Altered pancreatic function & Diabetes Mellitus

?
  • 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
1 of 21
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
2 of 21
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)
3 of 21
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)
4 of 21
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)
5 of 21
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
6 of 21
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
7 of 21
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)
8 of 21
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
9 of 21
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
10 of 21
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)
11 of 21
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)
12 of 21
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
13 of 21
What is the mechanism of action of biguanides?
Activate AMP kinase to decrease gluconeogenesis & increase glucose utilisation
14 of 21
What is the mechanism of action of sulphonylureas?
Stimulate insulin secretion via blockade of islet beta cell ATP-sensitive K+ channels
15 of 21
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
16 of 21
What is the mechanism of action of thiazdinediones?
PPAR gamma-agonists = "insulin sensitizers"
17 of 21
What is the mechanism of action of alpha-glucosidase inhibitors?
Delays digestions and absorption of starch & sucrose
18 of 21
What is the mechanism of action of GLP1-mimetics?
Promotes insulin release, decreases glucagon secretion, decreases gastric emptying & decreases hepatic glucose production
19 of 21
What is the mechanism of action of DPP-4 inhibitors?
Promotes insulin release, decreases glucagon secretion, decreases gastric emptying & decreases hepatic glucose production
20 of 21
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
21 of 21

Other cards in this set

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
View more cards

Comments

No comments have yet been made

Similar Medicine resources:

See all Medicine resources »See all Endocrinology resources »