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year 1 flash cards > GI strand: metabolism > Flashcards

GI strand: metabolism Flashcards

1
Q

what do we get glucose from

A

starch and glycogen

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2
Q

what do we get fructose from

A

sucrose (sugar)

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3
Q

what do we get galactose from

A

lactose (milk)

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4
Q

name 2 inherited disorders which are associated with absence of enzymes involved In the breakdown of sugars

A

hereditary fructose intolerence
galacrosaemia

NB- can be life threatening and cause sevre brain damage

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5
Q

is glycolysis an aerobic or aerobic process? what kind if cells does it take place in

A

anerorobic

all types of cells

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6
Q

what are the 2 phases to glycolysis

A

preparative phase

generating phase

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7
Q

what happens in the preparative phase of glycolysis? does this step require ATP

A

glucose –> fructose1,6biphosphate

ATP required

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8
Q

what happens in the generating phase of glycolysis ? what additional things are generated here

A

fructose1,6biphosphate –> 2x pyruvate

ATP and NADH generated here

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9
Q

what is generation of ATP in glycolysis called? how many ATPs are made in the aerobic and aerobic state of glycolysis

A

substrate level glycolysis

anaerobic: 2ATP
aerobic: 5-7 ATPs

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10
Q

in glycolysis what converts glucose –> glucose-6-phsopahte? why is this importnant

A

hexokinase in muscles and glucokinase in skeletal muscle

prevents glucose leaving the cell

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11
Q

name the molecules and enzymes which aid transition of glucose to pyruvate in glycolysis

A

glucose — (hexokinase/glucokinase)—> glucose-6-phosphate —–> fructose-6-phosphate —(phosphofructokinase)—-> fructose1,6biphosphate —>—->phosphoenolpyruvate —-(pyruvate kinase)—> pyruvate

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12
Q

in the absence of O2 what is pyruvate converted to and why is this important

A

pyruvate —> lactate

allows for regeneration of NAD

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13
Q

what is the Warburg effect ? what is this significant in and why?

A

high lactate productions in aerobic conditions

diagnostic of cancer as tumour cells absorb glucose more rapidly then normal cells but use aerobic glycolysis

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14
Q

where is glycogen mainly stored

A

liver and skeletal muscle

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15
Q

where are the glycosidic bonds made in glycogen, allowing it to be branched

A

1,4 and 1,6 glycosidic bonds

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16
Q

highlight the steps and enzymes involved in glycogen synthesis

A

glucose —-(hexokinase/glucokinase)—–>glucose-6-phosphate —(phosphoglucomutase)—-> glucose-1-phospahte + glucogenin +UDP-glucose —-(glycogen synthase enzyme) —-(branching enzyme) —-> glycogen

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17
Q

how does glucogen synthase enzyme work?

A

keeps adding UDP-glucose via 1,4 glycosidic bonds to make a long chain

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18
Q

how does branching enzyme work?

A

breaks of parts of the chain and adds it at the C6 of main chain =1,6 glycosidic chains

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19
Q

when do glycigenisis occur

A

in the fed state

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20
Q

when does glycogenlysis occur

A

in the fasting state

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21
Q

what hormones induce glycogenlysis

A

glucagon
noradrenaline
adrenaline

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22
Q

highlight the steps and enzymes involved which turn glycogen to glucose, in the liver and muscle cells

A

glycogen —(glucogen phosphorylase)—>. glucose-1-phosphate —-(phosphoglucomutase)—> glucose-6-phosphate

in muscle this goes into the glycolysis cylce

in the liver, kidneys and duodenum this is acted on by enzyme glucose-6-phosphatase –> turning it into glucose

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23
Q

where is the enzyme glucose 6 phosphatase found

A

in liver, kidneys and duodenum

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24
Q

highlight the steps that occur in the link reaction ? what other molecules are produced here ?

A

2 pyruvate —(pyruvate dehydrogenase)— 2 acetyl CoA

2NADH and 2CO2 produced

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25
Q

how does acetyl CoA get converted to fatty acids and what enzyme is required in this process

A

Acetyl CoA —-(Acetyl CoA carboxylase)—-> Maalonyl CoA —-> fatty acids

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26
Q

highlight the steps in the Krebs cycle and enzymes involved

A

Oxaloacetate + Acetyl CoA —(citrate synthase—> citrate —-(auto citrate)—-> isocitrate —-(isocitrate dehydrogenase) —>a-ketoglutarate —(a ketoglutarare dehydrogenase) —> succinyl —-(succinylCoA synthase) —-> sucinate —(complex 2/ sucinate deHgenase)—> fumate —-(Fumerase) —> malate —-(malate DH) —> OAA

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27
Q

highlight the steps in the electron transport chain

A

1) NADH into complex1, meanwhile FADH2 into complex 2
2) drop off electrons
3) e- from complex 1 and 2 to co-enzyme Q
4) e- to complex 3
5) e- to cytochrome C
6) e- to complex 4
7) e- donated to O2 and combine with H+ to H2O
8) H+ move through ATP synthase/F0F1ATPase
9) the movement of H+ combines ADP to ATP

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28
Q

what is the generation of ATP in Electron transport chain called?

A

oxidative phosphorylation

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29
Q

what can cause a lack of pyruvate dehydrogenase? how do we see this in and what can it cause

A

lack of thiamine seen in alcohol addicts can cause beriberi or Wernicke-Korsakoff syndrome

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30
Q

what activates and what deactivates pyruvate dehydrogenase?

A

activated by: sudden demands upon the cell- signalled by Ca2+

deactivated by: NADH, acetlyCoA, ATP, ADP (basically when energy levels are high)

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31
Q

what waste product is released from the Krebs cycle?

A

CO2

between isocitatre —> a-ketogluterate and —> succinyl

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32
Q

what do reduced NADH and FADH2 carry

A

electrons

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33
Q

when is the ATP made in the Krebs cycle

A

succinyl –> succinate

first GDP–>GTP then this turned into ATP

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34
Q

Why do diabetic patients synthesise ketones

A

cant use glucose effectively in the absence of insulin ….. so glycolysis is inhibited …. so pyruvate low …..

BUT STILL UNDERGO gluconeogensis … so oxaloacetate and malate being removed to form glucose

insulin low so fatty acids oxidised from adipose tissue = high levels acetlyCoA… lack of oxalactete prevents ACoA entering Krebs = ketones synthesised

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35
Q

how does cyanide effect ETC

A

blocks the formation of water at the end

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36
Q

how are protons able to move from a low [H+] in the maxtrix to a high [H+] in the intracellular membrane

A

each reduction step of electrons moving from complex to complex releases energy allowing H+ to pump across - like a game of hot potato

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37
Q

for one molecule of ATP how many protons cross the membrane

A

4 (should be 3 but an extra one for the movement of Pi)

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38
Q

what are uncouplers and what do they do

A

weak acids which are soluble in membrane and can associate with H+ at the inter membrane space and release the protons in the matrix

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39
Q

what is the aim of uncouplers

A

to dissipate the proton gradient and so the ETC can continue without ATP synthesis

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40
Q

what is the significance of high amounts of brown adipose tissue being found in newborns

A

has more mitochondria and contains thermogenin (uncoupling protein), when activated due to low body temps energy is released as heat

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41
Q

what happens when the ETC is uncoupled from ATP synthesis?

A

energy is released as heat

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42
Q

what is DNP? why is it dangerous

A

a ‘slimming’ pill

causes side effects: hyperthermia, tachycardia, excess sweating, blinding

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43
Q

other than energy what can fats be used to generate

A

phospholipds

cholesterol

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44
Q

same two essential fatty acids which are precursors for eicosanoids (prostaglandins, leukotrienes, thromboxanes)-ie. inflammatory and anti-inflammatory molecules

A

omega 3 and 6

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45
Q

what is cholesterol a precursor for?

A

membranes
vitamin D
steroid hormones
bile salts

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46
Q

what steroid hormones does cholesterol lead to the development of

A
  • androgens
  • oestrogen
  • progesterone
  • mineralocorticoids (eg.aldesterone)
  • glucocorticoids (eg.cortisol)
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47
Q

how do chylomicrons make their way from the intestines to the liver

A

intestinal epithelial cells —> into lymph lacteals –> enter circulation via thoracic duct and subclavian vein

NB: not a direct from GI tract to liver

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48
Q

what does the liver do to. chylomicrons

A

turns them into VLDL

this them turns into LDLs and HDLs

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49
Q

what happens when fatty lipids (ie. chylomicrons,VLDLs, LDLs) arrive at peripheral tissues the fed state ?

A

released by lipoprotein lipase

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50
Q

what happens when fatty lipids arrive at peripheral tissues the fasting state ?

A

form adipose tissue: triacylglycerols broken down by hormone sensitive lipase —> fatty acids released into blood —> transported to tissues bound to albumin

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51
Q

can fatty acids be used by the brain?

A

no because cannot cross BBB

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52
Q

What stimulates fatty acid oxidation

A

long chain fatty acids

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53
Q

what is the first step in the oxidation of FAs

A

activation to fatty acyl CoA from the long chain fatty acids

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54
Q

how do we move acyl CoA into the mitochondria

A

carnitine transport system adds a carnitine and removes a CoA making fatty acid carnitine, done by carnitine palmitoyl transferase 1 = so can be transported

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55
Q

what inhibits the carnitine transport system

A

malonyl CoA (prevents the synthesis and degradation of FAs at the same time)

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56
Q

what happens when fatty acyl cartatine enters the mitochondria

A

carnitine palmitoyl 2 removes the carnitine and adds a CoA creating fatty acyl CoA

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57
Q

during the oxidation of fatty acids in the mitochondria what is produced and released in each oxidation

A

each turn releases one acetyl CoA and produces NADH and FADH2

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58
Q

what happens to the products of fatty acid oxidation

A

NADH and FADH2 are oxidised in the ETC and Acetyl CoA enters the Krebs

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59
Q

can the oxidation of fats be done in a anaerobic environment

A

no has to be aerobic

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60
Q

what is the main thing which regulates fatty acid synthesis ? how does it do this

A

conc malonyl CoA

inhibits carnitine acyl-transferase 1

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61
Q

why does malonyl CoA inhibit fatty acid synthesis

A

ensures that fatty acid breakdown is inhibited when energy is plentiful

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62
Q

why do we get formation of ketone bodies

A

excess acetyl CoA

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63
Q

where does ketogenesis occur

A

liver

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64
Q

where does ketolysis occur

A

brain and muscle

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65
Q

why would ketogenesis occur

A

when the body is reliant of fatty acid oxidation for energy

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66
Q

in what states would we get ketogensis occurring

A

fasting
uncontrolled diabetes
low blood glucose conc

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67
Q

why cant acetyl CoA be used in the Krebs cycle when glucose levels are low

A

because meanwhile gluconeogensis is occurring and so OAA is pumped and used out of the cell a so cannot react with Acetyl CoA

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68
Q

how does low levels of glucose lead to ketone body formation

A

decreased kerb cycle activity = decreased citrate levels = body joins 2 Acetyl CoA –(acetlyCoA acyltransferase) –> Acetoacetyl CoA —–(acetlyCoA acyltransferase)—–> HMG-CoA —-(HMG-CoA lyase)—> AcetoAcetate —> 3hydroxybutyrate and acetone

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69
Q

what is the job of acetlyCoA acyltransferase

A

joins 2 Acetyl CoA molecules and removes a CoA in the process

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70
Q

what are the main organs which synthesise cholesterol

A

intestines and liver

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71
Q

what are high levels of cholesterol associated with

A

CV disease and Alzheimers

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72
Q

highlight the steps in cholesterol biosynthesis

A

Acetyl CoA —> HMG CoA —–(HMG CoA reductase) —> Mevalonate —-phosphorlyated —-> isoprene units —– 6 isoprene units phosphorylated —> squalene ——cyclisation to form ring structure —-> lanosterol —> cholesterol

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73
Q

where does cholesterol synthesis take place

A

smooth ER

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74
Q

which step in cholesterol synthesis is the most importnant and why?

A

first step as HMG CoA reductase controls the rate of synthesis

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75
Q

what is cholesterol synthesis controlled by

A
  • cholesterol levels (high levels = inhibit synthesis)

- energy levels (insulin stimulates and glucagon inhibits )

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76
Q

why would insulin stimulate and glucagon inhibit cholesterol synthesis

A

because insulin signals that there is energy availability whilst glucagon signals that there is a lack of energy and so energy is not ‘wasted’ on cholesterol synthesis

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77
Q

how do insulin and glucagon affect the activity of HMG CoA reductase

A

effect the phosphorylation enzyme which is inactivated at low energy levels

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78
Q

how does phosphorylation affect the activity of HMG CoA reductase

A
  • controls the amount of enzyme present
  • controls the transcription of enzyme (inhibited by high cholesterol)
  • rate of degradation of enzyme (inhibited by high cholesterol)
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79
Q

how does high levels of cholesterol affect the transcription enhancing signals from the ER

A

inhibits the movement of SREBP (sterol regulatory binding protein) into the nucleas of the ER and so inhibits the binding od=f SREBP to SRE (sterol regulatory element) = decreasing the levels of transcription of HMG coA reductase and so cholesterol

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80
Q

how do we break down cholesterol

A

we cant ! can only excrete via faces

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81
Q

how do saturated fats affect cholesterol levels in the blood

A

raise the levels of LDL cholesterol

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82
Q

how do we get the formation of Trans Fats

A

formed from hydrogeneation of oils

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83
Q

how do Trans fats affect cholesterol levels

A

raise LDL and lower HDL

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84
Q

what effects do mono-unsaturated and poly-unstaurated fats have on disease prevalence?

A

reduce CHD risk and other benefits?

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85
Q

how does familial hyperccholesterolaemia affect and individual, what are they at increased risk of?

A

lack of LDL receptors

increased risk of CHD

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86
Q

what are high levels of LDL associated with

A

increased risk of atherosclerosis

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87
Q

what is Tangier disease

A

lack of HDL (so sufferers at higher risk of CHD)

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88
Q

describe the formation and consequence of an atherosclerotic plaque

A

damage to endothelial cells —> LDL access to subintimal space (space behind epithelium) —>accumulation of foam cells —> create bulge in vessel wall = plaque —> fibrous collagen ‘cap’ is formed —> restrict blood flow in coronary arteries = angina

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89
Q

how can thrombosis occur from a plaque

A

inflammatory response: macrophages produce proteinase enzymes —> degrade fibrous cap —> plaque ruptures —> activates clotting mechanisms —> blood clot

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90
Q

how has high levels of cholesterol been associated with alzieherms

A

high cholesterol = accumulation of AB peptide

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91
Q

what is alcoholic steatohepatitis and how is it caused

A

liver disease

metabolism of large amounts of Alcohol inhibit fatty acid oxidation and activate triglyceride synthesis = accumulation of triglycerides

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92
Q

what is non alcoholic steatohepatitis and how is it caused

A

chronic liver disease

insulin resistance leads to increased insulin secretion = FA synthesis = accumulation of FA on liver

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93
Q

what are excess sugars usually converted to

A

fatty acids

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94
Q

what are fatty acids converted to

A
  • triacylglycerols (triglycerides) for storage

- other lipid synthesis (for membranes)

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95
Q

where does fatty acid synthesis mainly occur

A

liver , adipose tissue, breast tissue during lactation

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96
Q

how are is manlonyl CoA synthesised

A

citrate —(citrate lyase)—-> acetyl CoA —–(acetylCoA carboxylase) —–> malonyl CoA

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97
Q

how are FAs synthesised

A

x(malonyl CoA + Acetyl CoA) —-> palmitate —> longer chain FAs or unsaturated FAs

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98
Q

highlight the synthesis of triglycerols

A

3 fatty acids + glycerol-3-phosphate

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99
Q

what is a key modulator for metabolism

A

ATP availability: AMP-activated protein kinase

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100
Q

how does AMP-activated protein kinase work

A

phosphorylates key enzymes involved in metabolism in the heart, adipose tissue, liver, muscle

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101
Q

what are the overall effect of AMP-activated protein kinase

A

increase energy providing pathways and inhibit anabolic pathways (eg. FA synthesis, insulin secretion)

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102
Q

how does insulin influence glycolysis in muscle and adipose tissue

A
  • increases expression of enzymes coding for glycolysis

- decreases expression of genes coding for glucosneogensis enzymes

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103
Q

how does glucagon influence glycolysis in muscle and adipose tissue

A

regulates levels of fructose2,6biphosphate which activate glycolysis and inhibits gluconeogeneiss

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104
Q

what happens when fructose2,6biphosphate is phosphorylated in high glucagon levels

A

enzyme degrades F26-BP

105
Q

what happens when fructose2,6biphosphate is dephosphorylated in low levels of glucagon

A

enzyme synthesises F26-BP

106
Q

what can we form from AA

A
  • proteins
  • nitrogen containing metabolites
  • energy
  • fatty acids
  • ketones
  • glucose/glycogen
107
Q

what is kwashiorkor

A

disease in children of developing countries causing malnutrition, making them look fat

108
Q

what are the symptoms of kwashiorkor

A 
Poor growth
Susceptibility to infection
Changes in hair/skin colour
Poor skin condition and poor nutrient absorption
Abdominal bloating
lower limb oedema
109
Q

what kind of diet is kwashiorkor caused by

A

low protein high fibre diet

110
Q

why does nitrogen have to be exerted

A

because ammonia from the AA can be converted to ammonium which can result it hyperammonaemia

111
Q

what can hyperammonaemia cause

A 
tremor 
vomiting 
cerebral oedema 
coma 
death
112
Q

what is the main reason we get hyperammonaemia

A

liver disease: hepatitis or cirrhosis

113
Q

which organ disposes of NH3 and which excretes it ?

A

liver disposes it as urea and kidney excretes it as urine

114
Q

what are the 3 stages which convert NH3 to urea

A
  • transamination
  • deamination
  • urea synthesis
115
Q

highlight the steps in the process of transamination

A

1) AA combines with a-ketogluterate
2) amino group from AA and O2 from AKG swapped via pyrodoxial phosphate
3) AlanineAmino transaminase converts the AA to pyruvate and AKG is converted to glutamate
4) addition of another amino group to glutamate —> glutamine

116
Q

where do transaminase reactions occur

A

muscle/peripheral tissue

117
Q

where does demanination occur

A

in the liver

118
Q

highlight the steps involved in deamination

A

1) glutamine acted on by glutamate dehydrogenase to form AKG
3) this releases NADPH from NADP+
4) NH3 is also released

119
Q

what vitamin does pyrodoxial phosphate require

A

B6 - pyrodoxial phosphate is the active form of B6

120
Q

what is pyrodoxial phosphate used in

A
  • transamination and synthesis of AA
  • decarboxylation of NTs
  • haemorrhage synthesis
121
Q

what can a lack of B6 lead to

A
  • anaemia (lack of team synthesis)
  • neurological conditions (lack of NT synthesis)
  • poor growth and immune responses (lack of protein synthesis)
122
Q

what happens to the AKG formed at the end of deamination

A

combines with aspartate —> OAA and glutamate

OAA can go into Krebs

123
Q

what is the control step in urea synthesis

A

NH4+ enters the mitochondria + HC03- ——-(carbamoyl phosphate synthetase 1)—–> carbamoyl phosphate

124
Q

what is carbamoyl phosphate synthesise 1 allosterically activated by? how is this formed

A

N acetyl glutamate

formed when glutamate levels are high (due to high levels of AA so protein)

125
Q

what happens once carbamoyl phosphate enters the urea cycle

A

combines with ornithine to form citrulline via enzyme ornithine transcarbamoylase

126
Q

what happens to citrulline

A

A second amino group from aspartate is added —> arginine —-> urea

127
Q

how is uric acid different from urea

A

uric acid is derived from purine nucleotides rather than protein

128
Q

what can excess uric acid in blood lead to

A

hyperuricaemia which can lead to deposition of Na crystals in kidneys (kidney stones) and joints (gout)

129
Q

how can we get hyperuricaemia

A

over production of urate or poor excretion by the kidneys

high purine foods (red meat, seafood, yeast-containing -inc beer)

130
Q

what can we use the carbon Skelton of AA for

A

Krebs cycle (via OAA)

  • fatty acid and ketone synthesis
  • gluconeogenisis
131
Q

where does gluconeogensis occur

A

cytosol of liver and kidneys

132
Q

when does gluconeogenesis occur

A
  • low blood glucose : fasting or exercise
133
Q

what are the precursors for gluconeogensis

A

keto acids
lactate
glycerol

134
Q

how is lactic acid converted to glucose in gluconeogensis

A

lactic acid —> pyruvate —-> OAA —-> phodphornolpyruvate —> Frutose-1,6-biP —> fructose -6-phosphate—(glucose-6-phosphatase)—–>glucose

135
Q

what effect does type 1 diabetes have on glyconeogenisis

A

glycolysis is inhibited as insulin allows tissue enters of glucose to muscle and adipose tissue so gluconepogensis is stimualted

= increases glucose conc a lot as body doest realise we have glucose

136
Q

why does weight loss occur in individuals with diabetes type 1

A

muscle protein is broken down to provide AA for gluconeogenisis

137
Q

what is the cori cycle

A

converts lactate rapidly from respiring cells to glucose via pyruvate

138
Q

what does high levels of NADH cause

A

increases energy storage as triacylglycerol

139
Q

why does alchohol make you hungry ? how does this work

A

inhibits gluconeogensis

ethanol metabolism creates lots of NADH which decreases levels of NAD+

this prevents convertion of glycerol to glyceraldenhyde 3 phosphate as NAD+ too low

high NADH causes conversion of pyruvate to alanine to lactate

so pyruvate and glyceraldehyde-3-phosphate cannot join create glucose = inhibition glycogenesis

140
Q

what are glucocorticosteroids

A

class of steroid hormone

141
Q

what is the active form of glucocovrticosteroids

A

cortisol

142
Q

what is the pharmaceutical derivative of glucocorticosteroids

A

hydrocortisone

143
Q

what are glucocorticosteroids produced by

A

adrenal / suprarenal glands

144
Q

what part of the adrenal gland produces glucocorticoids

A

the zone fasiculata of adrenal - middle part of the adrenal cortex

145
Q

what are the differnt layers of the adrenal gland (from outer to inner)

A

zona glomerulosa
zona fasciculata
zona reticularis

146
Q

what are the 2 zones of the adrenal gland

A

medulla - the inner zone

cortex

147
Q

what does the zona glomerulosa (the outer layer of the adrenal cortex produce)

A

mineralcorticosteroids : aldosterone and corticosterone

148
Q

what does the zona fasciulata of the adrenal cortex ( the middle layer) produce

A

glucocorticoids : cortisol and cortisone

149
Q

what does the zona reticularis of the adrenal cortex (the inner layer) produce

A

androgens: oestrogen and testosterone

150
Q

what does the adrenal medulla produce

A

catecholamines : noroadrenaline and Adrenaline

151
Q

what is the process by which cortisol is released from the adrenal glands starting from the hypothalamus

A

hypothalamus releases CRH —> signals the anterior pituitary to release ACTH —> signals adrenals to release cortisol

152
Q

what us cortisol bound to

A

albumin

153
Q

when is the production of cortisol at its highest

A

30 minutes after waking

154
Q

do levels of cortisol stay high through the day

A

no they decline throughout the day

155
Q

what are the levels of cortisol regulated by

A

suprachiasmatic nucleas of the hypothalamus

156
Q

which cells are cortisol(GC) receptors present on

A

almost all cells - affecting all body systems

157
Q

during what times do we get an increase in cortisol production

A

during times of stress

158
Q

are levels of cortisol essential for feotal devlelopmemnt? do levels increase during pregnancy?

A

yes cortisol levels are essential for foetal development and thereby levels increase by 2-4 fold during pregnancy

159
Q

what are the actions of cortisol

A
  • reduce inflammation

- increase glucose availibity to the brain

160
Q

how does cortisol reduce inflammation

A
  • surpesssses B cell antibody production
  • apoptosis of T cells
  • reduce neutrophil migration
161
Q

how does cortisol increase glucose availability

A
  • acts on the liver, pancreas, muscle and adipose tissue to increase gluconeogenesis, lipolysis and reduce glycogen synthesis
162
Q

how does cortisol effect insulin and glucagon

A

reduces insulin production and increases glucagon synthesis

163
Q

what are the actions of cortisol on the CV system

A
  • circadian rhythm affects BP and HR

- Increased cardiovascular tone = can cause hypertension

164
Q

what is circadian rhythm

A

the day and night rhythm

165
Q

what are the actions of cortisol on the nervous system

A

GC receptors found throughout the CNS - part of fight or flight response

166
Q

what is Addisons disease

A

adrenal insufficiency - lack of cortisol

167
Q

does Addisons doses usually present by itself

A

no usually presents with another autoimmune disease e

168
Q

what are the primary causes of Addisons disease

A

problem is with adrenal gland itself:

  • chronic granulomatous disease
  • autoimmune (producing antibodies against)
  • malignancy
  • haemorrhage
  • infective
169
Q

what are the secondary causes of Addisons disease

A

insufficient ACTH production:

  • pituitary disease
  • exogenous steroids
170
Q

why is primary adrenal disease not as bad as secondary adrenal disease

A

because we have 2 adrenal glands - so if one affected still have another

171
Q

what are the signs and symptoms of Addisons disease

A
  • weakness and fatigue
  • orthostatic hypotension (feel dizzy when stand)
  • hypoglycaemia
  • weight loss
  • reduced body hair (due to reduced androgens)
  • hyperpigmentation
  • hyperkalaemia and hyponatraemia
172
Q

is hyperpigmentation seen in primary or secondary Addisons disease

A

only primary

173
Q

what is hyperkalaemia and hyponatraemia ? and why do we get it

A

hyperkalamia - is an increase potassium
hyponatraemia - is a decrease in sodium

due to lack of aldosterone

174
Q

what are the gastrointestinal symptoms we get with Addisons disease

A
  • nausea
  • diarrhoea
  • vomtting
  • constipation
  • abdominal pain
175
Q

why do we get an Addisonian crisis

A

due to inability to produce cortisol in stressful situations (eg. infection, trauma, surgery, non-compliance with medications)

176
Q

how serious is Addisonian crisis

A

very serious- life threatening

177
Q

do we get an increase or decrease in BP in an Addison crisis

A

decrease in BP - low BP

also hyperkalamia and hyponatraemia

178
Q

how might patients present in an Addisonian crisis

A

nausea
confusion
pyrexia (fever)
vomiting

179
Q

how would we investigate for Addisons disease

A
  • random cortisol level
  • U&Es
  • normocytic normochromic anaemia
  • SST (short synathen test)
  • ECG
180
Q

what are we looking for in U&Es if someone has presented with Addisons disease

A 
raised urea 
creatinine 
acidosis 
hyponatraemia 
hyperkalaemia
181
Q

why would we perform an ECG on someone in an Addisonian crisis

A

because the hyperkalaemia and hyponatraemia can effect the heart rate and functioning of heart

182
Q

what is a SST - short synacthen test

A

test for adrenaline insufficiency

183
Q

would we do an SST in a critically ill patient

A

no if the patient is critically ill give steroids straight away

184
Q

before you carry out a SST what medication would you need to stop

A

any form of hormone replacement therapy or oral contraceptive pill

185
Q

how does the SST work

A
  • take a basal cortisol level
  • synthetic injection of ACTH
  • take cortisol levels at each 30-60 minutes
  • cortisol > 420 at 30 mins is adequate
186
Q

what is the treatment for someone in an Addisonian crisis

A

must treat as ion life threatening

  • IV steroids - cortisol
  • IV fluids
187
Q

why would we give IV fluids to someone in an Addisonian crisis

A

to support low BP

188
Q

what is the long term treatment for Addisonian disease ? why do we give this ?

A

hydrocortisone

  • replicate circadian rhythm
  • increase
189
Q

how would you administer hydrocortisone

A

need to replicate circadian rhythm so high dose in the morning and lower doses in the evening
* if body under less need to double the dose of hydrocortisone as would happen normally*

190
Q

what is Cushings syndrome

A

when there is an excess amount of steroid

191
Q

what are the causes of Cushings syndrome

A

prolonged exposure to excess steroid- glucocorticoid meds:

endogenous or exogenous

192
Q

what age do we get the peak incidence of bushings syndrome

A

25-40 years

193
Q

are cushings disease and syndrome the same thing ? why

A

no Cushings disease is only concerned with a pituitary tumour - ACTH dependent

Cushings syndrome is is due to excess cortisol from any other cause : ectopic ACTH production

194
Q

what is the primary cause of cushings syndrome

A

excess iatrogenic - excess cortisol given

195
Q

what are the signs and symptoms of cushings syndrome

A

tomato with matchstick arms and legs:

  • weight gain
  • proximal muscle weakness
  • brusising
  • striae
  • hypertension
  • osteoporosis
  • diabetes
  • impaired immune function
  • personality changes
  • moon face
  • hyperglycaemia
  • thin extremities
196
Q

what are the extra symptoms off cushings syndrome in females

A

amenorrhea

hirsutism

197
Q

what investigations would you do to diagnose cushings syndrome

A
  • initial Ix:
    ONDST
    late night salivary cortisol
    24 hour burniangy cortisol
198
Q

how does ONDST work in diagnosing bushings syndrome

A

overnight dexomethozone suppression test - steroids given at night (11pm) given should suppress morning cortisol production

199
Q

what imaging tests would you carry out to diagnose for cushings syndrome

A
  • MRI pituitary (check brain)
  • CT adrenal
  • CT TAP
  • PET-CT
200
Q

what is the primary treatment given in cushings syndrome

A

primary treatment is surgery - removal of casual tumour : adrenal, adrenalectomy
surgery done from the back of the body

201
Q

what is the secondary treatment for cushings syndrome

A

medication

radiotherapy

202
Q

what medications are given to people with cushings syndrome

A
  • steroidogenesis inhibitors
  • somatostatin analogues
  • adrenal steroid inhibitors
  • anti-neoplastic drugs
203
Q

how do steroidogenesis inhibitors work

A

inhibits the enzyme that catalyses the last step of cortisol synthesis in adrenal cortex

204
Q

how do somatostatin analogues work

A

bind and activate human somatostatin receptors resulting in inhibition of ACTH secretion

205
Q

how do adrenal steroid inhibitors work

A

inhibit steroid synthesis

206
Q

how do anti-neoplastic drugs work

A

decrease steroid production - mitochondria destruction of cells

207
Q

how do thyroid hormones function

A

control basal metabolic rate

208
Q

what 2 hormones does the thyroid produce

A

T4 and T3

209
Q

what is T4 called

A

thyroxine

210
Q

what is T3 called

A

triiodothyronine

211
Q

is T3 or T4 or both biologically active?

A

T3 is biologically active

212
Q

out of T3 and T4 which one is mainly produced

A

T4 most abundant - but converted to T3 in the periphery

213
Q

what are the 2 essential components for thyroxine production

A

tyrosine and iodine

214
Q

how is thyroxine produced

A
  • iodine is taken up from blood by thyroid epithelial cells
  • tyrosine is produced from thyroglobulin
  • thyroglobulin is synthesised from the thyroid epithelial cells and secreted into lumen follicle
  • thyroid peroxidase on thyroid epithelial cells iodinasases tyrosine on thyroglobulin
  • synthesis of T4/ T3 from 2 iodotyrosines
215
Q

is hypothyroidism common?

A

yes very common endocrine disorder

216
Q

what are the usual causes for hypothyroidism

A

usually primary failure of thyroid to produce thyroxine

rarely secondary or tertiary

217
Q

what are the main causes for primary hypothyroidism

A
  • iodine excess or defiancecy
  • autoimmune disease
  • iatrogenic
  • thyroiditis
218
Q

what are the symptoms of hypothyroidism

A

range from asymptomatic to myxoedema coma:

  • thinning hair/ loss
  • enlarged thyroid
  • puffy face
  • slow heartbeat
  • dry and coarse skin
  • poor appetite
  • constipation
  • infertility
  • heavy menstration
  • weight gain
  • intolerance to cold
  • feeling tired
  • poor memory
219
Q

in who is hypothyroidism most common

A

females and elderly

220
Q

how do we treat hypothyroidism

A

improve symptoms:

- daily dose of levothyroxine (T4)

221
Q

do we give both young healthy individuals and elderly the same dose of levothyroxine to treat hypothryoidism

A

no :

in young healthy adults start treatment in full dose but in elderly give it gradually

222
Q

does treatment of hypothyroidism with levothyroxine have immediate effect

A

no can take up to 4-6 weeks to show

223
Q

what are the primary causes for hyperthyroidism

A
  • graves disease
  • toxic goitre
  • solitary goiture (only one nodule effected)
  • thyroiditis
224
Q

what are the secondary causes for hyperthyroidism

A
  • pituitary tumour

- iatrogenic

225
Q

what are the symptoms of hyperthyroidism

A
  • excessive sweating
  • heat intolerance
  • increased bowel movements
  • tremor
  • nervousness , agitation
  • rapid heart rate
  • weight loss
  • fatigue
  • decreased concentration
226
Q

are the presentation of symptoms in older and younger patients the same

A

no in younger patients there’s more symptoms of sympathetic activation and in older patents in mainly effects the CVS

227
Q

how can graves disease effect the eye

A
  • peri-orbital oedema
  • diplopia- seeing 2 images instead of one
  • proptosis = abnormal profusion of eye
228
Q

what us hyperthyroidism also known as

A

thyrotoxicosis

229
Q

how do we treat thyrotoxicosis

A
  • anti-thyroid agents
  • B blockers
  • glucocorticoids
  • radioactive iodine
  • surgery
230
Q

why is it risky to give radioactive iodine and in what patients should we really avoid giving this

A

there’s a risk of hypothyroidism and avoid in patients with eye dieseas

231
Q

in what state do we need increased thyroxine requirements

A

during pregnancy - for foetal development

importnant to raise levothyroxine dose in hypothyroid patients

232
Q

when does the foetal thyroid reach maturity

A

11 weeks

233
Q

when does the foetal thyroid begin secreting thyroid

A

16 weeks

234
Q

what kind fo development is the thyroid hormone essential for in a foetus

A

for the neurological development of the foetus

235
Q

what are the 2 reasons we may get hypothyroidism in babies

A

due to lack of maternal thyroxine or thyroid ageeneis

236
Q

what is growth hormone also known as

A

somatotropin

237
Q

what is growth hormone importnant in maintaining

A

lean body mass and controls metabolism

238
Q

when do we get the maximal release of GH

A

second half of the night

239
Q

what is GH release stimulated by

A

GHRH Secreted from hypothalamus

240
Q

what is GH release inhibited by

A

GHIH

somatostatin

241
Q

what kind of things affect GH release

A 
age 
gender 
puberty 
sleep 
exercise
242
Q

how does GH effect protein metabolism

A
  • anabolic effect
  • stimulates transcription
  • increased AA uptake and protein synthesis
243
Q

how does GH effect fat metabolism

A

promotes lipolysis

increase fat utilisation

244
Q

how does GH effect carbohydrate metabolism

A

antagonistic to insulin
promotes gluconeogensis
increases utilisation of glucose
inhibits glycolysis

245
Q

how does growth hormone induce growth

A
  • promotes linear growth in children
  • transforms cartilage to bone (condrocyte stimulation production)
  • increase bone mass
246
Q

what are the autogenic effects of GH

A
  • enhances milk production

- prolactin like effect

247
Q

what can hyper secretion of Gh lead to in children

A

gigantism : tall, large hands and feet, loss of libido, impotence, hyperglycaemia, macrocephaly, prognathism

248
Q

what can hyper secretion of Gh lead to in adults

A

acromegaly

249
Q

what are the features of acromegaly

A 
enlargement of hands and feet
coarse facial features (ie. large bulging head) 
prognathism - bulging of lower jaw 
macroglossia - large tongue 
hyperhidrosis- excessive sweating
250
Q

what can acromegaly lead to

A

hypertension
sleep apnoea
type 2 diabetes
cardiomyopathy

251
Q

what investigations can be done for acromegaly and giantism

A
  • IGF-1 levels (insulin-like growth factor-1 (IGF-1) test = indirect measure of the average amount of growth hormone)
  • GH levels after glucose challenge
  • prolactin levels (levels increase with increased levels of GH)
  • MRI pituarty
  • CT TAP (Computed Tomography of Thorax, Abdomen and Pelvis)
252
Q

What is the treatment for acromegaly and giantism: hyper secretion of GH

A
  • transsphenoidal surgery
  • endoscopic neurosurgical procedure
  • post op imaging to check for residual tumour
  • check for hypopituarism post op
253
Q

what is transsphenoidal surgery

A

remove tumors of the pituitary gland by inserting an endoscope into the brain by going through the nose and sphenoid bone

254
Q

what is the second line fo treatment for hyper secretion of GH (acromegaly and giantism)

A

medical treatment

radiation

255
Q

what medical treatment can we use for hyper secretion of GH (acromegaly or giantism)

A
  • somatostatin analogue (man made version of somatostatin)
  • dopamine receptor analogues - binds to dopamine type 2 receptors and decrease GH secretion
  • GH receptor antagonists
256
Q

how does somatostatin effect GH levels

A

slows down the production of GH

257
Q

how can radiation help with hyper secretion of GH (acromegaly and giantism)

A

prevent growth of pituitary tumour in most patients

258
Q

what are the risks of radiation in hyper secretion of GH levels

A

can lead to hypothyroidism

259
Q

does radiation in order to treat hyper secretion of GH hormone have an immediate effect

A

no takes years to reduce levels of GH hormone

year 1 flash cards (23 decks)

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