Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CPT > Diabetic drugs > Flashcards

Diabetic drugs Flashcards

You may prefer our related Brainscape-certified flashcards:
NASM ® CPT flashcards
1
Q

What stimulates the release of insulin?

A
  • Secreted by B cells in response to:
    1. Increase in glucose
    2. Incretins
    3. Parasympathetic activity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the half life of insulin?

A
  • ~5 minutes in plasma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What inhibits the release of insulin?

A
  • Decreased glucose concentration
  • Cortisol
  • Sympathetic activity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the role of insulin?

A
  • Decreases hepatic glucose output via inhibition of gluconeogenesis and glycogenolysis
  • Increases glycogen stores
  • Promote uptake of glucose into tissues - muscle and adipose especially
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How is insulin in the body regulated?

A
  • Secreted into blood even during fasting - prevents receptor downregulation
  • Rate and extent of glucose concentration change leads to biphasic pattern of insulin release
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the symptoms of type 1 diabetes mellitus?

A
  • Typically present in children and young adults
  • Polyuria
  • Polydipsia
  • Weight loss
  • Fatigue/lethargy
  • Generalised weakness
  • Blurred vision
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How is type 1 diabetes diagnosed?

A
  • Hyperglycaemia
  • Fasting glucose >6.9 mmol/L
  • Or random plasma glucose >11 mmol/L
  • Plasma or urine ketones in presence of hyperglycaemia
  • HbA1c >48 mmol/mol (>6.5%)
  • Single raised plasma glucose without symptoms not sufficient for diagnosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Compare plasma glucose with HbA1c

A
  • Glucose - immediate measure of glucose levels in blood mmol/L
  • HbA1c - measures percentage of red blood cells with a sugar coating (glycated haemoglobin)
  • HbA1c reflects average blood sugar over last 10-12 weeks
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the biochemical triad of diabetic ketoacidosis?

A
  • Hyperglycaemia
  • Ketonaemia
  • Acidosis
  • Predominantly in type 1 diabetes mellitus
  • Particularly common in children on diagnosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

When do we suspect diabetic ketoacidosis?

A
  • Blood glucose >11 mmol/L
  • Polydipsia
  • Polyuria
  • Abdominal pain
  • Vomiting and diarrhoea
  • Lethargy
  • Confusion
  • Visual disturbance
  • Acetonic breath
  • Symptoms of shock
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What do we test for when we suspect diabetic ketoacidosis?

A
  • Ketones
  • Urine or blood
  • Venous pH <7.3
  • Or HCO3- <15 mmol/L
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the precipitating factors for diabetic ketoacidosis?

A
  • Infection
  • Trauma
  • Non adherence to insulin treatment
  • DDIs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How must insulin treatment be given?

A
  • Parenterally to avoid digestion in the gut
  • Because insulin is a protein
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How is insulin formulated?

A
  • In 100 units/mL
  • 300 and 500 units/mL available to reduce volume
  • Be careful when measuring dose
  • Ensure you’re using correct vial so that you don’t prescribe an overdose
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the routine delivery of insulin?

A
  • Subcutaneous injection
  • Upper arms, thighs, buttocks, abdomen
  • I.V.I used for emergency treatment
  • Rotate site of administration to limit lipodystrophy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How do we slow insulin absorption?

A
  • Protamine and/or zinc complexes added to natural insulins (used less now)
  • Causes soluble insulin to form hexamers - delays absorption from site of injection
  • [plasma] is greatest after 2-3hours
  • Dosing 15-30 minutes prior to meals
  • Insulin analogues also used - a few amino acid changes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Which insulin types are fast acting?

A
  • Insulin aspart - rapid acting
  • Soluble insulin (Humulin S, Actrapid) - short acting
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Which insulin types are longer acting?

A
  • Isophane insulin (NPH) - intermediate
  • Insulin glargine - long
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What things do we need to consider when prescribing insulin?

A
  • Combinations often prescribed - by brand name
  • Short and long-acting mixtures
  • May take them separately
  • Basal-bolus dosing is common
  • Other dosing regimens can be used - patient centred
  • Syringes, pens, pumps, inhalers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the adverse side effects of insulin treatment?

A
  • Hypoglycaemia
  • Lipodystrophy
  • Lipohypertrophy or lipoatrophy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the contraindications for insulin treatment?

A
  • Renal impairment
  • Hypoglycaemia risk
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the DDIs for insulin treatment?

A
  • Dose needs increasing with systemic steroids
  • Caution with other hypoglycaemic agents
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is basal-bolus dosing?

A
  • Given rapid acting insulin - bolus e.g. aspart
  • Patient generally takes this before a meal
  • Given long acting insulin - basal e.g. glargine
  • Commonly used for young active T1DM patients
  • Allows flexibility if adherence is good
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is diabulimia?

A
  • When a type 1 diabetic stops or reduces their insulin to control their weight
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Give an overview of type 2 diabetes mellitus?

A
  • Slow progression of disease over many years
  • Many people are asymptomatic early on
  • Vast majority of T2DM patients are overweight or obese
  • Age profile of T2DM has decreased
  • Insulin into cells reduced due to cellular resistance associated with obesity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Outline the pathophysiology of insulin resistance

A
  • Insulin resistance initially overcome by increased pancreatic insulin secretion
  • Decreased insulin receptors
  • Decreased GLP 1 secretion in response to oral glucose
  • Response reduced at B cells
  • Eventually insulin production reduced
27
Q

Why is type 2 diabetes mellitus diagnosed later in life?

A
  • Blood sugar rise typically slower than type 1 DM
  • Symptoms are variable
  • Often diagnosed through midlife MOT
28
Q

How is type 2 diabetes managed?

A
  • Lifestyle
  • Education
  • Weight loss (surgery in more and more instances)
  • Initially non-insulin therapies
  • Adherence is challenging in many patients
  • Insulin forms part of treatment plan in poorly managed or later stage disease
  • Treat co-morbidities
29
Q

What are the different classes of hypoglycaemic agents?

A
  • Sulphonylureas
  • Biguanides
  • Thiazolidinediones (glitazones)
  • Dipeptidyl peptidase 4 inhibitors (gliptins)
  • SGLT-2 inhibitors (gliflozins)
  • GLP-1 receptor agonists
30
Q

Give an example of a biguanide

A
  • Metformin
31
Q

What is the mechanism of action of biguanides?

A
  • Decrease hepatic glucose production by inhibiting gluconeogenesis
  • Some gluconeogenic activity remains so hypoglycaemia risk is reduced
  • Supresses appetite so weight gain is limited
  • Typically first drug offered
  • Can be taken concomitantly with other hypoglycaemic agents
32
Q

What are the adverse side effects of metformin?

A
  • GI upset
  • Nausea
  • Vomiting
  • Diarrhoea
33
Q

What are the contraindications for metformin?

A
  • Stop if eGFR ,30 mL/min
  • Alcohol intoxication
34
Q

What are the DDIs of metformin?

A
  • Drugs that may impair renal function e.g. ACEi, diuretics, NSAIDs
  • Drugs that increase glucose levels e.g. loop and thiazide like diuretics
35
Q

Give an example of a sulfonylurea

A
  • Gliclazide
36
Q

What is the mechanism of action of sulfonylureas?

A
  • Stimulate B cell pancreatic insulin secretion
  • Blocks ATP-dependant K+ channels
  • Need residual pancreatic function to work
  • Weight gain through anabolic effects of insulin
  • Typically taken in combination with other agents
37
Q

What are the adverse side effects of sulfonylureas?

A
  • Mild GI upset
  • Nausea
  • Vomiting
  • Diarrhoea
  • Hypoglycaemia
38
Q

What are the contraindications of sulfonylureas?

A
  • Hepatic and renal disease
39
Q

What are the DDIs of sulfonylureas?

A
  • Other hypoglycaemic agents
  • Loop and thiazide like diuretics - increase glucose so reduce action of sulfonylureas
40
Q

Give some examples of glitazones

A
  • Pioglitazone
  • Rosiglitazone
41
Q

Outline the mechanism of action of glitazones

A
  • Insulin sensitisation in muscle and adipose
  • Decrease hepatic glucose output by activation of PPAR-g
  • Gene transcription
  • Weight gain because of fat cell differentiation
  • Used much less frequently than other agents
42
Q

What are the adverse side effects of glitazones?

A
  • GI upset
  • Fluid retention
  • Fracture risk
  • Bladder cancer
43
Q

What are the contraindications of glitazones?

A
  • Heart failure because of fluid retention
44
Q

What are the DDIs of glitazones?

A
  • Other hypoglycaemic agents
45
Q

Give some examples of gliflozins

A
  • dapagliflozin
  • canagliflozin
46
Q

What is the mechanism of action of gliflozins?

A
  • Decreased glucose absorption from tubular filtrate
  • Increased urinary glucose excretion
  • Competitive reversible inhibition of SGLT-2 in PCT
  • Modest weight loss, hypoglycaemic risk is low
  • Add on therapy in T2DM
  • Treats HFrEF
47
Q

What are the adverse side effects of gliflozins?

A
  • UTI
  • Genital infection
  • Thirst
  • Polyuria
  • Pancreatitis?
48
Q

What are the contraindications of gliflozins?

A
  • Hypovolaemia - possible hypotension
49
Q

What are the DDIs of gliflozins?

A
  • Antihypertensive and other hypoglycaemic agents
50
Q

Diabetic drugs are GLP-1 agonists. What are the physiological effects of GLP-1?

A
  • Increases insulin secretion and biosynthesis
  • Decreases glucagon secretion
  • Decreases food intake by increasing satiety
  • Decrease glucose production by the liver
  • Increase glucose uptake by muscles
  • Decrease gastric emptying
51
Q

Give some examples of DPP-4 inhibitors (gliptins)

A
  • Sitagliptin
  • Saxagliptin
52
Q

Outline the mechanism of action of gliptins

A
  • Prevent incretin degradation - increase incretin plasma concentration
  • Glucose dependant so acts after patient eats
  • Does not stimulate insulin secretion at normal blood glucose
  • Lower hypoglycaemic risk
  • Suppress appetite so they are weight neutral
53
Q

What are the adverse side effects of gliptins?

A
  • GI upset
  • Small pancreatitis risk
54
Q

What are the contraindications of gliptins?

A
  • Avoid in pregnancy
  • History of pancreatitis
55
Q

What are the DDIs of gliptins?

A
  • Other hypoglycaemics
  • Drugs that increase glucose can oppose gliptin action e.g. loop and thiazide like diuretics
56
Q

Give some examples of GLP-1 receptor agonists

A
  • Exenatide
  • Liraglutide
  • Semaglutide
57
Q

What is the mechanism of action of GLP-1 receptor agonists?

A
  • Increase glucose dependant synthesis of insulin and secretion from B cells
  • Activate GLP-1 receptor
  • Resistant to degradation by DPP-4
  • Given by subcutaneous injection
  • Promote satiety
58
Q

What are the adverse side effects of GLP-1 receptor agonists?

A
  • GI upset
  • Decreased appetite with weight loss
59
Q

What are the contraindications of GLP-1 receptor agonists?

A
  • Renal impairment
60
Q

What are the DDIs of GLP-1 receptor agonists?

A
  • Other hypoglycaemic agents
61
Q

Which type 2 diabetes drugs are modified/extended release?

A
  • Metformin
  • Incretin mimetics
62
Q

What are the advantages of modified/extended release preparation diabetic drugs?

A
  • Overcome GI upset
  • Less frequent dosing
  • Slower release changes PK properties
  • Improved adherence
  • But more difficult to modify dose
63
Q

Why swallow an extended release tablet whole?

A
  • Modified release preparation coats tablet
  • Crushing up tablets overrides effects

CPT (22 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions