Altered pancreatic function & Diabetes Mellitus

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  • Created by: Becca
  • Created on: 26-12-13 15:35
How is glucose homeostasis maintained?
Insulin LOWERS blood glucose by increasing tissue gutilisation. Glucagon (+adrenalin/GH/cortisol) RAISES blood glucose by increasing glucose production
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What is the role of adrenaline, cortisol & growth hormone?
Adrenaline: provision of energy for emergencies & exercise (severe hypoglycaemia). Cortisol: mobilisation of fuels during adaptation to stress. Cortisol & growth hormones both used in prolonged hypoglycaemia
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What is ketogenesis? What inhibits & synthesises ketogenesis? What is the result of ketosis?
Synthesis of ketone bodies by the liver, from fatty acid breakdown products (ketosis = state of excess ketones). Inhibited by insulin & stimulated by gluagon -> metabolic acidosis (decreased blood pH due to acidic ketone bodies)
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What is the consequence of loss of insulin action?
Decreased glucose intake, lipolysis -> FFA + glycerol, protein breakdown -> AA. Liver: glycogen breakdown, gluconeogenesis: increased glucose, ketones (metabolic acidosis) & glucose (osmotic diuresis: filtered load exceed absorption maximum)
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What is diabetes mellitus? What causes it?
Chronic metabolic disorder characterised by hyperglycaemia caused by insulin deficiency (type 1, destruction of islet B-cells, autoimmune) or impaired beta-cell function and/or loss of insulin sensitivity (insulin resistance, type 2)
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What are the symptoms common to both type 1 & 2 diabetes? What is specific to each type?
Thirst, polyuria, glucosuria, fatigue, malaise, blurred vision & infections. Type 1: weight loss, ketoacidosis. Type 2: complications (secondary), altered mental status
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What conditions/diseases are secondary causes of diabetes?
Endocrine: Cushing's, acomegaly, phaeochromocytoma. Pancreatic disease: chronic pancreatitis, surgery, CF, tumour. Genetic disorders: Down's syndrome, Prader-Willi. Drug induced: steroids, beta-blockers, diuretics
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What are the aims of management for diabetics?
Alleviate symptoms, normalise metabolic parameters, improve quality of life, educate & prevent complications (long term/secondary, micro/macrovascular)
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What is the strategy of treatment for type 2 diabetics?
Diet/lifestyle -> Oral hypoglycaemic agent e.g metformin (first line, contra-indicated in renal impairment), sulphonylurea (side effect weight gain) -> Combine 2 -> Combination of 3 or add insulin -> Add/increase insulin or insulin alone
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What are the sources of insulin?
Animal: porcine, bovine. Human: semi-synthetic (enzymatically-modified porcine insulin) or recominant (E. coli, yeast). Insulin is classified according to duration of action
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What are the different types of insulin?
Short-acting (soluble, analogues, bolus), intermediate-acing, long-acting (basal) & biphasic (pre-mixed, mix of short and intermediate acting insulins, injections twice daily)
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What are the problems with insulin therapy?
Injections (painful, bruising, lipodstrophy), hypoglycaemia (need for monitorying plasma glucose concentration), weight gain & high circulating insulin concentration (CV risk)
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What are future diabetes therapy options?
Oral insulin: Capsulin (enclosing insulin in stomach acid resisting capsule, passes intact into SI), oral-lyn (insuin spray absorbed across buccal mucosa). Artificial pancreas: continuous glucose monitoring system together with insulin pump
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What is the mechanism of action of biguanides?
Activate AMP kinase to decrease gluconeogenesis & increase glucose utilisation
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What is the mechanism of action of sulphonylureas?
Stimulate insulin secretion via blockade of islet beta cell ATP-sensitive K+ channels
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What is the mechanism of action of prandial glucose regulators (rapid-acting insulin secretagogues)?
Stimulate insulin secretion via blockade of islet beta cell ATP-sensitive K+ channels
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What is the mechanism of action of thiazdinediones?
PPAR gamma-agonists = "insulin sensitizers"
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What is the mechanism of action of alpha-glucosidase inhibitors?
Delays digestions and absorption of starch & sucrose
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What is the mechanism of action of GLP1-mimetics?
Promotes insulin release, decreases glucagon secretion, decreases gastric emptying & decreases hepatic glucose production
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What is the mechanism of action of DPP-4 inhibitors?
Promotes insulin release, decreases glucagon secretion, decreases gastric emptying & decreases hepatic glucose production
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What is the mechanism of action of sodium-glucose transporter 2 inhibitors?
Inhibit renal glucose reabsorption -> inhibits sodium-glucose co-transporter in renal promixal convoluted tubule. Decreases glucose reabsorption & increases urinary glucose excretion
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Card 2

Front

What is the role of adrenaline, cortisol & growth hormone?

Back

Adrenaline: provision of energy for emergencies & exercise (severe hypoglycaemia). Cortisol: mobilisation of fuels during adaptation to stress. Cortisol & growth hormones both used in prolonged hypoglycaemia

Card 3

Front

What is ketogenesis? What inhibits & synthesises ketogenesis? What is the result of ketosis?

Back

Preview of the front of card 3

Card 4

Front

What is the consequence of loss of insulin action?

Back

Preview of the front of card 4

Card 5

Front

What is diabetes mellitus? What causes it?

Back

Preview of the front of card 5
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