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171 Cards in this Set
- Front
- Back
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True or false:
insulin is stored and secreted from beta cells of the pancreas but is created in the liver |
False
Stored, secreted and created in the beta cells of the pancreas |
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Above what limit would blood glucose have to be to stimulate insulin release?
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>5mM
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Describe insulin biosynthesis
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Endoplasmic reticulum -> pre-proinsulin ->signal sequence removed -> proinsulin -> packed into secretory granules -> hydrolysed -> insulin + C-peptide -> release
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In the creation of insulin what is the function of C-peptide?
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When proinsulin is made, it holds the A and B chains (of the to be insulin) together
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What type of glucose transporter is present on the beta cells of the pancreas?
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GLUT-2
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What is the first step of glucose metabolism once it has been taken up by beta cells?
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phosphorylation by glucokinase (GK)
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How does the metabolism of glucose in beta cells cause the secretion of insulin?
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Metabolism of glucose causes K+ channels on cell surface to close -> disrupts negative membrane potential -> causes voltage-gated calcium channels to open -> Ca2+ flood in -> insulin secretion
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How does sulphonylureas work?
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inhibit K+ channel to stimulate insulin secretion
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What are some hormonal potentiators that are required for some beta cells respond to glucose?
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glucagon
glucagon polypeptide 1 gastric inhibitory polypeptide |
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What is the biphasic response of insulin?
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first respond is fast, then slows in the second phase even in the presence of continued glucose stimulation
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Explain the difference in the biphasic response of insulin
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Two pools of insulin
1. rapidly released pool: physically attached to the voltage gated calcium channel 2. Deeper vesicle: takes longer to be exocytosed |
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What are the key targets of insulin?
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liver
muscle adipose tissue |
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What is the main role of insulin, and briefly state how it fulfils this role
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main role: maintain glucose homeostasis
Stimulates glucose transport into muscle and adipose tissue and promotes the sythenesis of macromolecular fuel stores (lipid, glycogen and protein) Reduce glucose output from liver and prevent breakdown of macromolecules |
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What is insulin's effect on lipid metabolism?
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Inhibits lipolysis and ketone body formation
Stimulate FA and triacylglycerol formation |
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True or false:
Insulin regulates protein synthesis? |
True
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What type of receptor does insulin act through in their target tissues?
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Tyrosine kinase receptor
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How does that lack of insulin cause the decrease of glucose uptake into muscle and adipose tissue during carbohydrate deprivation?
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lack of insulin causes glucose transporters to move back in to golgi appartatus
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How does the decrease in insulin promote the release of glucose from liver?
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decrease insulin = increase cAMP -> activation of glycogen phosphorylase -> degrades glycogen -> glucose in blood
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What glucose concentration is mainatained in the body for adqueate supply to the brain?
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4mM
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How does the decrease in insulin cause the release of FAs?
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increase cAMP -> enzyme triacylglcerol lipase -> release of FA + glycerol
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What tissues are able to use FAs as an alternative fuel source?
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mucsle and liver
conserve glucose for brain |
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What can't the brain utilise FAs?
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FAs can't cross the BBB
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How does a cell utilise FAs instead of glucose for fuel?
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FA oxidation = inhibition of pyruvate dehydrogenase (PDH) complex -> prevention of glucose oxidation
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How does the utilisation of FAs promote the recycling of glucose in the body?
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inhibition of PDH allows for pyrvate -> lactate -> liver -> gluconeogenesis
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When are ketone bodies produced?
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Prolonged exposure to hypoinsulinaemia due to massive lipolysis
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In prolonged starvation how is the brain's energy supplied?
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1. lipolysis -> ketone bodies
2. muscle breakdown -> a.a -> ketone bodies and glucose |
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How does glycosuria occur in diabetes?
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insufficient insulin -> glucose accumlation in blood >10mM -> appears in urine
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In persistant hypoinsulinaemia,normal utilisation of glucose in tissues is inihibited, but there is increasing glucose concetration in the blood. Why?
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uncontrolled proteolysis and lipolysis -> FAs + A.A
A.A -> more ketone bodies and glucose F.A + ketone bodies -> inhibit PDH -> inhibit glucose utilisation and promote gluconeogenesis |
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Explain how uncontrolled diabetes can have frequent urination but unquenchable thirst
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hyperglycaemia changes osmotic potential of blood -> draws water out -> cellular dehydration -> thirst -> patient drinks more -> frequent urination.
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How does uncontrolled diabetes result in hyperkalemia?
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Acidotic environment created (ketone bodies, lactate, FAs) -> causes K+ to move out of cells.
Kidney have a reduced ability to push potassium into urine -> hyperkalemia |
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What are the counterregulatory hormones to prevent hypoglycaemia?
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glucagon
adrenaline GH cortisol |
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What is the normal range of glucose?
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between 4-6mM/L
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What are the symptoms of hypolgycaemia and what counterregulatory hormone are they attributed to?
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adrenalin -> SNS: tremor, tachycardia, palpitation, sweating, weakness, awareness of hypogylcaemia
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How would a patient develop hypoglycaemic unawareness?
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Long standing diabetes (>10 years), adr response to hypogylcaemia becomes impaired.
More likely to happen with recent severe episodes = vicious cycle |
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How would you improve autonomic dysfunction?
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Avoiding hypoglycaemia:
better dietary intake pattern cutting down insulin dosage |
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What is the major cause of severe hypoglycaemia?
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hypoglycaemia unawareness
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True or false:
hypoglycaemia unawareness is pathopneumonic for diabeties one |
False
It's more common in long standing diabetes 1, however a diabetes 2 patient of many years can develop it too |
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What are the common causes of hypoglycaemia that are not due to autonomic dysfunction?
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increase physical activity with insufficient food
continous consumption of alcohol without food delayed or missed meals errors in insulin dose inappropirate insulin regimens |
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True of false:
Many episodes of hypoglycaemia have no identifiable precipitating factor? |
True
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What symptoms might a patient experience if they have plasma glucose below those needed for normal CNS metabolism?
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headache
alterned mental status visual disturbance neuroglycopenic symptoms neurological deficit seizures coma death |
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How would you treat a conscious patient with hypoglycaemia?
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Mostly: 15-20g of oral glucose (6-7 jelly beans OR 150 mls normal coke) followed by complex carbs (slice of bread OR piece of fruit)
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How would you treat an unconscious patient or a patient who is unable to swallow?
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1. IV injection of 50% glucose or IM injection of glucagon
2. complex carbs when they regain conciousness |
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How would you treat hyperglycaemia which is a result of an episode of hypoglycaemia?
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Won't aggressively treat it with insulin for the next 24-48 hours or hypoglycaemia may return
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What are some of the factors are considered in whether or not the patient should be holding their driving licence?
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Frequency of hypoglycaemic episodes
Ability of the patient to detect epidsodes And ability of patient to treat themselves appropriately Vision acuity |
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As a doctor, what would be your duty in terms of notifying relevant driving authorities about your patient's diabetes
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Duty: inform patients to inform releveant authorities. But generally doctors are not required to inform authorities unless it is absolutely neccessary and only do so after discussing with patient.
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What is the physiological range for hydrogen ions?
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36-44 nmol/L
pH 7.37-7.45 |
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Between microvascular disease end macrovascular disease, which disease is specific for diabetes, and which disease occurs in the general population but is more severe in diabetes?
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Microvascular disease -specific for diabetes (neuropathy, rentinopathy)
Macrovascular disease -more severe in diabetes (atherosclerosis) |
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True or false:
Good control of blood glucose can reduce microvascular and macrovascular complications in diabetes |
False
Only has a positive correlation with microvascular disease. Macrovascular disease is prevented with treatment of cholesterol level and elevating high BPs |
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Describe non-proliferative retinopathy
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weakening, rupture, leakage and occulusion of BVs manifested as microaneurysms, dot and blot haemorrhages, hard exduates (due to lipid deposits) and soft exudates (local ischemia).
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Decribe proliferative rentiopathy
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Formation of new fragile vessels on the rentina.
Causes substantial risk of rupture and haemorrhage |
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Decribe macular oedema
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swelling, exduate or haemorrhage
more common in type 2 |
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What are the vision threathening retinopathies in a diabetic?
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proliferative retinopathy and macular oedema
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What would the treament be for vision threathening rentinopathies?
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laser photocoagulation (reduces progression to blindness)
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What kind of drug is used to treat diabetic nephropathy?
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renin-angiotensin inhibitors
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What is nephropathy characterised as in diabetes?
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proteinuria
hypertension oedema renal insufficiency |
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Histologically, what process is central to the development of diabetic nephropathy?
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mesangial expansion and basement membrane thickening
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What is used to classify a patient's diabetic nephropathy into the 5 different stages?
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estimated GFR calculated from serum creatinine levels
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Ture of false
Microalbuminuria has nothing to do with diabetic nephropathy |
False
a patient with microalbuminuria has a 10-20 fold increased risk of developing diabetic nephropathy |
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How would you measure microalbuminuria?
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1. 24hr urine collection
2. albumin/creatinine ratio from spot urine test Test should be preformed more than once because of day to day variations in albumin excretion. Generally 2/3 abnromal readings are needed to confirm |
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What types of drugs are the drugs of choice for a diabetic patient with hypertension who has some evidence of diabetic nephropathy?
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ACE inhibitors
OR angiotensin receptor antagonist |
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What is the most common form of diabetic neuropathy?
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Sensory neuropathy mainly affecting lower limbs
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What vessles are affected by macrovascular disease?
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coronary arteries
peripheral vessels cerebral vessles |
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How are diabetics affected by macrovascular disease compared to the rest of the popluation?
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Occurs at a younger age
More common More extensive More severe |
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True or false
Patients with microalbuminuria or proteinuria have an increased risk of CV disease |
True
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What should be kept undercontrol so as to decrease the risk of macrovascular disease in a diabetic?
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HT and hypercholesterolaemia
(no difference compared to everyone else) |
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What do statins inhibit?
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HMG-Coa reductase
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Is there any use in using statins and ACE inhibitors in diabetic patients who have normal cholesterol and are not hypertensive?
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Yes
There is evidence to show that taking it prophylactically reduces the risk of CV events (protective) |
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Explain how diabetic foot disease occurs
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1. neuropathy -loss of sensation leads to unawarness of surroundings and predisposes patient to ulcercations and infections
2. Vascular disease -reduces blood flow resulting in gangrene, infection and ulceration |
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When should a type 1 diabetic patient be assessed for diabetic complications?
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By 5 years after diagnosis and then annually
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How high blood glucose levels lead to diabetic complications is unclear. However, how might high glucose affect the body thus leading to complications?
(probably can skip Q unless you're interested/know it already) |
MAY CAUSE:
1. excessive binding of glucose to tissue resulting in accumulation of advanced glycation end products which damages tissues 2. increase accumulation sorbitol and deficiency of myoinositol through the polyol pathway 3. Increase EC matrix deposition in kidney -> glomerulosclerosis and declining function 4. activation of protein kinase C pathway -> increasing oxidative stress |
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A diabetic patient with type 1 diabetes has had an acute illness in the hospital and they're blood glucose is low even though they haven't eaten any food orally. Do you take them off their insulin so as to correct the blood glucose?
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No
Must continue insulin, but treat by replenishing carbohydrate intake either orally or through IV. |
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Would insulin therapy increase or decrease during pregnancy?
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increase
decrease risk of fetal abnormailities and prevent maternal ketoacidosis |
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How would the patient administer their own insulin?
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Subcutaneous, parenterally
because it's degraded by proteolytic enzymes in the GIT |
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What is the major route of elimination of insulin?
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Cellular uptake -internalisation of insulin receptor complex in liver and muscle
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What is the plasma half life of insulin?
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4 hours
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Describe short acting insulin
(synthetic soluble or regular) |
Onset: within 30secs of SC injection
Duration: 6-8 hours |
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Describe intermediate-acting insulin
(synthetic isophane or NPH) |
insulin bound protamine (fish protein)
Gradual release |
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Describe long acting insulin
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insulin zinc suspension
rarely used in Australia, replaced by long acting insulin analogues |
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Describe very rapid and short acting insulin analogues
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Absorbed rapidly
Acting time: 2-3 hours Injection must be followed by an immediate meal. They are used to control post-prandial hyperglycaemia |
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True or false:
Short acting insulins are more likely to cause hypoglycaemia because they act so rapidly that the body doesn't have time to compensate |
False
They are less likely to cause hypoglycaemia because they are so short acting |
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Describe premixed insulin
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Mixture of short and longer acting insulin (25/75, 30/70, 50/50 proportions)
Dosage: 1, 2 or 3x/day before meals Usage is less flexable due to the mix which cannot be adjusted |
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When are premixed insulin situable for patients?
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More suited to patients who have regular meal times and meal content
Also simply to use and more suited for patients who cannot handle complex insulin regimens |
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Describe very long acting insulin analogues
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Glargine: modified to have isoelectric pH which renders it insoluble after injection =slowly absorbed
Determir: binds to albumin = prolonged action |
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What are very long acting insulin analogues used for?
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provide basal level of insulin and complements injections of short acting insulin before each meal =basal bolus regimen)
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How many days will a normal store of glycogen last a person who is fasting?
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1 day
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What are the stimulators of insulin secretion?
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Increase glucose concentration
Increase AA concentration Gasto-intestinal hormones (Incretins) Parasympathetic stimulation |
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Which causes the release of more insulin -oral glucose or IV glucose? And why?
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Oral glucose
Releases GI hormones and PSNS stimulation. Incretins stay around longer and help insulin secretion |
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What factors inhibit beta cells from producing insulin?
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SNS
Somatostatin Phenytoin (epilepsy drug) Thiazide diurectics |
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How does insulin get released into the liver?
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Pancreas -> portal circulation -> liver
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What organ is exposed to a higher concentration of insulin and glucagon than peripheral tissues?
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Liver
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What is insulin's mechanism of action?
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Increase tyrosine kinase
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If you could use one word to summaries the actions of insulin, what would it be?
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Anabolic
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What is GLUT4 responsible for?
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GLUT 4 is in the peripheral tissues
It response to insulin and allows the diffusion of glucose down it's concentration gradient into the cell (facilitated cell membrane diffusion) |
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How does insulin influence fat cells to increase their uptake of glucose?
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increase low density lipoprotein receptor
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What are the effects of insulin on fat cells?
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increase uptake of glucose
increase fat as triglyceride decrease fat breakdown |
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What are insulin's effect on proteins?
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increase AA uptake
increase protein synthesis decrease protein breakdown |
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What are the effects of insulin on glucose?
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increase glucose's uptake in the peripherally. especially in muscle and fat tissue
increase glycogen synthesis decrease glcogenolysis |
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What are insulin's effect on the liver?
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insulin inhibits glycogen breakdown, gluconeogenesis, ketogenesis and liver output of glucose
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What is the first sign that insulin isn't working in a person?
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Liver output of glucose is not inhibited after a meal
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True or false:
Insulin has no effect of glucose transport in the kidney |
True
Filration rate of glucose is proportional to glucose concentration but it's reabsorbed |
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At what concentration is glucose in excess such that not all are reabsorbed?
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>16mmols
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What is the consequence of incomplete glucose reabsorption in the kidney?
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osmotic diuretic
Decreases water reabsorption therefore large volume of water loss |
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What does polyuria cause?
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loss of BV
polydipsia |
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What is the only part of the brain is glucose transport dependent on insulin?
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satiety centre
explains why diabetics can still feel hungry despite a high blood concentration of glucose |
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Is glucose uptake in muscle with exercise insulin dependent or independent?
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independent
for a well controlled diabetic who suddenly exercises a lot, they risk hypoglycaemia |
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True or false:
GH is one of the counter regulatory hormone of insulin. Since insulin inhibits proteolysis, GH must increase proteolysis. |
False
GH doesn't increase protein breakdown |
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Where is glucagon release?
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alpha cells of the pancreas
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What stimulates glucagon release?
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decrease glucose
decrease FA increase A.A (e.g. high protein, low CHO meal) |
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What is the general effect of glucagon
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Catabolic
-increase stored nutrients |
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What is glucagon's effect on CHO?
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Increase glycogen breakdown
Increase gluconeogenesis (liver) |
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What is glucagon's effect on A.A?
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Protein breakdown -> A.A (for liver gluconeogenesis)
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What is glucagon's effect on Fat?
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lipolysis -> products for ketogenesis (liver)
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In the diabetes diagnostic criteria, post fasting, what are the values for: normal glucose tolerance, impaired glucose tolerance and diabetes?
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Normal: <6mmol/L
Diabetes: > or = 7.0mmol/L Impaired: between normal and diabetes |
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What is the difference between type1a and type 1b diabetes?
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1a = autoimmune
1b = looks like type 1 (insulin treated) but don't have autoimmunity |
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What mediates the autoimmune destruction of pancreatic beta cells?
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T cell mediated immune destruction
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What is the honeymoon period in diabetes type1?
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The period lasting 2-3 years where the beta cells are able to produce insulin still and the patient isn't heavily reliant on insulin medication
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What are the shared clinical features of T1DM and T2DM?
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Non-specific features, generally related to hyperglycaemia
Thirst, polyuria Blurring vision Infection Poor wound healing Tiredness |
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Explain the features of thirst and polyuria
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hyperglycaemia
hyperosmolality |
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Explain the features of blurring of vision
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hyperglycaemia and sorbitol accumulation
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Ture or false:
The blurring of vision is always a sign of retinopathy |
False
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Explain how infection risk increases due to diabetes in relation to the immune system impairment
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white cell dysfunction with severe hyperglycaemia
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Explain the feature of poor wound healing
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Poor collagen formation
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What is the difference between T1DM's clinical picture, compared to T2DM
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T1 = acute
T2 = slow, asymptomatic |
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Is Acanthosis present in T1DM or T2DM?
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T2DM
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Is ketosis usually present in T1DM or T2DM?
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T1DM
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Is C peptide detectable in T1DM?
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No.
Detectable in T2 |
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Are antibodies detectable in T1DM or T2DM?
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T1DM
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Which type of DM might present with associated immune disease?
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T1DM
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What might the circulating Ab in T1DM be directed to?
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islet cells
GAD IA2 insulin ZnT8 |
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What is the differences in T1DM and T2DM in treatment?
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T1DM - always need insulin
T2DM -might try diet and oral agents first T1DM must not stop insulin (sick days, peri-operative) |
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Why might a T1DM patient have to settle for an imperfect diabetic control?
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hypoglycaemia
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What is HbA1c?
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HbA1c is the product formed by the non-enzymatically binding of glucose to the beta-chain of haemoglobin A
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What kind of vascular disorder is microalbuminuria under?
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microvasular
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What is the relationship of HbA1c to the risk of microvascular complications?
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the development of microvascular complications of diabetes is directly related to the level of HbA1c
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What does the level HbA1c let you look at?
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prior glycaemia in the past 120days
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What is the general target for glycaemic control?
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7.0% or less (53%mmol/mol)
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What is the concept of basal-bolus insulin?
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to mimick nature and give the correct insulin amount only when needed thereby attaining near normal daytime and nighttime glycemia
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List some reasons as to why T1DM is hard to control
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1. requires attention to diet, exercise and blood glucose monitoring from a young age
2. methods of delivering insulin and monitoring glucose are not perfect 3. can develop counter-regulatory response to hypoglycaemia and cannot detect hypoglycaemia |
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When might diabetic complications present in T1DM compared to T2DM?
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Unusual to be significant in the first 5 years of T1DM but T2DM might present with it at diagnosis
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In diabetic rentiopathy, when do symptoms start to present?
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When macula is involved or when new vessels bleed
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In diabetic nephropathy, when do symptoms occur?
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When creatinine is much eleveated
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How would you detect early stages of nephropathy?
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microalbuminuria is the first clinical sign (later +proteinuria) of diabetic damage to the kidney
Marker for both progressive kidney damage and CV disease |
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What might give a clue that diabetic nephropathy is deleveoping?
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Hypertension
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True or false:
Retinopathy is usually present with nephropathy? |
True
If not might have to rethink Ddx |
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List the autonomic neuropathy that can occur in T1DM and T2DM
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GI/GU effects:
post gustatory sweating Oesophageal dysmolilty Gastroparesis Autonomic diarrhoea Cardiovascular effects HR variability lost Orthostatic hypotension Silent ischaemia Hypoglycaemia unawareness |
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In diabetic males and females, how might the presentation of atherosclerosis differ?
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F>M
Present younger Myocardial infarction may be painless |
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List some autoimmune disease that may accompany T1DM
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Tyroid
Adrenal Celiac Hypogonadism |
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Why might alcohol cause hypos and ketoacidosis?
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inhibits gluconeogenesis and increases ketones
Alcohol metabolism increases NADH this causes: 1. Pyryvate -> lactate (less for gluconeogensis) 2. increase malate -> oxaloacetate = inhibit Kerbs in mitochondria + decrease gluconeogenesis 3. acetaldehyde -> increase acetyl CoA -> F.A. + ketones |
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How might alcohol have a minimal acute effect on glycaemia?
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If taken with food
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What is considered an OK amount to drink for a T1DM?
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1-2 drinks
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Why might sucrose containing foods need not be restricted but must be counted?
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Sucrose does not increase glycaemia more than isocaloric amounts of starch
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Are sugar alcohols and nonnutritive sweeteners safe?
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yes
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What is the bolus dose of insulin based on?
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CHO content of the meal
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What is the algorithm used when giving insulin dosage?
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ICR algorithm
e.g. 2 units of insulin for every 10g of CHO |
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What type of insulin is actrapid? and how long does it act for?
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Short acting
4 hours |
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What type of insulin is Protaphane? and how long does it act for?
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Intermediate acting
12 hours |
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When should patient's inject actrapid and why?
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Inject 30mins before meals
Exists as a hexamer and must dissociate before it can be absorbed. May take 20mins or longer |
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What are some of the problems with actrapid?
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inconvenient = compliance problems
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What do humalog and Novorapid have in common?
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Modified human insulin. Prevent hexamer formation for a more rapid absorption
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What is a normal level of HbA1c?
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<6%
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List some proportions of foods such that serving food =15g CHO
|
1 slice of bread
1/3 cup rice 1/2 pasta 1/2 cob corn 1 medium apple or orange 300g watermelon |
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What are the downsides of basal bolus regimen?
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More injections
Weight gain Makes diabetes more 24/7 |
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What are the pros for basal bolus regimen?
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decrease hypoglycaemia
flexibility |
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What are the cons associated with insulin pump?
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More blood glucose monitoring
Wearing the pump Cost 24/7 diabetes Only suitable for a small section of T1 Need medical staff to turn them off |
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What are the pros of insulin pump?
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more physiological insulin profile
decrease hypos flexible weight management less needles |
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How do you prevent diabetic ketoacidosis?
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T1 should never omit insulin
increase dosage in times of illness |
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How would you manage the patient during febrile intercurrent illness with ketones?
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Take normal dose of insulin + 20% of extra short acting insulin ever 2-3 hours until ketones disappear
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What are the causes of diabetic amputations?
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Neuropathy or vascular disease -> trauma -> ulcer -> failure to heal -> infection -> amputation
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What is the treatment of neuropathic ulcer?
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Reduce pressure e.g. orthowedge shoe or air-boots
Treat infection Adequate debridement of ulcer Rest Education |
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How would you treat an ischaemic ulcer?
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Rest
Treat infection Improve circulation if healing does not occur Education |
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True or false
well controlled T1DM with in an intensive insulin regime can be more flexible with their diet and diet regime |
True
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