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194 Cards in this Set
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Define diabetes mellitus |
An abnormal Metabollic state in which there is glucose intolerance due to inadequate insulin action |
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Where is insulin secreted from? |
Beta cells of islets of lagangerhams in the pancreas |
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Where is glucagon secreted from? |
Alpha cells in the pancreas |
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What stimulates the secretion of insulin? |
High blood glucose concentration |
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What inhibits the secretion of insulin? |
Epinephrine - think if it was fight or flight you would need more glucose to go to your muscles so we don't want it to be stored away |
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What stimulates the secretion of glucagon? |
Low blood glucose concentrations Increase in epinephrine (stress) |
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What inhibits the secretion if glucagon? |
Insulin. They act as opposites when one is high the other is low |
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The effect of insulin cancels the effect of glucagon, what do we call this? |
Counter-regulatory hormones Their secretion of insulin and glucagon mainly depends on blood glucose levels |
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How would insulin levels corresponds to glucose after a meal? |
Almost identical in shape and height |
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Define glycogenolysis |
The breakdown of glycogen in the liver to form glucose for the liver and skeletal muscle |
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Define glycogenesis |
The formation of glycogen from glucose |
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Define gluconeogenesis |
Production of glucose from non-carbohydrates |
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Define protein production |
Replenishment of cellular proteins |
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Define protein breakdown |
Breakdown of skeletal muscle |
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Define ketogenesis |
The production of ketones (a glucose alternative) made from the breakdown of fatty acids |
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What does TAG production involve? |
Triacylglyceride (fat stores in adipocytes) made from fatty acids and glycerol. Conversion of excess glucose |
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Define lipolysis |
Breakdown of triacylglycerides to fatty acids and glycerol |
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Explain the effect the Fed state will have on all of the previous metabolic pathways |
Increase glycolysis (liver) Increase in glycogenesis Decrease in glycogenolysis Decrease in gluconeogenesis Increase in protein production Increase in cellular glucose uptake Decrease in ketogenesis Increase in TAG production Decrease TAG breakdown (lipolysis) |
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Explain the effect the fasting state will have on the previous metabolic pathways |
Decrease in glycolysis Decrease in glycogenesis Increase in glycogenolysis Increase gluconeogenesis Decrease in protein production Increase in protein breakdown Decrease in cellular glucose uptake Increase in ketogenesis Decrease in TAG production Increase in TAG breakdown |
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Which type of food is the most calorofic? |
Fats |
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What happens to dietary nutrients that are surplus to immediate energy requirements? |
Converted to storage forms of energy (anabolic process) Fats, proteins and glycogen in the liver |
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Where can we get glycogen from during the fasting state? |
The liver (100g). We can't get it from the muscle (400g) as that glycogen can only be used in the muscle it can't be mobilised to the blood |
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What do triacylglycerides break down into? |
Fatty acids and glycerol |
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What can the products of lipolysis be used for? |
Glycerol - used to make glucose via gluconeogenesis FAs - oxidised and converted to ketones bodies in the liver |
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Explain how protein can be used as a energy source? |
Rapid breakdown into amino acids during initial fasting period. Amino acids can be de-aminated to form alpha ketogenic acids. They can enter Krebs cycle as Acetyl CoA. Glucogeneic amino acids can be converted to glucose. |
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What happens with proteins as an energy source after initial fasting? |
Slow breakdown of proteins In starvation loss of proteins leads to malfunction of vital organs |
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Why is it important that we have different energy sources? |
For humans to survive a prolonged fast period |
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What could happen if somebody had a glycogen storage deficiency? |
The people with this disease can become hypoglycaemic once they enter the fasting state |
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What does each trace represent? This shows glucose utilisation and starving time |
1 - dietary glucose 2 - glycogenolysis 3 - gluconeogenesis |
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What is the preferred energy source for the brain? |
Glucose |
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What are the back up sources of energy for the brain? |
Glucose (small) 3-hydroxybutyrate (large) Acetoacetate (both ketones bodies from fat breakdown) Amino acids (small) |
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During the Fed state where does glucose go? |
Brain for energy To make ATP in muscles and to make glycogen in skeletal muscle To make glycogen in the liver Undergoes glycolysis in the liver to produce fatty acids which are converted into TAG and then VLDL which are stored in adipose tissue. |
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Why are fats stored as TAG and not as fatty acids? |
Fatty acids are soluble and TAGs are insoluble so more can be packed into the same space |
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What does VLDL stand for? |
Very low density lipoprotein |
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Explain what happens during the fasting state |
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In which type of diabetes mellitus would you expect to see ketones? |
Type 1 due to the complete absence of insulin |
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How are ketones produced? |
The fatty acids from TAG breakdown form Acetyl CoA and this can then form ketones bodies |
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Where can ketones be used? |
In Krebs cycle where they can produce energy They can act as an energy source for the brain Produce acetone in the breath and ketones can be detected in the urine They can't be used in the liver |
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Name the three ketones bodies |
3-hydroxybutyrate Acetoacetate Acetone (not used) |
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What bonds are in glycogen? Briefly describe their structure |
Alpha 1-4 and alpha 1-6 glycosidic bonds. They are highly branched so that they are easily hydrolysed, increases space for enzyme activity |
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Approximately how much glycogen is in the liver? How much is in the muscle? What are the functions of each? |
Liver glycogen 100g in well fed liver Rapidly mobilise Rapidly depleted during fast Main role to maintain blood glucose levels during initial period of fast Muscle glycogen 400g Main role to provide energy to muscle during strenuous exercise |
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What promotes glycogenesis? |
Insulin |
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What promotes glycogenolysis? |
Glucagon |
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Explain how we would go from glucose to glycogen |
Enzymes Phosphoglucomutase UDP-glucose pyrophosphorylase Glycogen synthase |
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Why is glycogenolysis not the opposite of glycogenesis? |
Some of the reactions are irreversible so an enzyme called glycogen phosphorylase is needed to go from glucagon to glucose 1-P |
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What do glycogen synthase and glycogen phosphorylase do? |
Glycogen synthase - synthesises glycogen in the Fed state Glycogen phosphorylase - breakdown if glycogen in the fasting state |
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Explain the effect insulin and glucagon have on glycogen synthase and glycogen phosphorylase |
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Draw the squares to help |
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Roughly how long can glycogen produce glucose for in the absence of a carbohydrate? |
10-18 hours |
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What are the three substrates for gluconeogenesis? |
Oxaloacetate (Alpha ketoacids) Glycerol Lactate |
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Where does gluconeogenesis occur? |
Cytosol and mitochondria )mainly in the liver) |
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Does gluconeogenesis require energy? |
Yes it is a Catabolic process. The energy comes from FA oxidation |
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Explain how each gluconeogenesis substrate is converted into something useful |
Lactate - taken up by the liver and converted to pyruvate (Cori cycle) Glycerol - hydrolysis of TAG in adipose tissue. Taken up by the liver and converted to dihydroxyacetone (DHAP) Alpha-ketoacids - glucogenic amino acids can e converted in to oxaloacetate which can be converted to phosphenol pyruvate |
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What other organ can also undergo gluconeogensis? |
The Kidneys but only in very late stages of fasting |
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During FA synthesis, what happens to excess Acetyl CoA? |
Acetyl CoA from the mitochondria exported to cytoplasm and carboxylated to malonyl CoA (3C) by Acetyl CoA carboxylase (ACC) |
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What 3 things control AAC production? |
Activated when insulin levels are high Activated by citrate (excess energy) Inhibited by fatty acids (end product of FA synthesis) |
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Where does FA synthesis occur? |
Cytosol of the liver |
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How are fatty acids synthesised? |
FAs are synthesised from excess Acetyl CoA produced from excess carbohydrate catabolism |
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What enzyme catalyses the reactions in FA synthasis? |
Fatty acid synthase in the cytosol of the liver |
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What acts as the reducing power for fatty acid synthesis? |
NADPH the reduced form of NADP+ Nictinomide adenine denucleotide phosphate. NADPH is produced by the before monophosphate pathway |
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During fatty acid synthesis how are the chains lengthened? |
Continuous addition of malonyl CoA. This lengthens the FA chains |
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What do the newly formed fatty acids then combine with thlo be stored? |
Glycerol to form TAG. Liver Tags are packed into VLDLs and exported to adipocytes |
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What enzyme is needed to breakdown TAG? What activated this enzyme? |
Hormone Sensitive lipase Intracellular enzyme Activated epinephrine, norepinephrine from sympathetic nerve endings and glucagon |
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Where are the products of TAG breakdown transported to? |
Glycerol transported to the liver for gluconeogenesis FAs bind to albumin in the plasma and are transported into the blood where they can enter cells. |
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FAs have variable chain lengths, what are they? |
VLCFA >22 Carbons LCFA 12>22 Carbons MCFA 6>12 SCFA <6 |
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Where can FAs go after they're released? |
Enter Krebs cycle as Acetyl CoA in most tissues Acetyl CoA can be converted to ketones bodies in the liver They cannot go into the brain as fatty acids as they cannot cross the blood brain barrier. Only ketones bodies can do this |
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Depending on the lengths of the chains how do the fatty acids migrate into the tissues? |
VLCFA can't be transported into the mitochondria, they are degraded by peroxisome to shorter Far. LCFA transported into the mitochondrial matrix via the carnitine shuttle and activated to FAcyl CoA. MCFA and SCFA can diffuse through the mitochondrial membrane and are activated to FAcyl CoAs in the mitochondrial matrix. |
Think about whether they can get through the mitochondrial membrane |
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Explain briefly Beta oxidation of FAs |
It is oxidised by NAD+ and FadH and Acetyl CoA is lost. So the original fatty acid chain is reduced by two carbons |
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What would happen in beta oxidation if the person has a defect that means they can't break down MCFAs? |
They have to remain in the Fed state as they can't break down FAs to provide energy via ketogenesis |
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Describe protein metabolism in the Fed state |
Amino acids to to all tissues, skeletal muscle for protein synthesis. They also go to the liver for protein synthesis but also go on to make pyruvate - this makes glycogen. Acetyl CoA can also be made this can go on to make fatty acids and TAG which can be stored in adipose tissue |
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Describe protein metabolism in the fast state |
Skeletal muscle protein is broken down to provide amino acids. These amino acids can then make pyruvate which can enter glycolysis and form glucose or Acetyl CoA which can be oxidised to form ketones bodies |
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Why is ketoacidosis specific to type 1 diabetics? |
Ketoacidosis because the ketones bodies are produced as there is no insulin the body is tricked into thinking that it is fasting, so it breaks down amino acids and fats. As there is still lots of glucose in the blood the ketones aren't used they build up and cause the blood pH to lower |
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What us the front line pharmaceutical treatment for diabetes mellitus type 2? |
Metformin - associated with no net weight gain so it's perfect for overweight/obese patients with type 2 diabetes |
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State some consequences of over-nutrition |
CVS Musculoskeletal disorder Hypertension Lower self-esteem Heart problems Death |
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What are the BMI ranges for being underweight, healthy, overweight, obese? |
Underweight <20 Health weight 20-25 Overweight 25-30 Obese 30-40 Morbidly obese >40 |
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What are the main health problems that increase in risk when you're obese? |
Sleep apnea Type 2 diabetes Insulin resistance Dyslipidemia (high cholesterol) |
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What are the two types of obesity? |
Central obesity - associated with Metabollic syndrome, organs are jam packed with white fat. Higher risk of negative outcomes Apple's and pears - lower body obesity, they may be metabolically normal |
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What is this first line of treatment for diabetes mellitus type 2 patients? |
Lifestyle change - diet and exercise |
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We have exciters and inhibitors that affect how much we eat can you name any (general name)? |
Appetite stimulators lipostat-measures fat stores Ergostat-measure energy stores Satiation mechanisms |
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What part of the brain is for short term satiety? |
The brain stem |
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What part of the brain is in control to the long term response to calorie restriction? |
The hypothalamus - control of laying down fat stores |
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How do we know that the hypothalamus controls appetite? |
Injury to the hypothalamus has lead to change in behaviour towards food and the weight of patients |
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How does the brain stem control feeding (short term)? |
Controls feeding via the caudal nucleus of the solitary tract (NTS). In response to GI, circulatory and central cues |
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How does the hypothalamus controls appetite? |
Paraventricular nucleus - regulates appetite and energy balance Arcuate nucleus (ARC) - critical for food intake regulation |
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Explain how the arcuate nucleus stimulates and suppresses appetite |
NPY neurons - utilise peptides such as NPY and AgRP to stimulate appetite POMC/CART neurons utilise peptides to suppress appetite |
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Where does the paraventricular nucleus get an input for? |
Arcuate nucleus Also input from glucose sensors within the brain stimulate release of Vasopressin and corticotrophin-releasing hormone from parvocellular neurosecretaty cell |
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Name some appetite stimulators |
Neuropeptide Y Agouoti Related Peptide Ghrelin Orexin |
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Name some appetite supressors |
Leptin Peptide YY Glucagon like peptides 1 (GLP-1) alpha melanocyte - stimulating hormone Endorphins TNF, CRH inflammatory mediators |
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When might there be an increase NPY? |
After short term food deprivation In an animal preparing for hibernation In genetic models of obesity |
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What glands are affected by the release of NPY as a result of calorie restriction? |
Gonads - decrease in reproductive function Adrenal glands Thyroid (decrease in thermogenosis) |
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Does obesity have anything to do with genetics? |
People can have a polygenic predisposition to obesity or a monogenic obesity (rare) - for example a leptin deficiency |
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What are the functions of leptin? |
Alters fertility and puberty Measures fat stores Alters metabolic response to pregnancy and lactation |
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What are the main ideas for insulin resistance? |
Individuals mass: Same amount of insulin but in a greater volume Molecular mechanism: Insulin receptor adapts to high levels of insulin Leptin resistance: Leptin signalling is disrupted |
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Pathologically what is the main difference between diabetes mellitus type 1 and type 2? |
Type 1 produce no insulin to damage to the beta cells in their pancreas. Type 2 diabetics tens to produce insulin but due to the high levels of glucose in their blood their insulin receptors become intolerant to it |
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What is the difference that you would see between type 1 and type 2 patients? |
Type 1 patients would generally be much younger (children) Type 2 patients are generally overweight or obese and will be middle aged or older |
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What does the binding of insulin to insulin receptors do? |
It promotes the mobilisation of Glut4 channels to the membrane so that glucose can be taken in to cells |
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Why might a diabetic have glucose in their urine |
Either the absence of insulin or increase insulin resistance will mean that bone or fewer Glut4 transporters will migrate to the membrane so the glucose remains in the blood. When this glucose reaches the kidney it will surpass the renal threshold and end up in the urine |
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If we were to check insulin levels and antibodies how might this help us to decide between type 1 and type 2 diabetics |
Type 1 Insulin levels - low Antibodies may also be present Type 2 Insulin levels - high No antibodies will be present |
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Describe the clinical features of type 1 |
Type 1 "Acute" Young age Marked symptoms- weight loss, strong thirst (polydipsia) No family history No complications at time of diagnosis May present as an emergency |
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Describe the clinical features of type 2 diabetes |
Insidious Older and middle age May have no symptoms Family history usually positive May present with or because of complications |
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What medication can cause diabetes? |
Steroids - used to treat inflammatory diseases like asthma, COPD, IBS, Rheumatoid arthritis, Cancer. Pancreatitis or pancreatic surgery Cushings syndrome |
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How does hereditary of autoimmune diseases work? |
It isn't the specific autoimmune disease that is passed on it is more to do with the fact that the family has an autoimmune disease. E.g. the mum may have rheumatoid arthritis and the daughter type 1 diabetes |
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What does MODY stand for (type of monogenic diabetes) |
Maturity onset diabetes of the young |
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Explain gestational diabetes briefly |
The hormones produced during pregnancy increase insulin resistance causing gestational diabetes. More like I'm women who are overweight/obese women, people who have a family history or personal history of gestational diabetes or people from certain ethnic backgrounds |
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What can happen if a baby is born with a mother who has gestational diabetes? |
Large babies and a difficult labour Risk factor for type 2 diabetes |
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What is the fasting plasma glucose concentration for a diabetic? |
>7.0mmol/l Normal <6.1mmol/L |
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What is the random plasma glucose concentration for a diabetic patient? |
>11.1mmol/l |
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Can we use blood glucose monitors to diagnose someone? |
No they aren't accurate enough. The quality control is insufficient due to the consequences of being labelled with diabetes |
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What urine test can we do to decide between type 1 and type 2 diabetics? |
Dipstick test and check for ketones if they are present the patient is a type 1 diabetic |
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What is Hb A1C? How can it be used diagnostically? |
Hb A1C > 40mmol/mol shows chronic hyperglycaemia. The red blood cells are freely permeable to glucose molecules so glucose irreversible binds to Hb A1C to form glycolated haemoglobin. |
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What does a Hb A1C test tell us? |
Glucose levels of the patient over the last 2-3 months |
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How does the oral glucose tolerance test work? |
Drink 75g of glucose Blood test at baseline and 120 minutes Impaired glucose tolerance if >7.8mmol/L but less than 11.1mmol/L |
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What are the diagnostic values for gestational diabetes? |
A fasting plasma glucose level of 5.6mmol/L or above A 2 hour plasma glucose level of 7.8mmol/L |
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What can happen to blood vessels that is a direct result of diabetes? |
Endothelial cells take in glucose. These cells don't require insulin, this causes glycosylation of the blood vessels (narrowing of smaller vessels-type 2). This is a risk factor for CVS. |
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What diabetics do to prevent complications? |
Control their blood glucose levels |
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Explain the first type of insulin regime |
Fast acting insulin is taken twice a day with meals. This is pre-mixed |
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Explain the second type of dosing regime |
Intensive therapy 3 or more daily injections. 3 taken with each meal and one in the evening |
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What are the pros and cons of the intensive compared to the standard regime? |
Intensive therapy increase the risk of hypoglycaemia by 3x But it results in a large decrease in the incidence of long term complications |
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How can patients react negatively to insulin? |
Hypoglycaemia Headache Anxiety Vertigo Confusion Tachycardia Sweating Hypersensitivity - chronic inflammation round the site of injection |
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What are two types of insulin aensitizers? |
Biguanides Thiazolidinediones |
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What are the types of of secretagogues? |
Sulphonylureas Meglitinides Incretin analogues and DPP4 inhibitors |
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Name the two drugs that modify glucose absorption |
Alpha glucosidase inhibitors SGLT2 inhibitors - associated with UTI |
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What is the main type of biguanides? |
Metformin |
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Briefly how does metformin work? |
Decreases gluconeogensis and increases uptake of glucose in skeletal muscle |
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What are the main side effects of metformin? |
Gastrointestinal upset Nausea Vomitting Diarrhoea Abdominal pain Increases lactate production. Not suitable for renal patients or CKD |
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How do thiazplidinediones work? |
Activate gene transcription by binding to peroxisome proliferate activated receptors (PPAR). Promotes lipogenesis, decreases inflammation, increases cholesterol reflux Low risk of hypoglycaemia but it's potent at lowering Hb A1C levels. |
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What are the side effects of thiazplidinediones? |
Weight gain Bladder cancer Congestive heart failure due to water retention |
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How do sulfonylureas work? |
Constant presence of glucose me and that K+ channels are constantly open and so the membrane isn't depolarised. They block the potassium channels so that the cell can repolarise and insulin vesicles can migrate to the surface |
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State some side-effects of sulfonylureas |
Hypoglycaemia Weight gain GI upset Increased BP |
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What appetite suppressant does Incretin therapy include? |
Glucagon like peptide - 1 (GLP1) However it is rapidly metabolised by DPP4 and doesn't last long in the body |
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How could a DPP 4 inhibitor activate GLP - 1? |
It would stop GLP - 1 from being inactivated |
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How do alpha glucosidase inhibitors work? |
Mimic natural sugars and act as competitive inhibitors to reduce glucose absorption |
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What are the main disadvantages of alpha glucosidase inhibitors? |
Flatulence Abdominal cramps Bloating (glucose gets digested by the bacteria in the gut) Headaches |
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Describe the difference between essential and non-essential amino acids |
Essential amino acids can't be produced by the body they must be in the diet. Non-essential amino acids don't have to be in the diet as the body can produce them |
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Define substrate level phosphorylation |
The formation of ATP by transfer of a phosphate to ADP from another phosphorylated molecule |
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What are the uses for ATP? |
Muscle contraction Active transport Biosynthesis Cellular processes Adaptive thermogenosis |
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What are the two types of phosphorylation? What's the difference? |
Substrate level phosphorylation - ATP formed by the transfer of a phosphate group Oxidative phosphorylation - ATP produced by the oxidation of molecules |
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What acts as the final electron acceptor? |
Oxygen |
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What kind of reaction is ATP hydrolysis, exothermic or endothermic? |
Exothermic it releases 30.6KJ/mol |
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Why do we not fun out of ATP? |
Energy is used to form ADP and Pi but we also produce energy from the oxidation of fats, proteins and carbohydrate |
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What are the coenzymes called involved in respiration? |
NAD+ (Nicotinamide adenine dinucleotide) and FAD (flavin adenine dinucleotide) They are electron acceptor they become reduced |
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Write equations for the reactions that NAD+ and FAD undergo |
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NADH has a higher reducing potential than FADH2, what do i mean by that? |
Produces more ATP NADH produces 3 ATP molecules FADH2 produces 2 ATP |
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Is ATP a stable molecule? |
No, it prefers to be hydrolysed |
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What makes up sucrose? |
Fructose and glucose |
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Where is fructose processed? |
In the liver |
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Does fructose in the blood cause insulin secretion? |
No unlike glucose |
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What channel protein transports fructose? |
Glut 5 |
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What are the two main enzymes involved in fructose metabolism? What do they convert? |
Fructokinase - converts fructose to fructose-1-phosphate Aldolase B - converts fructose-1-phosphate to glyceraldehyde and dihydroxyacetone (DHAP) |
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What are glyceraldehyde and dihydroxyacetone then converted to? |
Glyceraldehyde-3-phosphate |
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What is it called if someone lacks the fructokinase enzyme? What does this mean clinically? |
Essential fructosuria. The patient can't digest fructose so they just get fructose in their urine. Mild condition |
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How is essential fructosuria inherited? |
Autosomal recessive |
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What can happen if you have an Aldolase B deficiency? |
Severe health complications. It results in a condition known as hereditary fructose intolerance. It causes lover damage and hypoglycaemia. |
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How is hereditary fructose intolerance inherited? |
Autosomal recessive |
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When does hereditary fructose intolerance become a problem? |
When the children are weaned from breast milk as they start to invest products containing fructose |
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What clinical features can patients with hereditary fructose intolerance have? |
Nausea Vomiting Abdominal distress Chronic growth restriction/failure to thrive Liver damage Hypoglycaemia |
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Why can patients with hereditary fructose intolerance get hypoglycaemia? |
They can convert fructose to fructose-1-phosphate as they still produce the fructokinase enzyme but they can't progress any further. The phosphate remains locked in the fructose-1-phosphate so it can't be used in other reactions to make ATP. This causes problems with glycolysis where ATP is needed so there's a decrease in glycolysis causing hypoglycaemia |
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Explain where the channels GLUT1- 4 transfer glucose to |
GLUT1 - RBCs GLUT2 - liver and kidney (in and out) GLUT3 - Neurons GLUT4 - Adipose tissue and skeletal muscle (numbers available increase with insulin) |
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Apart from facilitated diffusion how else can glucose be transported into cells? |
Co-transport: Na+/glucose or SGLT I'm the intestines |
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What's the difference between essential non-essential amino acids? |
Essential amino acids need to be taken in in the diet whereas non-essential amino acids can be synthesised by the body either by using the essential amino acids or other compounds in the body |
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What are the 3 main stages from large molecules to producing ATP |
Hydrolysis in to smaller monomers Conversion of building blocks to Acetyl CoA Oxidation of Acetyl CoA to produce ATP |
General terms not specific steps |
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What is the basic structure of an amino acid? |
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What happens to amino acids once they enter the cell? |
They are de-aminated. The amine group is removed and either goes on to make nitrogen containing compounds or urea (non-toxic). The carbon skeleton gets oxidised to form Acetyl CoA and goes on to make ATP |
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Where are the places that we can get amino acids from? |
Hydrolysis of dietary proteins Synthesis - non-essential amino acids Degradation of tissue proteins |
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Name some nitrogen containing compounds that there are in the body |
Cellular proteins Hormones Neurotransmitters Haemoglobin Cytochrome Melanin Nucleotides |
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How can amino acids be used as an energy source? |
They can be oxidised and converted to glucose and oxidised or stored as glycogen. They can also be converted to TAG (fat stores) or ketone bodies |
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The amino acid pool should always be in balance, what do we mean by this? |
Nitrogen intake= Nitrogen excretion |
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What are the 3 possible fates of amino acids once they enter the amino acid pool? |
Protein biosynthesis Biosynthesis of other nitrogen containing compounds Oxidation for energy and excretion of nitrogen atoms |
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What do we mean by positive nitrogen balance? Who would have this? |
When nitrogen intake is greater than excretion. Occurs during childhood and pregnancy - they are growing so they will use the extra amino acids so they don't need to be excreted |
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What do we mean by negative nitrogen balance? |
Nitrogen intake is less than nitrogen excretion -protein deficiency. This is pathological |
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What happens to excess amino acids? |
Catabolised to make energy (main site is in the liver) |
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What are the 2 steps involved in the removal of amino groups? |
Transamination Oxidative examination |
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Explain transamination |
Occurs in the cytosol and mitochondria of most tissues. Amine group is transferred to alpha-ketoglutarage forming glutamate and an alpha keto-acid. This is catalysed by aminotransferases |
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Explain oxidative deamination |
(Mainly liver and kidney) The amino group of glutamate is released forming alpha-ketoglutarate (reproduced from the first step) and ammonia. Catalysed by glutamate dehydrogenase. NAD is also reduced at this point |
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Is ammonia toxic? |
Yes it is a neurotoxin |
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What are the 2 types of alpha-ketoacids? |
Glucogenic and ketogenic |
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What's the difference between glucogenic and ketogenic alpha-ketoacids |
Glucogenic amino acids can be converted into pyruvate or Krebs cycle intermediates (they can as substrate of gluconeogenesis). Ketogenic amino acids Are converted to acetoacetate, Acetyl CoA or acetoacetyl CoA |
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How do we get rid of NH3? |
It can combine with glutamate to form glutamine catalysed by glutamine synthetase. It can also bind with pyruvate to make alanine. Alanine are transported to the liver, ammonia is removed and it's converted to urea via the urea cycle |
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Can you name any other nitrogen waste products that are in the urine? |
Uric acid from purine breakdown Free ammonia Creatinine |
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Does the liver usually struggle to maintain the urea cycle? |
No the urea cycle of the liver is normally well in excess of ammonia production. |
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What could cause hyperammonia? What would the effects be? |
Viral hepatitis Cirrhosis Acute excessive alcohol abuse Congenital hyper-ammonia Ammonia is a neurotoxin, excess leads to CNS related symptoms. Zit can lead to come, death, tremors, encephalopathy (brain damage), slurring |
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Define metabolism |
The chemical process by which cells produce the substances and energy need to sustain life |
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Which uses ATP and which makes ATP, anabolic or catabolic reactions? |
Anabolic - makes ATP Catholic - used ATP |
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What is adaptive thermogenosis? |
Generating heat without shivering |
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When fatty acids are oxidised what do we call this? |
Beta oxidation |
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Is oxidation catabolic or anabolic? |
Catabolic |
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Where is insulin secreted from? |
Beta cells of the isletsof langerhans in the pancreas |
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Where does glycolysis occur? |
Cytosol |
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What is the main function of glycolysis in the liver and adipose tissue? |
To convert glucose into TAG for storage |
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In other tissues what is the main function of glycolysis? |
To make ATP |
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What are the end products of glycolysis? |
2 pyruvate 2 NADH 2 ATP |
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What are the end products of glycolysis in anaerobic respiration? |
2 Lactate 2 ATP |
Per glucose molecule |
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What is key about stage 1 of aerobic glycolysis? |
It requires energy investment - 2 ATP molecules |
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What are the three key enzymes and steps that we need to know in glycolysis? |
Hexokinase (other tissue) and glucokinase (liver) - glucose to glucose-6-phosphate Phosphofructokinase-1 - converts fructose-6-phosphate to fructose-1,6-bisphosphate Pyruvate kinase (regulated only in the liver) - converts phosphoenolpyruvate to pyruvate |
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Which enzyme acts as the rate determining step? |
Phosphofructokinase-1 |
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