapy, erectile dysfunction, foot ulceration, diarrhoea, constipation, painful peripheral neuropathy. (Retinopathy, nephroopathy, neuropathy)
211
Q

What are the two main functions of the pancreas?

A
  • Production of digestive enzymes, secreted into duodenum (exocrine)
  • Hormone production (Islet of Langerhans)
212
Q

Where are Insulin and Glucagon secreted from?

A
  • Insulin = beta cells

- Glucagon = alpha cells

213
Q

How does blood glucose concentrations in the blood change in the presence of : a) Insulin?
b) Glucagon?

A
  • Insulin decreases by fat cells taking in glucose from the blood
  • Glucagon increases by liver releasing glucose into the blood
214
Q

What is the signal, target tissue and action of Insulin?

A
  • Feeding
  • Adipose, skeletal, liver
  • Anabolic
215
Q

What is the signal, target tissue and action of glucagon?

A
  • Fasting
  • Liver, adipose
  • Catabolic
216
Q

What conditions can increase/decrease the renal threshold for glucosuria?

A
  • Pregnancy decreases

- Being elderly increases

217
Q

Give 4 properties of Insulin.

A
  • Glycogenic
  • Anti-gluconeogentic
  • Anti-lipolitic
  • Anti- ketotonic
  • Favours storage
218
Q

Outline how insulin is synthesised.

A
  • Insulin mRNA translates to preproinsulin as a precursor.
  • Insert into ER -> pro insulin
  • Exposed to several specific endopeptidases -> mature insulin (C peptide is excised)
  • Insulin and free C peptide are packaged -> Golgi -> secretory granules.
  • Accumulates in cytoplasm
  • Margination - granules move to cell surface
  • Exocytosis
219
Q

How is insulin secreted from beta cells?

A
  • Stimulus = increase in glucose levels
  • Glucose -> beta cells by facilitated diffusion via GLUT 2
  • Increase in glucose conc in ECF = Increase in beta cells
  • Depolarisation of membrane - influx of Ca
  • This triggers Exocytosis of insulin-containing secretary granules
220
Q

What does Insulin do in the liver, muscles and adipose tissues?

A
  • Increase in glucose uptake into target cells & glycogen synthesis
  • In the liver it stimulates glycogen formation and inhibits breakdown of AA
  • In muscles it stimulates uptake of AA promoting protein synthesis
  • In adipose tissues it stimulates storage of triglycerides
  • Inhibits breakdown of FA
221
Q

Outline the structure of an Insulin receptor.

A
  • Alpha chain on exterior

- Beta chain spans cell membrane in single segment.

222
Q

Outline how the insulin receptor is activated.

A
  • Alpha chains move together when insulin is detected and folds around insulin- moves beta chains together
  • Beta chains form on active tyrosine kinase
  • Initiates a phosphorylation cascade resulting in an increase in GLUT 4 expression
  • Result - cells can take up more glucose.
223
Q

What are the 5 effects of glucagon?

A
  • Increases Gluconeogenesis (glucose from AA)
  • Increases glycogenolysis
  • Increases lipolysis to increase FA in the blood
  • Overall increase in glucose in blood plasma
  • Ketogenesis
224
Q

What are the hormones that are produced by the pituitary gland?

A
  • TSH (thyrotrophs)
  • ACTH (corticotrophs)
  • GH (somatrophs)
  • LH and FSH (gonadotrophs)
  • Prolactin (lactotrophs)
225
Q

What hormones does the adrenal gland cortex produce and give examples.

A
  • Mineralocorticoids, aldosterone
  • Glucocorticoids, cortisol & corticosteroid
  • Androgens, dehydroepiandrosterone
226
Q

What hormone does the adrenal medulla produce?

A
  • Adrenaline
227
Q

Outline the structure of the adrenal cortex?

A
  • Zona glomerulosa
  • Zona fasciculata
  • Zona reticularis
228
Q

What does each section of the adrenal cortex produce and its role?

A
  • Zona glomerulosa: mineralocorticoid, regulate Na and K production
  • Zona fasciculata: glucocorticoids, regulation of carb metabolism
  • Zona reticularis: glucocorticoids and androgens
229
Q

How are steroid hormones produced? Give a key characteristic.

A
  • Synthesised from cholesterol via progesterone.

- Lipophilic

230
Q

How is cortisol secretion controlled?

A
  • ACTH from corticoids from anterior pituitary

- ACTH controlled by CRF in response to physical, chemical and emotional stressors.

231
Q

How do ACTH levels fluctuate during the day?

A
  • Highest in early hours and decreases throughout the day.
232
Q

How does ATCH result in cholesterol esterase production?

A
  • Interacts with high affinity to receptors on Zona fasciculata and reticularis.
233
Q

What are the results of over secretion of ACTH?

A
  • Increased pigmentation due to partial MSH activity
  • Adrenal hyperplasia
  • Over production of cortisol
234
Q

How is cortisol transported in the blood stream?

A
  • Via plasma proteins as it’s Lipophilic
235
Q

How does cortisol act?

A
  • Crosses plasma membrane of target cell and binds to cytoplasmic receptors
  • Hormone/receptor complex enters nucleus to interact with specific DNA regions
  • Changes rate of transcription of specific genes.
236
Q

What does cortisol cause in response to stress?

A
  • Decreased amino acid uptake, decreased protein synthesis and increased proteolysis in most tissues (not liver)
  • Increased hepatic Gluconeogenesis and glycogenolysis
  • Increased lipolysis in adipose tissue
  • Decreased peripheral uptake of glucose
237
Q

What neurotransmitters does the adrenal medulla produce?

A
  • Noradrenaline

- Dopamine

238
Q

Outline catecholamine synthesis.

A
  • Tyrosine -> dopamine -> noradrenaline -> adrenaline
239
Q

What effects does adrenaline have on the body?

A
  • Increased cardiac output and blood supply to muscle
  • Increased mental alertness
  • Increased glycogenolysis in liver and muscle
  • Increased lipolysis in adipose tissues
240
Q

What effects are there if there’s an over secretion of adrenaline?

A
  • Hypertension
  • Anxiety
  • Palpitations
  • Pallor
  • Sweating
  • Glucose intolerance
  • All due to a tumour.
241
Q

Hypoactivity of the adrenal cortex can be due to what, and what is this also known as?

A
  • Addison’s disease
  • Autoimmune destruction of cortex reduces glucocortoids and mineralcorticodis.
  • Disorders of pituitary/hypothalamus = decrease in ACTH/CRF
242
Q

How does hyperactivity of adrenal cortex occur? And what are the effects?

A
  • Increased secretions of glucocorticoids (Cushing’s syndrome)
  • Increased activity due to adenoma (tumour)
  • Disorders in secretion of ACTH caused by pituitary adenoma or ectopic secretion of ACTH.
243
Q

What is congenital adrenal hyperplasia?

A
  • Genetic defect in enzymes needed for cortisol synthesis
  • No feedback to pituitary = no control, ACTH continues to be produced
  • Increased ACTH means increase of size of adrenal cortex
244
Q

What are the signs and symptoms of excess cortisol?

A
  • Increased muscle proteolysis and hepatic gluconeogenesis => hyperglycaemia with polyuria and polydipsia (steroid diabetes)
  • Thin arms and legs due to muscle wasting
  • Increased lipogenesis in adipose tissues and deposition of fat in abdomen, neck and face hence MOONFACE and weight gain
  • Purple striae on lower abdomen, upper arms and thighs
  • Easily bruised due to thinness of skin
  • Acne and bacterial infection susceptibility increase due to immunosuppression
  • Osteoporosis
  • Hypertension
245
Q

What are the signs and symptoms of too little cortisol?

A
  • Addison’s
  • Tiredness, extreme muscle weakness, anorexia, vague abdominal pain, weight loss and dissiness
  • Increased pigmentation at points of friction, buccaneer mucosa, scars and palmor creases due to ACTH mediated melanocyte stimulation
  • Decreased bp. due to Na and fluid depletion
  • Hypoglycaemic episodes on fasting
246
Q

When can a crisis occur? And what are the results?

A
  • Stress/trauma/severe infection

- Nausea, vomiting, extreme dehydration, hypotension, confusion, fever, coma

247
Q

What are the tests for adrenocarticol function?

A
  • 24 hour cortisol free urine
  • DST low dose
  • ACTH stimulation tests
  • Plasma cortisol levels
248
Q

What can over secretion of aldosterone cause?

A
  • Hypertension and muscle weakness
  • Increase Na+ reabsorption in kidney in exchange for K+
  • Too much exchanges so no K+
249
Q

What are the consequences of over-secretion of adrenal androgens?

A
  • Increased hair growth
  • Increased muscle bulk
  • Deepening of voice
  • Broadening of shoulders.
250
Q

Where is the thyroid gland found?

A
  • Base of neck
  • Wraps around trachea below cricoid cartilage
  • 2 lobes connected by isthmus
251
Q

What is an enlarged thyroid called?

252
Q

How is thyroid secretion increased?

A
  • Nervous impulse from the sympathetic NS
253
Q

What are the cells that make up the thyroid gland and their structure?

A
  • Colloid cells
  • Surrounded by string of epithelium to form follicles
  • Darker cells surrounding colloid are C cells
254
Q

What do c cells produce?

A
  • Calcitonin
255
Q

How are thyroid hormones synthesised?

A
  • From tyrosine residues.
256
Q

How are T3 and T4 secretions regulated?

A
  • By Thyroid stimulating hormone from pituitary
  • TSH is regulated by TRH (thyrotropin releasing hormone) from hypothalamus
  • T3 and T4 cause negative feedback to control levels of TSH and TRH.
257
Q

What does T3 and T4 stand for?

A
  • T3: Tri-iodothyronine

- T4: Tetra-iodothyronine

258
Q

What are the chronic affects that TSH has on the thyroid?

A
  • Simulates growth and division of follicle cells

- Gland enlarges to form goitre

259
Q

What are the acute effects TSH has on the thyroid?

A
  • Stimulates storage, synthesis and secretion of T3 and T4
260
Q

What are the differences between T3 and T4?

A
  • T3: more potent, shorter half life, less produced

- T4: less potent, longer half life, more produced

261
Q

How can T4 be converted into T3?

A
  • Deiodination
262
Q

How are T3 and T4 synthesised?

A
  • Needs iodine from diet
  • Follicular cells concentrate iodine using an iodine trap
  • Iodine is activated by peroxidase enzyme
  • Reactive iodine associates with thyroglobulin
  • Protein containing the iodothyronines are stood red as colloid in follicular cells.
263
Q

Why is T4 used to treat hypothyroidism?

A
  • Easier to maintain constant blood conc.
264
Q

What are the standard amounts of free T3 and T4 in the blood?

A
  • T3: ~8 pmol/l

- T4: ~20 pmol/l

265
Q

What are the effects of thyroid hormones?

A
  • Increased basal metabolic rate (Increase: no. and size of mitochondria, O2 consumption, Nutrient utilisation)
  • Stimulates metabolic pathways (catabolic>anabolic)
  • Promotes growth and development of tissues
  • Increases responsiveness of tissues to SNS (noradrenaline), metabolic and reproductive hormones
266
Q

What effects do thyroid hormones have on the NS?

A
  • Increased myelination of nerve fibres and neurone development
  • Increased speed of reflexes
  • Increased mental activity
267
Q

What effect do thyroid hormones have on the CVS?

A
  • Increased cardiac output
268
Q

What effect do thyroid hormones have on the skin and subcutaneous tissue?

A
  • Increased turnover of proteins and glycoproteins
269
Q

What can hypothyroidism cause?

A
  • Cretinism in new borns
  • Severe muscle retardation (CNS development)
  • Coarse features and protruding tongue
  • Diminished liver growth
  • Delayed sexual development.
270
Q

What are the effects of hyperthyroidism?

A
  • Increased BMR and catabolic activity
  • Increased sympathetic and CNS activity
  • Reach mental peak earlier in life
271
Q

What are the signs and symptoms of hyperthyroidism?

A
  • Heat intolerance, increased perspiration, warm, moist hands
  • Weight loss
  • Tachycardia (often irregular) increased cardiac output
  • Increased bowel movement and appetite
  • Nervousness, irritability, emotional lability
  • Exphthalmus (bulging eyes)
  • Hyper reflexive
272
Q

What can be the cause of hyperthyroidism?

A
  • Grave’s disease

- Autoimmune: production of antibodies that stimulate TSH receptor on follicle cells

273
Q

Give some treatments for hyperthyroidism.

A
  • Radioactive I2 destroys thyroid and leads to hypothyroidism
  • Surgery, risky as easy to remove the parathyroid too
  • Carbimazol inhibits iodine incorporation into thyroglobulin.
274
Q

What are the signs and symptoms of hypothyroidism?

A
  • Cold intolerance, decreased perspiration
  • Mild weight gain
  • Decreased cardiac output
  • Mood swings
  • Poor concentration
  • Oedema and dry, firm, waxy swelling of the skin.
  • Brittle nails, hair loss, dry skin.
275
Q

What are the causes of hypothyroidism?

A
  • Hashimoto’s
  • Autoimmune destruction of thyroid follicles
  • Production of antibody blocking TSH receptor on follicle cells
  • Treat with T4
276
Q

What is the normal level of free calcium in the body and where is it stored?

A
  • 1-1.3mM

- Skeleton

277
Q

How much calcium is needed to be taken in daily to maintain levels?

A
  • 500-1500mg
278
Q

Where is calcium taken up and secreted?

A
  • Taken up: Duodenum and jejunum

- Secreted: Gut rich in calcium

279
Q

What is bone’s priority?

A
  • Maintaining serum calcium levels
280
Q

Where in the bone is calcium found?

A
  • In collagen fibrils as calcium phosphate crystals
281
Q

Outline briefly bone metabolism.

A
  • Bone deposition: osteoblasts, produce collagen matrix, mineralised (by hydroxyopetite)
  • Bone reabsorption: osteoclasts, acid breaks down bone.
282
Q

What form of calcium can be reabsorbed?

283
Q

What are the signs and symptoms of hypocalcaemia?

A
  • Hyper-excitability of NMS
  • Pins and needles
  • Tetany (muscle spasms)
  • Paralysis
  • Convulsions
284
Q

What are the signs and symptoms of chronic hypercalcaemia?

A
  • Renal calculi (stones)
  • Kidney damage
  • Constipation
  • Dehydration
  • Tiredness
  • Depression
285
Q

How are calcium levels increased?

A
  • Parathyroid hormone (PTH)

- Vitamin D

286
Q

How is PTH synthesis regulated?

A
  • Low serum calcium up-regulates gene transcription.
  • High serum calcium down-regulates
  • T½ = 4mins
287
Q

Why is PTH continually synthesised?

A
  • There’s little store of it.
  • Chief cells degrade and synthesise PTH
  • Cleavage of PTH in chief cells is accelerated by high serum calcium levels
  • Released PTH is cleaved in the liver.
288
Q

How is secretion of PTH regulated?

A
  • Plasma conc of calcium decreases => increased PTH

- Plasma conc of calcium increased => decreased PTH

289
Q

What is the effect of PTH on bone?

A
  • PTH induces osteoblastic cells to synthesise and secrete cytokines
  • Cytokines protect osteoclasts from apoptosis
  • PTH causes a decrease in osteoblasts
  • Reabsorption of mineralised bone and release of Pi and Ca into ECF
290
Q

What are the effects of PTH on the kidneys?

A
  • Affects tubular cells in kidneys
  • PTH increased calcium reabsorption in DCT reducing Ca excretion
  • Pi is removed by kidney reabsorption inhibition
  • Prevents calcium stone formation
291
Q

What are the two forms of vitamin D and how are they formed?

A
  • D3: made in skin and from dairy
  • D2: from yeast and fungi added to margarine as supplement.
  • Both form calcitriol by hydroxylation in liver and kidney
  • T½: ¼ day
292
Q

What effect does PTH have on the gut?

A
  • Stimulates conversion of Vit D to its active form which increases the uptake of Ca from gut.
293
Q

What effect does calcitriol have on the gut, bone and kidneys?

A
  • Active uptake of Ca
  • Transcellular transport
  • Endocytosis and exocytosis of Ca
  • Erodes bone
  • Decreases urinary loss of Ca by stimulating reabsorption
294
Q

What is the saying that signifies hypercalcaemia?

A
  • Stones, moans (depression) and groans (abdominal pain)
295
Q

What effect does hypercalcaemia have on PTH?

A
  • Increased level of calcium leads to decreased levels of PTH
296
Q

What are the effects of hypercalcaemia on the kidneys?

A
  • Decreased calcitriol
  • Less Ca taken from gut
  • Ca absorption decreased
  • Together= plasma Ca decreased
297
Q

What are the treatments of hypercalcaemia?

A
  • Fluids, as patients have lost excess fluid in urine

- Removal of benign tumour in parathyroid glands

298
Q

What happens if there’s a deficiency of PTH?

A
  • Abnormal Ca levels

- Hypocalcaemia is life threatening

299
Q

How is serum phosphate regulated?

A
  • Vitamin D stimulates Ca and Pi uptake in gut.

Medicine Semester 1 (6 decks)

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