Type 2 Diabetes Mellitus Flashcards

1
Q

what is the pathophysiology of type 2 diabetes?

A

combination of insulin resistance and beta-cell failure, resulting in hyperglycemia and associated with obesity

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

what is the initial treatment for someone with type 2 diabetes?

A

lifestyle changes and weight loss

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

can type 2 diabetes be reversible?

A

yes

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

what level of fasting glucose is normal?

A

less than or equal to 6mmol/L

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

what level of fasting glucose classes as impaired fasting glycaemia (intermediate state) ?

A

from 6 to 6.9 mmol/L

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

what level of fasting glucose classes as type 2 diabetes?

A

greater than or equal to 7 mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

2 hour glucose in the OGTT at which values is considered normal?

A

<7.7mmol/L

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

2 hour glucose in the OGTT at which values is considered impaired glucose tolerance (an intermediate state) ?

A

7.7-10.9mmol/L

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

2 hour glucose in the OGTT at which values is considered diabetic?

A

greater than or equal to 11

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

hbA1c at which values is considered

  1. normal
  2. pre-diabetes (intermediate state)
  3. diabetes
A
  1. <42mmol/mol
  2. 42-47.9mmol/mol
  3. greater than or equal to 48mmol/mol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

how do insulin resistance and insulin production change going from normal to intermediate state to diabetic state?

A

Normal -> intermediate: insulin resistance increases and insulin production increases to compensate

Intermediate -> diabetic: insulin production decreases and insulin resistance plateaus.

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

when can we use random glucose to diagnose diabetes type 2?

A

when someone also has symptoms of diabetes

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

why do people with type 2 diabetes not tend to get ketosis?

A

enough insulin is present in circulation to inhibit/suppress lipolysis and fatty acid beta-oxidation

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

why do people with long-duration type 2 diabetes sometimes get ketoacidosis?

A

because all their beta cell function has been lost

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

In healthy people, what is the relationship between insulin secretion and insulin sensitivity?

A

as insulin sensitivity decreases, insulin production increases

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

In type 2 diabetes, what happens in the liver, adipocytes and muscle?

A

Liver: produces excess glucose (insulin usually causes glucose to convert to glycogen whereas lack of insulin converts glycogen to glucose)

Muscle: no uptake of glucose from blood by GLUT transporter

Adipocytes: No uptake of glucose into adipocytes and number of triglycerides in the blood rising (because insulin encourages the conversion of triglycerides to NEFA)

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

adipocytes produce adipokines, what are these?

A

inflammatory chemicals which contribute to development of type 2 diabetes

18
Q

MODY stands for what and what is it caused by?

A

Maturity Onset Diabetes in the Young and it is caused by a single gene mutation

19
Q

Diabetes mellitus types 1 and 2 have what type of genetic inheritability?

20
Q

where is the part of the body that poses the highest risk for type 2 diabetes when it has more body fat?

A

visceral obesity > subcutaneous obesity

21
Q

what is the presentation of type 2 diabetes mellitus?

A
hyperglycaemia
overweight
dyslipidaemia
fewer osmotic symptoms
complications
insulin resistance
later insulin deficiency
22
Q

What are the risk factors for T2DM?

A
age
BMI
ethnicity
PCOS
family history
inactivity
23
Q

first line test for diagnosis of type 2 diabetes mellitus?

24
Q

what is the key management for hyperosmolar hyperglycaemic state in people with type 2 diabetes?

A

rehydration with IV fluids

25
what is the management of type 2 diabetes?
``` diet/lifestyle changes oral medication structured education may need insulin later remission/reversal ```
26
what monitoring do people with type 2 diabetes need?
``` HbA1c, glucose monitoring if on insulin Medication review weight assessment blood pressure dyslipidemia: cholesterol profile screening for complications eg. foot check and retinal screening ```
27
What are the four main goals for drug treatments for T2DM?
- Reduce hepatic glucose production - Improve insulin sensitivity - Boost insulin secretion - Inhibit carbohydrate gut absorption and inhibit renal glucose absorption
28
what does metformin do?
reduce hepatic glucose output and improves insulin sensitivity
29
Thiazolidinediones have what effect? Give an example.
Improve insulin sensitivity Pioglitazone
30
sulphonylureas, DPP4-inhibitors, GLP-1 agonists all do what? What do we do if these stop working?
boots insulin secretion move onto insulin
31
what do alpha-glucosidase inhibitor and SGLT-2 inhibitor do?
inhibit carbohydrate gut absorption and inhibit renal glucose reabsorption
32
what is the first line drug for T2DM?
metformin
33
what are the side effects / cautions of metformin?
GI side effects | Contra-indicated in severe liver, severe cardiac or moderate renal failure
34
normal insulin release requires closure of which channel? What do sulphonylureas do to this channel?
ATP-sensitive potassium channel They close the channel independent of glucose, boosting insulin production
35
Pioglitazone has what side effect?
peripheral weight gain
36
Pioglitazone is an agonist at which receptor?
PPAR-gamma
37
What does GLP-1 do?
- incretin/gut hormone, secreted in response to nutrients in the gut. Transcription product of pro-glucagon gene, mostly from L-cell. - stimulates insulin, suppresses glucagon, increases satiety
38
Give 2 examples of GLP-1 agonists?
Liraglutide, semaglutide
39
what does DPPG-4 enzyme do? What happens if you inhibit it?
Metabolises GLP-1 Longer half-life of GLP-1
40
GLP-1 agonists cause: 1.weight loss 2, weight gain 3. weight neutral
1
41
What do SGLT-2 inhibitors do?
inhibit Na-Glu transporter, increasing glycosuria (makes you pee out more glucose)