DIABETES Flashcards
risk factors of type 2 diabetes for Ben and in general
In general;
- obesity
- glucose intolerance
- family history of glucose intolerance or diabetes
- gestational diabetes
- sedentary lifestyle
- advanced age
- pancreatitis or pancreatic cancer
- certain infections
For Ben;
- previous acute pancreatitis
- increasing obesity
- possibly excess alcohol consumption (high alcohol consumption increases the risk of glucose intolerance, insulin resistance and therefore possibly type 2 diabetes
signs and symptoms of type 2 diabetes for Ben and in general
in general;
- hyperglycaemia (main one)
- polyuria (urinating a lot)
- prolonged wound healing
- fatigue
- polydipsia
- glycosuria (glucose in the urine)
- ketoacidosis (body breaks down fat at too fast a rate)
- polyphagia (eating excessive amounts of food)
- weight loss
-recurrent infections
For Ben;
- hyperglycemia
- glycosuria (the presence of reducing sugars in the urine)
- polydipsia (excessive thirst)
- polyuria (urinating a lot)
-ketoacidosis (body breaks down fat fast)
pathophysiology of type 2 diabetes.
- it is the decrease of insulin production or insulin resistance from the beta cells in the pancreas which leads to hyperglycaemia (elevated blood glucose levels)
- Normal blood glucose levels should be between 3-8mmol.
- without the necessary insulin, glucose will not enter most body cells leading to excess glucose remaining in blood (hyperglycaemia) and cell glucose deprivation. excess glucose in the blood results in an excess amount of glucose being filtered at the kidneys
HAVING TOO MUCH GLUCOSE IN THE BLOOD
a lot of glucose gets filtered from the kidneys and some gets reabsorbed back but there is a capacity to how much can be reabsorbed so the rest goes out in the urine. Having glucose in the urine draws water to be in the urine which causes us to lose water and leads to polyuria (excessive urination) and there is an increase in plasma osmolarity which makes us thirsty so we have polydipsia (increased thirst).
Neurons use glucose to generate ATP and they take it up based on glucose concentration so if there is a lot of glucose then they take up a lot. Excess glucose then starts to build up on the neurons called glycosylation. This leads to disruption in action potential conduction and issues with neurons receiving and sending signals. Glycosylation also occurs on the wall of the blood vessels which stops gas, nutrient and waste exchange which leads to inflammation, poor wound healing, recurring infections and further vascular tissue damage.
Cells also do not get enough glucose because there is not enough insulin or they are insulin resistance. Cells send signals that affect parts of the brain causing polyphagia (hunger) because they need glucose and can not use lipids exclusively. Adipocytes release more lipids into the blood because body cells now rely on lipids to produce ATP resulting in more and more lipids going into the blood and cells can only take up so many so it leads to hyperlipidemia and leads to atherosclerosis. The increased use of fats for cellular metabolism also results in the production of ketone bodies, which are acidic and can lead to ketoacidosis, a significant complication of diabetes.
complications of type 2 diabetes for Ben and in general- retinopathies
RETINOPATHIES: eyes
- vascular glycosylation which leads to ischemia and hypoxia which leads to microvascular damage
- this causes an increase in permeability which leads to macular oedema which is when the blood vessels in the eye are damaged resulting in leakage which leads to swelling of the macula. The swelling affects how the light rays stimulate the photoreceptors.
- microvascular damage also causes vascular proliferation where the new vessels are very weak and more susceptible to damage which leads to micro-aneurysm and micro haemorrhage. These are known as proliferative retinopathy.
- these cause blurred vision and blindness
- hyperglycemia can lead to glycolysation of blood vessels, whereby glucose gets deposited in the basement membrane of capillaries. This decreases effective gas, nutrient and waste exchange and can lead to localised tissue damage, including microvascular damage. The capillaries of the retina are particularly susceptible to this, as they are very delicate networks of blood vessels. In Bens case, the vascular damage has allowed leakage of fluid into the macula causing macular oedema.
comparison to type 1 diabetes
- type 1 diabetes means lack of adequate insulin production from the pancreas. The beta cells arent producing insulin
patients tests and assessments used for type 2 diabetes for Ben and in general
- fasting BGL
- oral glucose tolerance tests (fasting BGL done and then given a glucose rich drink and then blood glucose is taken again, often used to diagnose diabetes in pregnancy)
- HbA1C test- glucose is taken up by red blood cells proportionally to blood glucose concentration. Glucose deposits (glycosylation) occurs over the life of the red blood cell. This test tells us what your average blood glucose level has been over the past 3-4 months.
- HbA1c ‘three month sugars’ are glycosylated hemoglobin. Hemoglobin accumulates glucose over the lifetime of a RBC and therefore glycosylated hemoglobin/HbA1c reflects the average plasma glucose concentration over the previous few months
management of type 2 diabetes for Ben and in general
The goal of diabetes treatment is to obtain normal blood glucose levels and correct any metabolic disorders
treatment of type 2 diabetes
1. Where possible identify and treat/ eliminate underlying causes
2. dietary changes, weight loss and exercise may be sufficient
3. oral hypoglycemic drugs
- Ben has been on various diabetic treatment regimes, including different insulin preparations, oral hypoglycemics or a combination of the two. After his initial presentation of acute pancreatitis with diabetes he was on high doses of insulin, but after 6 weeks he no longer exhibited signs of diabetes and his insulin treatment was ceased. In subsequent years, his blood sugar levels began to rise again.
- Ben progressively made some changes to his diet, including decreasing alcohol intake, but for many years he struggled with weight control. As his diabetes progressed, his glycemic control became inadequate and eventually he was put on Metformin- an oral biguanide hypoglycemic agent that decreases gluconeogenesis and increases peripheral uptake/utilization of glucose
- Ben’s regular insulin treatment is with Humulin NPH (isophane insulin), a long acting insulin suspension using protamine. He supplements this with humalog as necessary. This is a rapid onset, short acting insulin that can be taken before or after meals to lower blood sugar levels. Ben uses a chart to calculate insulin requirements. This is easy for people who have trouble figuring out how much insulin to take. A disadvantage is that the chart could be generic and not specific to ben and how his body handles insulin.
- Ben made changes to his diet and exercise to further enhance his diabetes management and glycemic control. He has regular visits to the podiatrist and undertakes daily evaluations of his feet and lower limbs
complications- nephropathies and atherosclerosis
NEPHROPATHIES: nephrons of kidneys
- vascular glycosylation which leads to microvascular damage of the glomeruli of the kidneys
- leads to an increase in permeability of glomeruli which leads to loss of protein in the urine (proteinuria)
- microvascular damage also causes hypertrophy and fibrosis
- these eventually cause a decrease of GFR and lead to renal failure
- Ben’s renal function tests show he is in the safe zone, this could become a more significant complication for Ben in the future
ATHEROSCLEROSIS: increased lipolysis
- increased lipolysis leads to hyperlipidemia which leads to fatty plaque formation (atherosclerosis)
- this can lead to hypertension, peripheral artery disease and coronary artery disease and stroke
complications- neuropathies
NEUROPATHIES:
- neural glycosylation and vascular glycosylation that leads to tissue damage
- this leads to neuronal damage and AP disruption
- if somatic nerves are affected is causes tingling sensation, numbness or decreased sensation, skeletal muscle weakness, decrease reflexes. Distal symmetric polyneuropathy. If you step on something and injure yourself or burn yourself you may not feel it and this is dangerous
- Ben has peripheral neuropathy and has no feeling in his feet, ben had cellulitis in his feet from cuts he had that wouldn’t heal. He had charko joint in his feet so they feel tight
- autonomic nerve complications are orthostatic hypotension (hypotension from sitting down and then standing up quickly), incontinence, erectile dysfunction, resting tachycardia, gastric complications
- hyperglycemia leads to glycolysation of neurons. This disrupts normal action potential conduction, and when this occurs on neurons of the autonomic nervous system it can affect a variety of functions
- Gastrointestinal complications associated with autonomic neuropathy can include gastroparesis (delayed gastric emptying), diarrhea and/or constipation. Ben suffered from bloating, constipation and diarrhoea. To manage his bloating he only eats one meal a day and does not have it before bed
- Ben also has erectile dysfunction which is because his parasympathetic NS is affected.
- Ben also has postural hypotension and when he stands up too quickly especially after lying down can lead to a drop in BP
complications- ketoacidosis
KETOACIDOSIS
- where there is increased glucose combined with low insulin levels and increased counterregulatory mechanisms (glucagon, adrenaline)
- this leads to an increase in ketones which leads to acidosis (electrolyte imbalances)
- also leads to increased water-loss from hyperglycaemia which pulls water into the urine which leads to dehydration
- acetone breath, ketones in urine, postural dizziness, nausea and vomiting, CNS depression and kussmauls respiration are signs and symptoms
- need insulin, fluids and electrolytes
- when Ben was first admitted into hospital with abdominal pains he has ketoacidosis, likely complication of his hyperglycaemia
complications- diabetic feet
neuropathy and vascular complications both play a role in many pathologies associated with the feet and legs in those with diabetes.
some problems commonly recognised as diabetic foot pathologies are
- infections
-ischaemia
- ulcers
- charcot joints
- edema
- fallen arches
- hammer toe
Ben experienced a number of foot pathologies, which are;
- sensorial loss
- skin alterations
- ischemia and ulceration
- poor wound healing
- charcot joints
- fallen arches
- gait alterations
medications for diabetes
sulphonylurea
- should only be used if dietary and exercise management unsuccessful
- they stimulate basal insulin secretion by the pancreas- so must have functioning beta cells
- can cause hypoglycemia and have a tendency to promote weight gain
biguanides- metformin
- used in the treatment of NIDDM when diet, exercise and sulphonylurea drugs have been insufficient
- only works for patients with some residual beta cell function
- decreases liver gluconeogenesis
- increases glucose utilization by peripheral cells
- reduces LDL, VLDL and increases HDL
- hypoglycemia not usually a problem
- lower incidence of weight gain
- can cause anorexia, diarrhoea and nausea
- may cause potentially fatal lactic acidosis
- insulin therapy may need to be instituted temporarily due to illness, surgery or pregnancy
release mechanism of insulin
the B cells have K= + channels that are regulated by intracellular ATP.
when blood glucose increases more glucose enters the B cells which increases the intracellular ATP which closes the + ATP channels
This depolarisation of the B cell initiates an influx of Ca2+ ions triggering insulin release
The insulin receptors are membrane spanning glycoproteins
