Diabetes Pharmacological treatment Flashcards
which elements are present on the physical activity checklist to manage diabetes?
- minimum of 150min of moderate-to-vigorous intensity aerobic exercise per week (brisk walk)
- resistance exercise (strength training) > 2x/week (arms, chest, back, legs, abdomen)
- PA goals and involve multidisciplinary team
- minimize uninterrupted sedentary time
on which evidence does the PA checklist base itself?
- delay progression of disease itself and complication
- help in glycemic control and reducing medication for insulin resistance
why is a multidisciplinary team required when engaging in PA
when you start a new program of PA/exercise the whole treatment of diabetes will be affected -> medication and diet changes
which conditions must be assess before prescribing an exercise regimen
- neuropathy
- retinopathy
- coronary artery disease
- peripheral arterial disease
what are the ABCDES^3 of diabetes care and their targets
- A1c: optimal glycemic control (usually <7%)
- BP: optimal blood pressure control (<130/80)
- Cholesterol: LDL <2.0mmol/L or >50% reduction
- Drugs to protect the HEART
- Exercise/Healthy Eating
- Screening for complications
- Smoking cessation
- Self-management, stress and other barriers
which are the 2 insulin therapies for type 1 diabetes
- Basal [once a day] and bolus [at meals times] injection therapy
- continuous subcutaneous insulin infusion (insulin pump therapy)
why is insulin secretion so rapid?
when beta cells produce insulin, insulin is stored in vesicles which are ready to be released when there’s an increase in blood glucose
why is the blood glucose response at breakfast higher than at other meals?
during the overnight fasting period there are enzymatic reactions occurring promoting glucose anabolism (gluconeogenesis/glycogenolysis) which have to be stoped due to incoming glucose -> this switch takes time
what does basal insulin injection cover
the minimal amount on insulin circulating in blood - 50pm
used for overnight fasting period and in between meals
what are analogue types of insulin
human insulin produced by bacteria.
they are just formulated differently so that the release will be slower and cover only basal needs for basal injection or they can react faster with a higher peak and be removed from circulation more rapidly which reduces risks of hypo and hyperglycemia
what is the more conventional type of regiment for treating T1D compared to the intense regimen?
only 2 injections per day (vs. minimum of 3)
consistes of a premix which consists of rapid acting and intermediary acting insulin
NO BASAL
advantages and disadvantages of conventional type of regimen
advantage: doesn’t require education, good for someone who does not want to count their CHO or does not like to inject themselves
However, this is a last resort regimen because there is a risk of hyperglycemia at lunch time and hypoglycaemia after breakfast and dinner
=> more chronic hyperglycemia although controlled
+ FIXED insulin plan: it requires a strict meal plan in regards to CHO content, no skipping meals, as meal revolves around the insulin injection + physical activity could lea dot hypoglycemia
characteristics of Bolus types of insulin
- rapid acting has a short onset, peaks sooner, and lasts for a shorter amount of time
- short acting has a delayed onset, peaks later, but lasts for a longer time
characteristics of Basal types of insulin
- intermediate acting has a delayed onset with a peak much later ans lasts for 3/4 day
- long acting has a faster onset, no peak is observed and can last up to 24h => covers basal needs
both require only one injection per day
intensive insulin regimen is recommended for ____
better glycemic control
advantages of intensive insulin therapy
- more flexibility in timing and content of meals: insulin is adjusted according to CHO intake [must learn carb counting]
- insulin dose may be adjusted to exercise
- delays onset and slows progression of complications
what was observed during the follow-up of patients who underwent conventional vs intensive therapy
A1c levels maintained very high for conventional regimen (9%) where as goal is around 7% which was achieved by intensive therapy
+ there was a decrease in retinopathy, nephropathy, and neuropathy for those who followed intensive regimen+ significant reduction in MI, stroke, or CV death
insulin injection is done intravenously. True or false
FALSE, it is a subcutaneous injection: in the belly or button or leg by doing a simple pinch
what are the drugs called for management of type 2 diabetes?
antihyperglycemic agents
what is the first line medication prescribed to treat T2D? why?
Metformin because it is highly effective and doesn’t come with major side effects: we know of its safety, no risk of hypoglycemia, helps with weight control, affordable and easily accessible
what is the mechanism of action of metformin?
- decreases gluconeogenesis in liver which decreases glucose production
- increases insulin sensitivity and in turn increases glucose uptake
what are a few side effects of metformin?
- affects mostly the GI (transient), B12 deficiency (10-30% of cases)
mechanism of action of alpha-glucosidase inhibitors
delay intestinal glucose absorption
mechanism of action of insulin secretagogues
stimulate insulin secretion by pancreas
short-acting (4-7h), long-acting (once daily)
mechanism of action of incretin mimetics
stimulate insulin and reduce glucagon secretion; delay gastric emptying [induces satiety]
what are two examples of incretin mimetics
DPP-4 inhibitors
GLP-1 receptor agonists
mechanism of action of thiazolidinediones (TZDs)
increase insulin sensitivity in peripheral tissues and liver
mechanism of action of SGLT2 inhibitors
reduce glucose absorption by the kidney by blocking glucose transport in the proximal renal tubule -> glucose is excreted in the urine: glycosuria
when do you take antihyperglycemic agents other than metformin
when metformin is no longer efficient, when it reaches maximum dosage and glycemic target is not reached
what is the problem associated with insulin secretagogues
they have an associated risk of hypoglycemia because they stimulate insulin secretion [too much stimulation relative to the meal/amount of CHO consumed]
what is the particularity of incretin mimetics
they are peptides and must be injected, cannot be taken as capsules or else they will be digested/broken down
mode of action of DPP-4 inhibitors
they inhibit DPP-4 enzyme which allows for GLP-1 secretion by the intestine which stimulates insulin release, inhibits glucagon release, slows gastric emptying which overall lowers blood glucose and increases satiety [better weight control]
mode of action of GLP-1RA
GLP-1RA is a receptor agonist that binds to GLP-1 receptor and acts like GLP-1
effects of semaglutide
those who took this drug and had predisposition to developing prediabetes => reverted
advantages of SGLT2 inhibitors
when added to metformin there is a better efficacy on lowering A1c than other agents
rare hypoglycemia, lower BP, limit progression of chronic kidney disease, raise HDL
what are the stages in treatment at diagnosis of type 2 diabetes
- assess glycemic control, cardiovascular/renal status, dietary patterns and weight change
- select individualized A1c target
- start healthy behaviour interventions
- lifestyle changes help attain A1c target by 3 months -> no pharmacotherapy, if not reached within 3 months: start metformin
- start metformin is A1c is >1.5% above target, if target not reached after 3 months: adjust or advance therapy
- symptomatic hyperglycemia: start insulin + metformin
which antihyperglycemic drugs are the least favored
insulin secretagogues (hypoglycemia) and TZDs (weight gain)
which antihyperglycemic drugs are preferred
GLP-1RA [very expensive though] and SGLT2 inhibitor
which is the first factor to consider when prescribing an antihyperglycemic drug?
the relative A1c lowering when added to metformin
why is there weight gain when injecting exogenous insulin but not with endogenous insulin secretion
the amount of insulin injected to have the same effect on reducing blood glucose is higher in terms of units compared to what is secreted naturally by pancreas
[pancreas Secretes insulin which goes straight to liver through portal vein -> suppress endogenous glucose production [less glucose production by liver] as opposed to exogenous insulin -> doesn’t go straight to insulin, reaches liver after those tissues -> glucose production continues during that time -> more insulin is injected vs than what would be secreted by pancreas facing same glucose challenge -> anabolic action of insulin explains weight gain
which antihyperglcemic drugs are associated with weight loss
GLP-1RA and SGLT2 inhibitors
drug-nutrient interaction associated with metformin
can reduce vitamin B12 absorption, take with meals
drug-nutrient interaction associated with alpa-glucosidase inhibitors
take with first bite of meal (3X) or else NO EFFECT on lowering glucose absorption
limit alcohol
drug-nutrient interaction associated with insulin secretagogues
avoid alcohol due to possibility of hypoglycemia with this drug
drug-nutrient interaction associated with incretin mimetics
caution with alcohol, GI side effects: heartburn, belching, nausea, diarrhea
drug-nutrient interaction associated with TZDs
none
when diabetics are at risk of dehydration due to vomiting/diarrhea, what are the 2 recommendations
- rehydrate appropriately [water, broth, diet soft drinks, diet Jell-O]
- Hold SADMANS meds, restart once able to eat/drink normally [secretagogues, ACE-inhibitors, diuretics, metformin, angiotensin receptor blockers, non-steroidal anti-inflammatory drugs, SGLT2 inhibitors]
who patients are recovering from illness and can eat and drink again, what should they do?
- take DM medications as prescribed
- may need more frequent small meals/snack
- SMBG often: >4/d
who should receive statins on top of antihyperglycemic agents and metformin regardless of baseline LDL-c
- CVD or
- age >40yrs or
- microvascular complications or
- DM >15yrs duration and age >30yr
- warrants therapy
