Metabolism Flashcards
1
Q
What are the classifications for BMI weights
A
2
Q
What is malnutrition
A
a condition caused by imbalance in what an individual eats and what is required
3
Q
what is malabsorption
A
a condition caused by the failure to absorb nutrient properly
4
Q
What is undernutrition
A
a condition caused by an eating disorder
5
Q
what is homeostasis
A
the maintenance of a constant internal environment within limits of a dynamic equilibrium
6
Q
How do you calculate the BMI
A
BMI = Weight (kg) / Height ^ 2 (meters)
7
Q
what is metabolism
A
the chemical reactions that happen in organisms to sustain life
8
Q
What enzyme turns HMG acid into Cholesterol
A
HMG Co enzyme A reductase
9
Q
In metabolism of Acetyl Co-A, what regulates the production of ketone bodies or cholesterol
A
Ketone Bodies are increased in response to Glucagon
Cholesterol is increased in response to Insulin
10
Q
What is the intermediate between Acetyl Co-A and Ketone Bodies or Cholesterol?
A
Hydroxylmethyly Glutaric Acid
11
Q
What is the level of ketone bodies in the blood that suggest diabetes?
A
More than 10mM
12
Q
What are the products of Beta Oxidation of fatty acids
A
Acetyl Co-A, NADH, FADH2
No ATP
13
Q
What are the three ketone bodies and their properties
A
Acetone, acetoacetate and beta-hydroxybutyrate. water soluble and can enter the tri-carboxycylic acid chain.
14
Q
Which parts of the body requires glucose for energy exclusively
A
Cornea of the eye, medulla of the kidney, testes, RBC, CNS preferentially
15
Q
Name 3 different classes of lipids and 2 examples of each
A
Fatty Acids - triacylglycerols, phospholipids, fatty acids
Hydroxy Methyl Glutaric acid derivatives - Ketone Bodies and Cholesterol
Vitamins - A, D, E, K
16
Q
Where are ketone bodies and cholesterol synthesised
A
liver
17
Q
Where are fatty acids metabolised
A
Most tissues in the body with mitochondria, except CNS as difficulty in crossing the blood brain barrier.
18
Q
where is glycogen stored
A
liver and muscles
19
Q
what are the advantages of glycogen
A
stable, large surface area for rapid access, osmotically neutral
20
Q
What is glycogenesis
A
Creation of glycogen, using hydrolysis -
Glucose - glucose 1 phosphate - glucose 6 phosphate + UTP - UDP glucose + glycogen
21
Q
What enzymes are used in glycogenesis
A
1, Hexokinase = glucose - glucose 6 phosphate
2, Phosphoglucomutase = glucose 6 phosphate - glucose 1 phosphate
3, Glycogen synthase and Branching Enzyme - UDP glucose + glycogen
22
Q
What is gycogenlysis
A
Degradation of glycogen, phosphorylation reaction
glycogen - glucose 1 phosphate - glucose 6 phosphate - glucose
23
Q
What are the enzymes in glycogenlysis
A
1, Debranching enzyme & amp; Glycogen phosphorylase = Glycogen - glucose 1 phospate
2, Phosphoglucomutase = glucose 1 phospate - glucose 6 phosphate
3, Glucose 6 phosphatase = glucose 6 phosphate - glucose
24
Q
What effect does glucagon have on glycogen
A
Activates glycogenlysis - phophorlyation of glycogen synthase decreasing activity and phosphorylation of glycogen phosphorylase increasing activity
25
What effect does insulin have on the glycogen
Glycogenesis - dephosphorylation of glycose synthase leading to activation, dephosphorylation of glycogen phosphorylase leading to inhibition
26
Give two examples of glycogen storage diseases and the enzymes they effect
Von grieke disease - glucose 6 phosphatase, cannot convert glucose 6 phosphate to glucose in the liver
McArdle disease - glycogen phosphorylase cannot breakdown glycogen in liver or muslce
27
What are the advantages of lipid storage
bulk, energy rich, anhydrous, highly calorific - stoerd as triacyglycerol in adipose tissue.
28
What effect does glucagon and insulin have on fat stores
Glucagon - phosphorylates Hormone sensitive lipase activation
Insulin - dephosphorylates Hormone sensitive lipase deactivation
29
Name three energy storing molecules apart from ATP
Phosphoenolpyruvate
1,3 - Bisphosphoglyerate
Creatine Phosphate
30
Where is Creatine Phosphate, what does it do and how is it made
Creatine is transformed into creatine phosphate with the enzyme creatine kinase, this requires energy of ATP.
Creatine Phophate is a more stable form of energy than ATP but only lasts a short time and is produed in muscles when there are high concentrations of ATP
31
What is creatinine
Creatinine is formed spntaneously from the breakdown of creatine or creatine phosphate. High levels in urine suggest muscle wasting.
32
What are the characteristics of monosaccharides and give examples
Partially oxidised, hydrophilic - glucose, fructose, galactose, ribose, glyceraldehyde
33
What is the first step in glycolysis
glucose to glucose 6 phosphate
enzyme - hexokinase or glucokinase in liver
34
What is the commiting step in gycolysis
Fructose 6 phosphate - fructose 1,6, bisphosphate
Phosphofructokinase
35
What is the second step in glycolysis
glucose 6 phosphate - fructose 6 phosphate
Isomerase
36
Which two steps require ATP in glycolysis
Step 1 creation of glucose 6 phosphate
| Step 3 creation of fructose 1,6 bisphosphate
37
What are the net products of gycolysis
2 x (pyruvate + 2ATP + NADH + H + H20)
38
What are the two products of step 4 in glycolysis
Dihydroxyacetone phosphate - that can become glycerol phosphate making phospholipids and TAG
Glyceraldehyde - 3 - phosphate
Enzyme is Aldolase
39
What is substrate level phosphorylation
direct creation of ATP from carbohyrates, rather than indirectly from ATP synthase in the electron transport chain
40
What are the advantages of glycolysis
Many small steps makes, Little energy lost, can be controlled by multiple enzyes, versatility to connect with other metabolic pathways
Anaerobic
41
Name an enzyme that breaksdown polysaccharides and disaccharides
Amylase - polysaccharides in the mouth a1,4 glycosidic bonds
Sucrase - glucose/fructose
lactase - galactose/glucose
Maltase - glucose/glucose
42
Absorption of Glucose
In gut - sodium dependent glucose transporter SGLT
GLUT 1- RBC
GLUT 2 - both ways - liver, basolateral surface of epithelia, kidneys
GLUT 3 - nerurons
GLUT 4 - insulin dependent muscle / adipose tissue
43
Name 2 alternative products of glycolysis
2,3 Bisphosphoglycerate (2,3BPG) - from 1,3, BPG in step 6. uses enzyme bisphosphoglycerate mutase
Glycerol phosphate - from dihydroxyacetone phosphate in step 4, used in producing lipids
44
How is glycolysis regulated
Product inhibiton - high NADH leads to inhibition of Step 6
Allosteric inhibition - Phosphofructokinase in Step 3 activated by ATP inhibitied by AMP
Dephosphorylation - Glucagon activates protein Kinase A, which phosphorylates Pyruvate Kinase in step 10 of glycolysis
45
What is the purpose of the lactate pathway
To generate oxidised NAD+ to be used in RBC for glycolysis
| Cannot be retrieved from stage 4 of carbohydrate metabolism in electron transfer chain
46
When does lactate pathway happen
In RBC to generate NAD+, in muscle when insufficient oxygen
47
What is the process of lactate pathway
NADH + H + pyruvate --- lactate + NAD+
lactate dehydrogenase is the enzyme, reversibly
48
Which tissues can use lactate
Cardiac muscle converts it back to pyruvate
Liver can convert it back to glucose / glycogen
49
What are the consequences of high lactate
Lactic acidosis >5mM
50
Fructose pathway involves which steps
Fructose - Fructose 1 phosphate - 2x Glyceraldehyde-3-phosphate - glycolysis
51
What are the consequences of difunctional enzymes in the fructose pathway
Fructokinase - no problem, fructose excreted in urine
| Aldose - fructose 1 phosphate builds up in the liver causing toxic damage
52
What is the galactose pathway
Galactose - Galactose 1 phosphate - Glucose 1 phosphate - Glucose 6 phosphate - Glycolysis
Enzymes - galactokinase and galactose 1-P uridyl transferase
53
What are the consequences of enzyme deficiencies in the galactose pathway
galactokinase - increase in galactose which is forced into the galactitol pathway
glactose 1-P-uridyl transferase - galactose 1 phosphate builds up in liver causing disease and build up of galactose
54
What are the consequences of increased galactose
galactose converted into galactitol. Using NADPH in NADP+. By aldose reductase
NADPH is important in creating reduced glutathione, which prevents formation of inappropriate disulphide briges. So without it can cause cataracts in the eye
55
At what stage in glycolysis can the pentose pathway begin? what is the purpose of the pentose pathway?
Stage 1 - glucose 6 phosphate to C5 sugar?
Produces reducing power NADPH required for lipogenesis and glutathione reduction
Produces C5 sugars for nucleotides
56
What enzyme works on the pentose 5 pathway
glucose 6 phosphate dehydrogenase
57
What are the products of each rotation of the Kreb's cycle
3 NADH, 1 FADH2, 1 GTP, oxoacetate, 2 CO2
58
What are the 2 irreversible steps in the Kreb's cycle and the enzymes that regulate them
Isocitrate - ketoglutarate & amp & CO2 = isocitrate dehydrogenase
Ketoglutarate - Succinyl CoA = keoglutarate dehydrogenase
59
What effects the rate of reaction in the Kreb's cycle
ADP - activates isocitrate dehydrogenase
ATP/ NADH - inhibit isocitrate dehydrogenase and ketoglutarate dehydrogenase
60
What are the products of the Kreb's cycle used for
citrate = fatty acids
ketoglutatrate / malate = amino acids
FADH NADH2 = carriers of reducing power in electron transport chain
61
Where does glycolysis, Kreb's cycle, and Electron Transport Chain take place
cytoplasm, matrix of mitochondria, inner membrane of mitochondria
62
Where does the fructose, galactose and pentose 5 sugar metabolism take place in the cell.
liver, liver, all cells but mostly liver - all take place in cytoplasm
63
What enzyme converts pyruvate to acetyl CoA, where is it found and what does it produce
pyruvate dehydrogenase, takes pyruvate into the mitochondria, produces CO2 and NADH + H
64
Pyruvate dehydrogenase is activated and inhibited by what products
Activated by - ADP, NAD+, Insulin, Pyruvate
| Inibited by - ATP, NADH, Glucagon, Acetly CoA
65
What is the difference between substrate and oxidative phosphorylation
substrate - direct transfer of phosphate group to ADP or GDP, happens in cytoplasm, not oxygen dependent, produces less ATP
oxidative - happens on inner membrane of mitochondria, using energy from electrons to generation a proton motive force that activate ATP synthase, requires oxygen, produces more ATP
66
How many ATP molecules do the reducing agents create
NADH - 2.5 ATP
FADH2 - 1.5 ATP
67
What is the molecule that transports protons across the inner membrane of the mitochondria
proton translocating complext - 3 types
ATP synthase - inward bound
The inner membrane of the mitochondria is highly impermeable to protons.
68
What regulates the proton transport chain
Build up of ATP, lowers ADP, meaning less H+ can re-enter the matrix build up of H+ on intermembrane space is such that hydrogen pumping trhrough proton translocating membrane ceases
69
What inihibits the oxidative phosphorylation
cyanide - blocks one of the proton translocating complexes preventing the passage of electrons to oxygen.
CO - blocks provision of oxygen
70
What are uncouplers and give examples
They separate the proton translocating complex from the ATP synthase. By increasing the permeability of the inner mitochondial membrane.
Thermogenin, UCP 1, dinitrophenol
Common in brown adipose tissue and hibernating animals to produce heat
71
What are the essential amino acids
Isoleucine, leucine, threonine, histidine, lysine, methionine, phenylalanine, tryptophan, valine
72
What is transamination
Exchange of and amino group between an amino acid and keto acid, creating a different amino acid. Uses an aminotransferase enzyme - example alanine transaminase, aspartate transaminase
Alpha ketoglutarate - glutamate
Oxaloacetate - aspartate
73
What is deamination, and give example
Removal of amino group from amino acids for excretion
Glutamine - Glutamate - ketoglutarate
74
GIve two examples of amino acid clinical problems
Phenylketonuria: Phenylalanine - tyrosine, using phenylalnine hydroxylase. High phenylalanine causes mental retardation by inhibitin mitochondrial metabolism. Detected in urine, or heel prick of new borns.
Homocystinuria: Homocysteine - Cystathionine, by cystathionine beta synthase. High homosysteine damages connective tissue, CNS, muscle.
75
What are the two ways of processing ammonia and transporting it in the blood
Glutamate + ammonia = glutamine in tissues safe to transport in blood, used in liver to convert to urea or excreted in kidneys
Pyruvate + ammonia = alanine
76
What are the advantages of urea?
Non toxic, metabolically inert, high nitrogen content, soluble, chemically inert
77
What is the urea cycle inputs
glutamate and aspartate
78
what are the dangers of ammonia
extremely toxic to brain, readily dissolvable, alters pH, effects Kreb's cycle, metabolism
79
What is refeeding syndrome
When patients are severly malnourished, they have insufficient protein and exnzymes to process amino acids into safe urine. Consequently ammonia levels increase severely. This can cause death, BMI
80
Give uses for 5 amino acids
```
Histidine - histimine
Cystein - glutathione
Arginine - nitric acid
Glycine - hae
Tyrosine - Thyroid hormones
```
81
What are apoproteins
They are proteins that provide structural support to phospholipid bilayers, and idenitify the vessicles and act as cofactors.
82
What are lipoproteins
Phospholipid vesicles, with apoprotein structural units containing a hydrophobic lipid core
83
Where are lipoprotein lipases found and what interacts with them
On capillary walls, interact with apo C on chylomicrons, VLDL, IDLs
84
How is artherosclerosis caused
LDLs, lack Apo E and Apo C, they are not effectively cleared by the cells in the body. The cholesterol contents can get oxidised, as they hang in the blood for so long. The LDLs are then consumed by macrophages, which turn into foam cells, causing a fatty streak in the intima of blood vessels, this can narrow the lumen, or burst and cause a MI/ stroke
85
What Apoproteins do HDL have and what are their purpose
ATP Binding Cassete Protein (ABCA1) needed on tissues to form and HDL with cholesteroll and it will transport the cholesterol to the liver for processing. Deliver to liver for use in producing bile, or steroidal cells producing hormones
86
Give two examples of hyperlipoproteinaemias
Type 1 - High chylomicrons, defective LPL
Type 2 - Defective LPL, high chance of artherosclerosis
Type 3 - High IDL and chylomicrons, defective Apo E
87
Give three symptoms of hypocholerstolaemia and three treatments
Xanthelasma - yellow eyelid blotches
Tendon Xanthoma - nodules on tendons
Corneal Arcus - white rings around iris
diet, exercise, cholesterol sequestration in diet, statins target HMG-CoA reductase
88
What disease are aused by oxidative stress
Mulitple Sclerosis, CVD, Parkinson's,, Arthritis, Alzheimers
89
What is a free radical and give examples
an atom with an inpaired electron - hydroxyl radical (most damaging), superoxide, nitric oxide
90
What damage can free radicals cause
DNA - misspairing of nucleotides, strand breaks, damage to the backbone
Protein - change structure, gain or loss - eg. create cysteine and inappropriate disulphide bonds
Lipids - bind ot unsaturated fatty acids creating lipid radicals - eg. lipid peroxyl radical. Last a long time in the blood
91
Soures of biological oxidation
Endogenous - electron transport chain, nitric oxide synthase, NADPH oxidase
Exogenous - radiation, pollutants, tobacco, toxins
92
What is a respiratoy burst
A release of free radicals by a phagocyte to destroy pathogens - typically using NADPH oxidase, Nitric oxide, and hydrogen peroxide
93
Name 4 different defences against free radicals in the body
Glutathione - in reduced from can accept free radicals to form a disulphide bridge between two cystein amino acids
Catalase - Catalase - hydorogen peroxide to water and oxygen
Vitamin E - prevents lipid peroxidation with the help of vit C
Superoxide dismutase converts super oxide to hydrogen peroxide and oxygen.
94
Two diseases that increase free radival vulnerability
Galactosaemia - causes Galactose to be converted to Glactitol by the enzyme aldose reductase. Using NADPH and preventing any for regenerating Glutathione
Glucose 6 posphate dehydrogenase non function - cannot produce pentose sugars from gluose 6 phosphate, so not creating NADPH.
Consequences Heinz bodies and anaemia from RBC, cataracts
95
What are the consequences of Paracetamol
Excess paracetamol creates NAPQI - depletes gluthione and causes oxidative damage to the liver.
Antidote is acetylcysteine - regenerates the glutatione
96
give three examples of positive feedback in the body
ovulation, lactation, blood clotting
97
What is a zeitgeber
environmental stimuli - light, temperature, activity, diet
98
what is a suprachiasmatic nucleus
collection of neurons in the brain
99
What is an osmole
the amount of substance required to dissociate in water to form one mole of osmotically active particles
100
What is osmolality
the number of osmoles per kilogram of solution
101
How many litres of water in a 70kg man
42 L - 28L intracellular, 9.4L extracellular, 4.6L blood,
102
Give examples of 5 hormones produced by organs not glands
```
stomach - ghrelin, gastrin
Liver - IGF1
Adipose - Leptin
Kidney - Renin Calcitrol
Heart - ANP / BNP
```
103
What type of hormone are insulin and glucagon
small polypepetide, soluble hormones
104
What are examples and characteristics of amino acid hormones
adrenaline, noradrenaline, thyroid - former water soluble latter lipid soluble.
105
Give examples of glycoprotein hormones and their character
Large, water soluble - Lutenizing hormone, Follicle stimulating hormone, thyroid stimulating hormone
106
What are the advantages of binding proteins to non-soluble hormones
Increase solubility, half life and accessability.
107
What are the differences between the water soluble hormones and lipid soluble hormones
Cannot cross the plasma membrane for water soluble hormones, require carrier protein. Eg. G-protein for adrenaline and Insulin for Tyrosine Kinase
108
What is the region of the skull that holds the pituitary gland
sella turcica
109
What does the hypothalmic / pituitary axis control
growth, lactation, reproduction, adrenal gland, thyroid gland, water , puberty
110
Where does the pituitary develop from
anterior pituitary - ectoderm
| posterior pituitary - nervous system
111
What are tropic hormones and their examples
They effect the release of other hormones. Released from anterior pituitary gland, following neurosecretory stimulation from the hypothalamus.
thyrotropin releasing hormone - thyroid stimulating hormone
cortiotropin releasing hormone - adenocorticotropic hormone
prolacti releasing hormone - prolactin
112
what is diabetes
chronic hyperglycaemia
113
List the main differences between Type 1 and Type 2 diabetes
Type 1 - in young people, rapid onset, destruction of beta cells, treated with insulin
Type 2 - generally occurs in middle age, gradual onset, simultaneous loss of beta cells and tissue resistance to insulin, initially untreatable with insulin
114
What are the genetic markers for diabetes type 1 and symptoms and diagnostic
polydipsia, polyuria, weight loss - HLA DR3 and HLA DR4
115
what are the symptoms of ketonacidosis
hyperventilation, prostration, nausea, vomiting, dehydration
116
what are the symptoms of type 2 diabetes
polydipsia, polyuria, weight loss
tiredness, lethargy, persistent infections, infected feet.
117
what are the diagnostic blood tests for diagnosing diabetes
>7mMol fasting
| >11.1mMol/L random
118
Name two medicines for type 2 diabetes and their function
Metformin - decrease insulin resistance and decrease gluconeogenesis
Sulphonureas - increase insulin release from pancreas cells
119
what level of HBA1c suggests hyperglycaemia
>10% glycated HBA1c
120
what are the consequences of hyperglycaemia
high glucose creates sorbitol via aldose reductase, using NADPH, which can no longer be used for reducing glutathione and protecting against disulphide bridges.
Macrovascular - stroke, MI, poor circulation
Microvascular -
retinopathy weak vessels burst,
glaucoma (change in osmotic pressure of the eye),
nephropathy (decrease blood vessel diameter and infection), neuropathy (change in micro blod vessels for neurons)
diabetic feet (poor blood supply)
121
What is the structure of insulin and how is it produced and released
alpha and beta chain, 3 disulphide brides, 110amino acids long.
preproinsulin chain in ER
proinsulin in Golgi apparatus
storage granules Insulin and c peptide
secretion - high glucose, absorbed through GLUT2, increase ATP, open ATP sensitive K+channels, depolarsing cell releasing Ca2+, releasing granules.
122
At what stage in glycolysis can the pentose pathway begin? what is the purpose of the pentose pathway?
Stage 1 - glucose 6 phosphate to C5 sugar?
Produces reducing power NADPH required for lipogenesis and glutathione reduction
Produces C5 sugars for nucleotides
123
What enzyme works on the pentose 5 pathway
glucose 6 phosphate dehydrogenase
124
What are the products of each rotation of the Kreb's cycle
3 NADH, 1 FADH2, 1 GTP, oxoacetate, 2 CO2
125
What are the 2 irreversible steps in the Kreb's cycle and the enzymes that regulate them
isocitrate - ketoglutarate & CO2 = isocitrate dehydrogenase
ketoglutarate - Succinyl CoA = keoglutarate dehydrogenase
126
What effects the rate of reaction in the Kreb's cycle
ADP - activates isocitrate dehydrogenase
| ATP/ NADH - inhibit isocitrate dehydrogenase and ketoglutarate dehydrogenase
127
What are the products of the Kreb's cycle used for
citrate = fatty acids
ketoglutatrate / malate = amino acids
FADH NADH2 = carriers of reducing power
128
Where does glycolysis, Kreb's cycle, and Electron Transport Chain take place
cytoplasm, matrix of mitochondria, inner membrane of mitochondria
129
Where does the fructose, galactose and pentose 5 sugar metabolism take place in the cell.
liver, liver, all cells but mostly liver - all take place in cytoplasm
130
What enzyme converts pyruvate to actyl CoA, where is it found and what does it produce
pyruvate dehydrogenase, takes pyruvate into the mitochondria, produces CO2 and NADH + H
131
Pyruvate dehydrogenase is activated ad inhibited y what products
Activated by - ADP, NAD+, Insulin, Pyruvate
| Inibited by - ATP, NADH, Glucagon, Acetly CoA
132
What is the difference between substrate and oxidative phosphorylation
substrate - direct transfer of phosphate group to ADP or GDP, happens in cytoplasm, not oxygen dependent, produces less ATP
oxidative - happens on inner membrane of mitochondria, using energy from electrons to generation a proton motive force that activate ATP synthase, requires oxygen, produces more ATP
133
How many ATP molecules do the reducing agents create
NADH - 2.5 ATP
| FADH2 - 1.5 ATP
134
What is the molecule that transports protons across the inner membrane of the mitochondria
proton translocating complext - 3 types
ATP synthase - inward bound
The inner membrane of the mitochondria is highly impermeable to protons.
135
What regulates the proton transport chain
Build up of ATP, lowers ADP, meaning less H+ can reenter the matrix build up of H+ on intermembrane space is such that hydrogen pumping trhrough proton translocating membrane ceases
136
What inihibits the oxidative phosphorylation
cyanide - blocks one of the proton translocating complexes preventing the passage of electrons to oxygen.
CO - blocks provision of oxygen
137
What are uncouplers and give examples
They separate the proton translocating complex from the ATP synthase. By increasing the permeability of the inner mitochondial membrane.
Thermogenin, UCP 1, dinitrophenol
Common in brown adipose tissue and hibernating animals to produce heat
138
What are the essential amino acids
Isoleucine, leucine, threonine, histidine, lysine, methionine, phenylalanine, tryptophan, valine
139
What is transamination
Exchange of and amino group between an amino acid and keto acid, creating a different amino acid. Uses an aminotransferase enzym - example alanine transaminase, aspartate transaminase
Alpha ketoglutarate - glutamate
Oxaloacetate - aspartate
140
What is deamination, and give example
Removal of amino group from amino acids for excretion
Glutamine - Glutamate - ketoglutarate
141
GIve two examples of amino acid clinical problems
Phenylketonuria: Phenylalanine - tyrosine, using phenylalnine hydroxylase. High phenylalanine causes mental retardation by inhibitin mitochondrial metabolism. Detected in urine, or heel prick of new borns.
Homocystinuria: Homocysteine - Cystathionine, by cystathionine beta synthase. High homosysteine ddamages connective tissue, CNS, muscle.
142
What are the two ways of processing ammonia and transporting it in the blood
Glutamate + ammonia = glutamine in tissues safe to transport in blood, used in liver to convert to urea or excreted in kidneys
Pyruvate + ammonia = alanine
143
What are the advantages of urea?
Non toxic, metabolically inert, high nitrogen content, soluble, chemically inert
144
What is the urea cycle inputs
glutamate and aspartate
145
what are the dangers of ammonia
extremely toxic to brain, readily dissolvable, alters pH, effects Kreb's cycle, metabolism
146
What is refeeding syndrome
When patients are severly malnourished, they have insufficient protein and exnzymes to process amino acids into safe urine. Consequently ammonia levels increase severely. This can cause death, BMI
147
Give uses for 5 amino acids
```
Histidine - histimine
Cystein - glutathione
Arginine - nitric acid
Glycine - hae
Tyrosine - Thyroid hormones
```
148
describe glucagon and its effects
29 amino acids in length, produced by alpha cells in the pancrease, no dsulphde bridges, amino acid hormone
increases glycogenlysis, gluconeogenesis, ketogenesis, lipolysis
inhibits lipogenesis
149
What are the three regions of the adrenal cortex and their products
zona glomerulosa - mineralcorticcoids - salts Na+/K+, aldosterone
zona fasciculata - glucocorticcoids - sugars, cortisol
zona resticularis - androgens - glucocorticoids testosterone
150
Describe the adrenal cortex axis
1- hypothalamus detects pain, heat, emotion releases CRF corticotropin releasing factor
2- anterior pituitary responds by releasing 29 aa Adrenocorticotropic Hormone (from POMC)
3 - ACTH reacts with receptors on zona fasiculata and reticularis of the the adrenal gland
4, stimulates cholesterol esterase, producing cortisol
151
What are the effects of cortisol
increase proteolysis, glycogenlysis, gluconeogenesis, lipolysis
decrease glucose absorption in blood by blocking GLUT4
Stress hormone, increases metabolites
152
What are the catecholamines
adrenal hormones from the medulla, a modified symptathetic ganglion
153
What are the effects of adrenaline and where is it synthesised from
increase CNS, cardiovascular, glycogenlysis, lipolysis
Origin is tyrosine
154
What is Addion's disease
low cortisol - lethargy, postural hypotension, low glucose, low
In some case ACTH may be expressed at high level without stimulating cortisol but causing pigmentation of the skin. Melanocyte Stimulating Hormone MSH, is part of the ACTH
155
What is Cushing's disease
Chronic high coritsol - moon face, buffalo hump, hypertension, striae, muscle wasting in the limbs, mood swings. Cortisol causes redistribution of fat in body.
caused excess ACTH, cortisol or external steroid influence
156
What is exogenous cushing's and an example of a causative
A source of steroid that mimics the effects of elevated cortisol taken. Often anti-inflammatory drugs fro arthritis, asthma, inflammatory bowel disease
eg. dexamethasone /Prednisolone
157
How do you diagnose Cushing's
Look at natural ACTH and cortisol cycle. Test reaction to anacthen (ACTH analogue) and dexamethosone (cortisol analogue)
158
What are the two types of cells in the thyroid
follicular cells - T3/T4
| parafollicular cells - calcitonin
159
How is T3 and T4 created
Tysoine is taken into follicular cells
Converted into thyroglobulin
Thyroglobulin is sereted into the colloid of the cell
Iodinating species are also concentrated in the colloid
Iodination of thyroglobulin creates Mono iodotyrosine or Di-iodotyrosine (MIT and DIT). Form together to make T3 and T4
160
How is coritsol spread around the body
transcortin, overcomes hydrophobic nature of crotisol. Cortisol crosses cell membrane and enters the nucleus
161
What stimulus produces T3 and T4
stress and temperature, causes hypo to release thyrotropin releasing hormone TRH, which stimulates ant pit to release thyroid stimulating hormone TSH
162
What are the characteristics of TRH and TSH
TRH is a tri-peptide hormone
| TSH is a glycoprotein, 2 sub-units
163
How are T3 and T4 transported
thyronine binding globulin, albumin, pre-albumin. When bound to the carrier, it is not biologically active.
164
What are the metabolic effects of T3 and T4
General increase in metabolism across the body. Increase BMR, glucose uptake, lypolysis, protein metabolism, heat production, bone production
165
How do T3 and T4 work
Directly effect the DNA of the cell, receptos have a greater affinity for T3 than T4. Ratio of 1:10. Generally increase metabolism
166
Describe Hashimoto's Disease
1% of population - destruction of thyroid follicular cells, espcially TSH receptors. Symptoms - lethargy, mood swings, cold intolerance, constipation, brittle skin, ataxia
167
Describe consequences of low thyroid hormone in childhood
Cretinism - lack of thryoid hormone, leads to large tongue, pronounce brown, poor eyes, short stature and mental retardation. Effects neural development in children
168
Causes of hypothyroidism
destruction of thyroid gland, congenital defect, lack of TSH, lack of iodine
169
Describe Hyper thyroidism
Grave's disease - 1% population, autoimmune disease, antibody constantly stimulates TSH receptor. Thyroid stimulating immunoglobulin. Syptoms- high heat, bulging eyes, tachycardia, rapid bowel movements, weight loss.
170
What is the treatment of hyperthyroidism
carbimazole inhibits thyroglobulin, radioactive iodine obliterates thyroid, surgical removal of the thyroid
171
What are the functions of the parathyroid gland
Regulate calcium serum levels closely between 1-1.3mol / L
172
What regulates serum calcium levels
parathyroid hormone PTH, vitamin D, calcitonin
173
What are the symptoms of hypocalaemia
Hyperexcitability, tetany, paralysis, convulsions
174
What are the symptoms of Hypercalcaemia
kidney stones, constipation, depression, tiredness
175
How can tumours effect calcium levels
Common breast and pancreatic tumours release PTHrP - parathyroid hormone related peptide
176
What are the differences between PTH and Vitamin D (calcitrol) effects on calcium.
Both increase osteoclasts to release calcium from bone hydroxy apatite
PTH stimulates Vit D to increase Ca uptake in the gut
PTH increases reabsoption of Ca in kidneys, Vit D increases reabsorption of Ca and K in kidneys.
PTH increases blood Ca, Vit D increases serum Ca and K
177
What is Ricket's
A deficiency in dietary Ca leading to Ca serum levels maintained at the expens of bone. Symptoms - bony necklace, bow legs, soft kull, lumpy joints
178
Where is Ca absorbed
In the gut, jejunum and ileum mainly, chaperoned across gut epithelia by the Vit D
179
What are the three regions of the adrenal cortex and their products
zona glomerulosa - mineralcorticcoids - salts Na+/K+, aldosterone
zona fasciculata - glucocorticcoids - sugars, cortisol
zona resticularis - androgens - glucocorticoids testosterone
180
Describe the adrenal cortex axis
1- hypothalamus detects pain, heat, emotion releases CRF corticotropin releasing factor
2- anterior pituitary responds by releasing 29 aa Adrenocorticotropic Hormone (from POMC)
3 - ACTH reacts with receptors on zona fasiculata and reticularis of the the adrenal gland
4, stimulates cholesterol esterase, producing cortisol
181
What are the effects of cortisol
increase proteolysis, glycogenlysis, gluconeogenesis, lipolysis
decrease glucose absorption in blood by blocking GLUT4
Stress hormone, increases metabolites
182
What are the catecholamines
adrenal hormones from the medulla, a modified symptathetic ganglion
183
What are the effects of adrenaline and where is it synthesised from
increase CNS, cardiovascular, glycogenlysis, lipolysis
Origin is tyrosine
184
What is Addion's disease
low cortisol - lethargy, postural hypotension, low glucose, low
In some case ACTH may be expressed at high level without stimulating cortisol but causing pigmentation of the skin. Melanocyte Stimulating Hormone MSH, is part of the ACTH
185
What is Cushing's disease
Chronic high coritsol - moon face, buffalo hump, hypertension, striae, muscle wasting in the limbs, mood swings. Cortisol causes redistribution of fat in body.
caused excess ACTH, cortisol or external steroid influence
186
What is exogenous cushing's and an example of a causative
A source of steroid that mimics the effects of elevated cortisol taken. Often anti-inflammatory drugs fro arthritis, asthma, inflammatory bowel disease
eg. dexamethasone /Prednisolone
187
How do you diagnose Cushing's
Look at natural ACTH and cortisol cycle. Test reaction to anacthen (ACTH analogue) and dexamethosone (cortisol analogue)
188
What are the two types of cells in the thyroid
follicular cells - T3/T4
| parafollicular cells - calcitonin
189
How is T3 and T4 created
Tysoine is taken into follicular cells
Converted into thyroglobulin
Thyroglobulin is sereted into the colloid of the cell
Iodinating species are also concentrated in the colloid
Iodination of thyroglobulin creates Mono iodotyrosine or Di-iodotyrosine (MIT and DIT). Form together to make T3 and T4
190
How is coritsol spread around the body
transcortin, overcomes hydrophobic nature of crotisol. Cortisol crosses cell membrane and enters the nucleus
191
What stimulus produces T3 and T4
stress and temperature, causes hypo to release thyrotropin releasing hormone TRH, which stimulates ant pit to release thyroid stimulating hormone TSH
192
What are the characteristics of TRH and TSH
TRH is a tri-peptide hormone
| TSH is a glycoprotein, 2 sub-units
193
How are T3 and T4 transported
thyronine binding globulin, albumin, pre-albumin. When bound to the carrier, it is not biologically active.
194
What are the metabolic effects of T3 and T4
General increase in metabolism across the body. Increase BMR, glucose uptake, lypolysis, protein metabolism, heat production, bone production
195
How do T3 and T4 work
Directly effect the DNA of the cell, receptos have a greater affinity for T3 than T4. Ratio of 1:10. Generally increase metabolism
196
Describe Hashimoto's Disease
1% of population - destruction of thyroid follicular cells, espcially TSH receptors. Symptoms - lethargy, mood swings, cold intolerance, constipation, brittle skin, ataxia
197
Describe consequences of low thyroid hormone in childhood
Cretinism - lack of thryoid hormone, leads to large tongue, pronounce brown, poor eyes, short stature and mental retardation. Effects neural development in children
198
Causes of hypothyroidism
destruction of thyroid gland, congenital defect, lack of TSH, lack of iodine
199
Describe Hyper thyroidism
Grave's disease - 1% population, autoimmune disease, antibody constantly stimulates TSH receptor. Thyroid stimulating immunoglobulin. Syptoms- high heat, bulging eyes, tachycardia, rapid bowel movements, weight loss.
200
What is the treatment of hyperthyroidism
carbimazole inhibits thyroglobulin, radioactive iodine obliterates thyroid, surgical removal of the thyroid
201
What are the functions of the parathyroid gland
Regulate calcium serum levels closely between 1-1.3mol / L
202
What regulates serum calcium levels
parathyroid hormone PTH, vitamin D, calcitonin
203
What are the symptoms of hypocalaemia
Hyperexcitability, tetany, paralysis, convulsions
204
What are the symptoms of Hypercalcaemia
kidney stones, constipation, depression, tiredness
205
How can tumours effect calcium levels
Common breast and pancreatic tumours release PTHrP - parathyroid hormone related peptide
206
What are the differences between PTH and Vitamin D (calcitrol) effects on calcium.
Both increase osteoclasts to release calcium from bone hydroxy apatite
PTH stimulates Vit D to increase Ca uptake in the gut
PTH increases reabsoption of Ca in kidneys, Vit D increases reabsorption of Ca and K in kidneys.
PTH increases blood Ca, Vit D increases serum Ca and K
207
What is Ricket's
A deficiency in dietary Ca leading to Ca serum levels maintained at the expens of bone. Symptoms - bony necklace, bow legs, soft kull, lumpy joints
208
Where is Ca absorbed
In the gut, jejunum and ileum mainly, chaperoned across gut epithelia by the Vit D
