Diabetes management and therapeutics-Type 2 Flashcards
The gut is made up of organs like your stomach and intestines. When you eat, incretins (hormones such as glucagon-like peptide-1 [GLP-1] and gastric inhibitory peptide [GIP]) are released to help the body use glucose from the meal as well as suppressing your body from making more glucose. With type 2 diabetes, there is a decreased incretin effect due to a lack of what incretins and what effect
lack of GLP-1 and resistance to the action of GIP in the body. This results in less insulin and increased blood sugar.
in T2DM the pancreas can release to much glucagon causing what
high blood sugar
muscles can die to insulin resistance as can’t get the glucose they need
the hypothalamus helps regulate how much you eat, affecting your body’s sensitivity to insulin, and affects how your body metabolizes glucose and fats. In people with type 2 diabetes, changes in brain signaling can occur resulting in less of a response from signals, such as insulin or GLP-1, from the rest of the body
Just like muscle cells and liver cells, fat cells can be insulin resistant if you are overweight and/or have type 2 diabetes. This can cause higher blood sugar levels.
One job of the kidneys is to reabsorb blood sugar to help keep the energy that is stored from being lost. When you have type 2 diabetes, the kidneys reabsorb too much sugar back into the blood, making it hard to keep blood sugar levels under control.
ominous octet in type 2
decreased insulin secretion
decreased incretin effect
increased lipolysis
increased glucose reabsorption
decreased glucose uptake
neurotransmitter dysfunction
increased hepatic glucose production
increased glucagon secretion.
He highlighted that sulfonylureas only improve insulin secretion, which is transient, and that these agents do not preserve β-cell function
what is type 2
insulin resistance due to increased insulin numbing the receptors or a loss of receptors to invagination of vesicles.
what drugs promote insulin secretion
sulphonylureas( SUR1 receptor on ATPkcuasing depolarisation and calcium out nroamlyl causing insulin secretion ) and GLP-1 agonists( increase insulin secretion in response to food, decreasing appetite and slowing gastric emptying therefore stimulating insulin secretion and suppression glucagon secretion.
DPP4 degrade GLP 1 normally
what drugs target insulin resistance
metformin(AMPK) and thiazolidines( PPARy)
what drugs increase glucose excretion
SGLT2 inhibitors ( glucose passes from blood stream into nephron and SGLT2 reabsorbs glucose form nephron back into bloodstream normally) - inhibitors block It so glucose lost
theses are your flozins
what drugs cause slow glucose uptake
Alpha-glucosides ( glucosidase inhibitors)
norm the small intestine enzymes cleave polysaccharrised to monos and these are absorbed causing rise in blood glucose. predigestion begins in mouth thanks to a-glucosidase breaking down sugar chains. with acarbose tablet inhibits the enzyme so fewer monosaccharides prodcued so lower blood glucose levels
someone diagnosed with type 2 what is the first choice of treatment
think not drug
increase physical activity and restrict her energy intake
metfomin reduces blood glucose level by
suppressing hepatic gluconeogensis
facilitating glucose uptake in skeletal muscle and adipocytes
decreasing glucose absorption from the gut
how do DDP4 inhibitors act in increases insulin secretion from the bet a cells
prevent the breakdown of GLP-1
biguanides like metformin increase what by product
lactate
if someone is over weight what do you advice first second line etc
lose weight you fat fuck
metform
thiazolidines( PPARy)
numerous infections indicates CF leading to stunted growth what complication of this
diabetes mellitus
