Brainscape's Knowledge GenomeTM

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


See full index

M2 > Drugs used in the management of Diabetes Mellitus > Flashcards

Drugs used in the management of Diabetes Mellitus Flashcards

1
Q

Which glucose transporter is found at the pancreatic beta cells?

A

GLUT 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How does an increase in glucose level stimulate insulin release?

A

Increased intracellular glucose
= ncreased ATP production
= increase ATP/ADP ratio
= closing of K+ channels and depolarisation of the cell
= opens voltage gated Ca2+ channels
= exocytosis of insulin containing vesicles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How does insulin regulate blood glucose levels?

A

1.Facilitating cellular glucose uptake (GLUT 4 receptors)

2.Regulating carbohydrate, lipid and protein metabolism (glucogenesis inhibition, glycogenolysis)

3.Promoting cell division and growth (PI3K-Akt pathway, MAPK/ERK pathway)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How is exogenous insulin mainly cleared?

A

Kidneys

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

When is insulin therapy indicated?

A

In all Type 1 diabetes patients, and in
Type 2 diabetes patients with
1. Severe hyperglycaemia or
2. When glycemic targets are NOT reached with 2 or more oral hypoglycaemic agents (OHAs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the main types of insulins?

A
  1. Rapid
  2. short / intermediate/ long
  3. ultra long acting
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Which of the insulin types has the longest peak duration of action?

A

NPH (Intermediate acting insulin)

since there long acting insulins have no peak

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Which of the insulins are commonly used in an emergency to rapidly lower blood glucose levels?

A

Short acting regular human insulin
Note: It is administered intravenously

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Which of the insulins have the highest risk for hypoglycaemia?

A

NPH (Intermediate acting insulin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Which insulins cannot be mixed with any other insulin in a single syringe?

A

Glargine, detemir
Long-acting (Glargine, detemir) cannot be mixed with short or rapid-acting insulins in the same syringe

due to long acting insulins having a low pH formation
= if mixed with other insulins (neutral pH)
= premature precipitation
= incomplete insulin absorption
= unpredictable blood glucose levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What adverse effects are associated with insulin use?

A

Hypoglycaemia and lipodystrophy (abnormal distribution of fat, with less fat near areas of insulin injection)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How is insulin commonly administered?

A

Subcutaneous injection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What factors affect the absorption of insulin?

A

Site of injection, Depth of injection, Volume and concentration of the dose injected, exercise, heat (e.g. sitting in a sauna), massage of insulin site

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How does corticosteroids or an acute infection affect insulin demands?

A

It is likely to increase insulin demands as it can cause an increase in blood glucose levels (likely due to insulin resistance)

steroids:
corticosteroids cause increased gluconeogenesis
= hyperglycemia

infection:
body releases inflammatory mediators
= cytokines intefere with insulin signalling
= more glucose remain in blood stream
= increase in blood glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Which oral hypoglycaemic agent is commonly used as the first line of treatment in the absence of any contraindications?

A

Metformin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is metformin’s mechanism of action?

A

Metformin decreases hepatic glucose production, increases the density of insulin receptors at the tissues and reduces intestinal glucose absorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What factors could contraindicate the use of metformin?

A

Renal dysfunction, lactic acidosis, hepatic dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is thiazolidinedione’s mechanism of action?

A

Primary mechanism of action is via the activation of the nuclear transcription factor peroxisome proliferator-activated receptor-γ (PPAR-γ).

PPAR-γ ligands
= increase trasncription of genes invovled in glucpse and lipid metabolism
= regulate glucose metabolism, adipogenesis
= improve insulin sensitivity at adipose tissues, liver and skeletal muscles
= increase glucose uptake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the key adverse effects associated with the use of thiazoldinediones?

A

Weight gain, peripheral edema, increased risk of heart failure (fluid retention) and bone fractures

increase PPAR gamma (PPAR causes more production of adipocytes and less production of osteoblasts = more succeptible to bone fracture)
= increase transcription of genes to glucose uptake
= increase glucose uptake (increase water uptake = oedema and fluid retention = weight grain & HF due to fluid retention)

20
Q

Will an obese patient be suitable for thiazolidinediones?

A

Ideally not recommended as the drug can cause weight gain

21
Q

What is sulfonylurea’s mechanism of action?

A

Sulfonyureas (SU) bind to the SU receptor proteins subunits of the K+ATP channels
= inhibits KATP channel mediated K+ efflux
= depolarisation of pancreatic β-cells
= calcium-dependent exocytosis of insulin granules

22
Q

Name a sulfonylurea with a long duration of action

A

Glibenclamide - High risk of hypoglycaemia compared to the others

23
Q

What are the key adverse effects associated with the use of sulfonylureas?

A

Weight gain, hypoglycaemia

24
Q

What patient profile may have a higher risk of hypoglycaemia with sulfonyureas?

A

Elderly, poor renal function, or hepatic dysfunction, people with irregular eating habits

25
Q

What is meglitinide’s mechanism of action?

A

Meglitinides bind and close the ATP-dependent potassium (KATP) channels on the pancreatic beta cells in a **glucose-dependent manner **stimulating insulin release

26
Q

Why are meglitinides commonly used at meal times?

A

They have a rapid onset and short duration of action

27
Q

What is acarbose’s mechanism of action?

A

The α-glucosidase inhibitors reversibly inhibit membrane-bound α-glucosidase in the intestinal brush borders
= slow down the rise in glucose levels after a meal
= inhibit post prandial hyperglycemia

**must be taken with food

28
Q

What are some side effects associated with the use of acrbose?

A

Flatulence, GI discomfort

29
Q

In which groups of patients will acarbose be contraindicated?

A
  1. GIT diseases like IBD
  2. severe renal and hepatic disease
30
Q

What are the 2 classes of drugs that work by incretin based therapy?

A

Dipeptidyl peptidasae-4 inhibitors, GLP-1 receptor agonist

31
Q

What are the mechanisms of action of DPP-4 inhibtors?

A

DPP-4 inhibitors binds and inhibits DPP-4 thus prolonging the action of the endogenous incretins, which then
1. stimulate pancreatic β-cells to increase glucose-stimulated insulin release
2. suppress α-cell mediated glucagon release
3. supress hepatic glucose production

32
Q

Name 3 DPP-4 Inhibitors

A

Sitagliptin, Linagliptin and Vildagliptin

33
Q

Name 2 examples of glucagon-like 1 peptide 1-receptor agonist

A

Liraglutide, Semaglutide

34
Q

How are GLP-1 receptor agonists administered?

A

Subcutaneous injection
Semaglutide is also available as an oral tablet

35
Q

What are the mechanisms of action of glucagon-like 1 peptide 1-receptor agonist?

A

They activate the GLP-1 receptor (membrane-bound cell-surface receptor in pancreatic beta cells)
= Increase insulin release in the presence of elevated glucose concentrations

**does not cause hypoglycemia, as insulin secretion subsides as blood glucose concentrations decrease and approach euglycemia (normal blood glucose level)

36
Q

What are the potential adverse effects associated with the use of DPP-4 inhibitors and GLP-receptor agonist?

A

GI related issues, pancreatitis (not recommended for patients with a history of pancreatitis

37
Q

Other benefits of GLP-1 receptor agonists

A

Weight loss, improved cardiovascular outcomes

38
Q

What are examples of sodium glucose co-transporters?

A

Dapagliflozin, empagliflozin, canaglifloziin

39
Q

What is SGLT-2’s mechanism of action?

A

SGLT2, expressed in the PROXIMAL RENAL TUBULES, is responsible for 90% of the reabsorption of filtered glucose from the tubular lumen.

Inhibiting SGLT2
= decrease reabsorption of filtered glucose
= increase urinary glucose excretion

40
Q

What other benefits does SGLT-2 have?

A

Favourable cardiac outcomes - including reduced risk of hospitalizaton due to heart failure and reduced risk of worsening renal function

41
Q

What are some of the key adverse effects associated with the use of SGLT-2 inhibtors?

A
  1. Urinary tract infection
  2. increased urination
  3. female genital mycotic infections (fungal infection)
  4. increased risk of lower limb amputation (Canagliflozin, since it has a more potent diuretic effect = hyperviscocity = decrease oxygen to lower limbs)
  5. diabetic ketoacidosis
42
Q

Which hypoglycaemic agents are associated with weight gain?

A

sulfonyureas, thiazolidinediones, meglitinides

43
Q

Which hypoglycaemic agents have been found to have significant cardiovascular benefits and are favoured for patients with Atherosclerotic cardiovascular disease?

A

SGLT-2 inhibitors, GLP-1 receptor agonist

44
Q

compare GLUT 2 vs 4

A

GLUT 2
- insulin INDEPENDENT
- glucose transport in and out of cells
- low affinity for glucose

GLUT 4
- insulin regulated
- glucose uptake into cells after insulin stimulation
- high affinity for glucose

45
Q

what is the triad for diagnosing diabetic ketoacidosis

A
  1. hyperglucemia
  2. ketonemia (elevated ketones in the blood)
  3. metabolic acidosis
46
Q

acidosis vs alkalosis

A

M2 (20 decks)

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