DM Flashcards
what are the characteristics only associated with type II diabetes?
> 30 yrs old (60yrs = peak), obesity, family history, complications (long term) gradual onset, osmotic symptoms, no ketones in urine, high HbA1c
what are the characteristics only associated with type II diabetes?
> 30 yrs old (60yrs = peak), obesity, family history, complications (long term) gradual onset, osmotic symptoms, no ketones in urine, high HbA1c
what are the characteristics only associated with type I diabetes?
where is type II diabetes more common?
Asia, Africa, Carribean
where is type I diabetes more common?
Northern Europe
what are the symptoms of diabetes?
polyuria and polydypsia (osmotic diuresis) thrush (puritis vulvae and balaritis) gunger? blurred vision (glycated lens proteins) fatigue (impaired use of glucose)
what is the cause of type I diabetes?
pancreatic b cell destruction so insufficient insulin produced, autoimmune
what is the cause of type II diabetes?
insulin resistance of tissues - impaired cellular response to insulin: receptor down-regulation, reduced signalling
what is latent autoimmune diabetes in adults?
onset 40-60 years of type 1 diabetes develops more slowly
what is mature onset diabetes of the young?
early onset of type 2 diabetes no insulin autosomal dominant
what is gestational diabetes and what does it increase the risk of in later life?
diabetes during pregnancy increases the risk of getting type 2 later in life
why might diabetes occur secondary to another condition?
pancreatic obstruction, cushings, acromegaly
2 of which 3 symptoms are needed in order to diagnose type 1 diabetes?
weight loss
severe symptoms for short history
ketones in urine
2 of which 3 symptoms are needed in order to diagnose type 1 diabetes?
weight loss
severe symptoms for short history
ketones in urine
what are the characteristics only associated with type I diabetes?
where is type II diabetes more common?
Asia, Africa, Carribean
where is type I diabetes more common?
Northern Europe
what are the symptoms of diabetes?
polyuria and polydypsia (osmotic diuresis) thrush (puritis vulvae and balaritis) gunger? blurred vision (glycated lens proteins) fatigue (impaired use of glucose)
what is the cause of type I diabetes?
pancreatic b cell destruction so insufficient insulin produced, autoimmune
what is the cause of type II diabetes?
insulin resistance of tissues - impaired cellular response to insulin: receptor down-regulation, reduced signalling
what is latent autoimmune diabetes in adults?
onset 40-60 years of type 1 diabetes develops more slowly
what is mature onset diabetes of the young?
early onset of type 2 diabetes no insulin autosomal dominant
what is gestational diabetes and what does it increase the risk of in later life?
diabetes during pregnancy increases the risk of getting type 2 later in life
why might diabetes occur secondary to another condition?
pancreatic obstruction, cushings, acromegaly
which type of diabetes has ketones in the urine?
type 1
2 of which 3 symptoms are needed in order to diagnose type 1 diabetes?
weight loss
severe symptoms for short history
ketones in urine
what must random plasma glucose levels be with symptoms to diagmnose DM?
> 11mmolo/l
what must random plasma glucose be on 2 occassions without symptoms in order to diagnose DM?
> 11mmol/l
what must fasting plasma glucose be greater than with symptoms to diagnose DM?
> 7mmol/l
what must GTT - glucose tolerance test - (75g) be at fasting and after 2 hours in order to diagnosis diabetes without symptoms?
after fasty >7mmol/l after 2 hours >11mmol/l
what must HBA1c be greater than in order to diagnose diabetes?
> 48mmol/l
when is HBA1c unsuitable to diagnose diabetes?
stress hyperglycaemia, children and young adults, DMT1 for less than 2 months, haemotological abnormalities affecting HBA1c, pregnancy, drug induced diabetes, symptoms less than 2 months
what effect does insulin have on metabolsim?
signals fed state with lots of energy
growth hormone
promotes the use of energy for synthesis or storage
name 5 processes promoted by insulin
glycolysis, protein synthesis, fatty acid synthesis, glucose uptake, glycogen synthesis
how does insulin cause glucose uptake by cells?
binds to tyrosine kinase receptor –> PKB, P13K phosphorylate proteins –> GLUT4 inserted into membranes of insulin sensitive cells
which reactions are promoted if insulin is low?
-ase enzymes are increased so things are broken down
gluconeogenesis, glycogenolysis, ketogenesis, lipolysis, proteolysis
what does glucagon signal?
starvation so tries to increase plasma glucose levels for the brain
what do very high levels of glucagon stimulate?
lipolysis, preteolysis
which enzyme is responsible for breaking down lipids in the fasting state?
hormone senstive lipase breaks down adipose tissue into fatty acids
why do diabetics have high blood glucose?
low insulin or tissues not responsive to insulin so GLUT4 not expressed so high glucose levels in blood
gluconeogenesis and glycogenolysis stimulated producing more glucose, glycogen synthesis inhibited
why do diabetics have glucose in their urine?
high plasma glucose exceeds the renal threshold
why do diabetics have ketone body formation?
gluconeogenesis in the liver uses krebs cycle intermediates. accelerated fatty acid breakdown leads to more acetyl coA available
XS acetyl coA can’t be metabolised by krebs cycle so ketone bodies are formed instead
what do diabetics have high HBA1c?
RBCs have a memory! glycated form of Hb
covalkent bond between N-terminal of Valine and Hb
index of average blood glucose concentration over the lifetime of Hb
what sort of acidosis do diabetics have and what compensation occurs?
metabolic acidosis, respiratory compensation to decrease co2
what are the 4 main long term microvascular complications of DM?
retinopathy, nephropathy, neuropathy, lens damage
why does retinopathy occur?
basement membrane of capillaries damaged so increased permeability of capillaries leads to small haemorrhages in the eye
how does hyerglycaemia and fluctuating insulin affect minor metabolic pathways?
increased use of minor metabolic pathways such as POLYOL pathway producing sorbitol and fructose that are osmotically active so lead to swelling
what sort of proteins could be glycated in DM?
basement membrane, HBA1c
why does lens damage occur in DM?
glycation of proteins in the lens –> cataracts
osmotic changes due to sorbitol from polyol pathway
why does neuropathy occur?
demyelination of neurones due to blood vessel damage and sorbitol accumulation so decreased sensitivity and do not feel damage (loss of sensory perception)
vascular degeneration decreses healing so ulcers and infection can occur
why does nephropathy occur?
thickening of the basement membrane, disrupted filtering ability so leakage of large molecules
at what level of glucose in the blood does coma and seizures occur?
1mmol/l
how much higher is the risk of CHD?
2-3x
why is there an increase in circulating LDLs in DM?
glycated LDLs and receptors reduces uptake so more in blood
what can increased levels of LDL lead to?
LDL –> arteriole endothelium –> atherosclerosis
why is there a danger of stasis in DM?
glycation of proteins in capillary membrane
why are there higher ciculating levels of fatty acids?
xs lipolysis
what are the treatments for retinopathy?
regular eye tests, laser treatment
what are the negatives of tight glucose control?
increased risk of hypoglycaemia
how can nephropathy be prevented?
urine test for microalbumin = very early sign
U+Es
what is the important triangle?
lower blood glucose (control it), limit glucose variability, avoid hypoglycaemia
what is the treatment for DMT2?
insulin
2 x daily mixture short/ mild acting insulin
basal bolus 1 or 2x daily and pre meal
what must DMT2 patients taking insulin be aware of?
judging CHO intake
awareness of blood glucose being lowered by exercise
at what level of glucose in the blood does irreversible brain damage occur?
at what level of glucose in the blood does coma and seizures occur?
1mmol/l
what are the autonomic consequences of hypoglycaemia?
nausea, sweating, tremor, tachycardia, pallor, anxiety
what are the neuroglycogenic symptoms of hypoglycaemia?
slurred speech, confusion, lethargy, coma, drowsiness, aggression, lack of concentration
what is the blood glucose target for before meals?
4-7nM
what is the blood glucose target for after meals?
what is the target HBA1c?
what are the positives of tight glucose control?
decreased risk of complications
what are the negatives of tight glucose control?
increased risk of hypoglycaemia
what 2 things should reverse DMT2 if substancial?
weight loss and exercise
which medication can be used for DMT2?
hypoglycaemic agents to prevent complications
where does metformin act and what does it do?
liver - inhibits gluconeogenesis
whwre do a-gl;ucosidae inhibitors act?
inhibit glucose absorption in the stomach but not used because of flatulence
how do glifoxins work?
increase glucose loss from the kidneys and decrease reabsorption leading to weight loss. -ve = UTIs
how do sulphonylureas work?
increase insulin secretion from the pancreas
WHERE DOES glp-1 ACT AND WHAT DOES IT DO?
GLUCAGON LIKE PEPTIDE 1 CAUSES PANCREASE TO PRODUCE INSULIN SO YOU FELL FULL
HOW DO glp-1 ANALOGUES ACT?
like GLP-1 they increase insulin production from the liver so you decrease sugar and lose weight
where does pioglitazone act?
liver, muscle, adipose increases insulin sensitivity but too many side effects so not used
