Brainscape's Knowledge GenomeTM

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


See full index

BRS 4: Endocrinology > 4.8: An introduction to diabetes mellitus (part 1 of 2) > Flashcards

4.8: An introduction to diabetes mellitus (part 1 of 2) Flashcards

1
Q

Insulin action on glucose (2)

A

Decreases hepatic glucose output
Increases muscle uptake of glucose

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

Insulin action on fats (2)

A

Decreased lipolysis
Decreased ketogenesis

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

What two tissues is GLUT-4 commonly found in

A

Myocytes and adipocytes

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

Do GLUT-4 transporter proteins responds to insulin?

A

Yes

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

How does insulin affect

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

Insulin effects on proteins

A

Decreases proteolysis

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

What effect does GH and IGF-1 have on protein synthesis in myocytes?

A

Stimulates it

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

What effect does cortisol have on proteolysis in myocytes?

A

Stimulates it

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

What is a gluconeogenic amino acid?

A

An amino acid that can be converted into glucose through gluconeogenesis

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

What hormone leads to an increase in uptake of gluconeogenic amino acids in the liver?

A

Glucagon

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

What role does glucagon have in the liver?

A

Stimulates proteolysis to produce more gluconeogenic amino acids (converted to glucose)

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

What effect does insulin have on the hepatic glucose output in the fed state?

A

Reduces hepatic glucose output as gluconeogenesis is inhibited, so less glucose synthesised

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

What does lipoprotein lipase break triglycerides down into and what hormone stimulates this process?

A

Glycerol and non-esterified fatty acids (NEFA)
Insulin

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

2 effects of insulin in adipocytes?

A

Increases uptake of glucose via GLUT-4

converts glycerol and NEFA into triglycerides- when required

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

Why does insulin use glucose instead of NEFA as a substrate for triglyceride re-synthesis

A

To reduce glucose levels
And Inhibit breakdown of triglycerides in adipocytes back into glycerol and NEFA

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

What effects do GH and cortisol have on triglycerides in adipocytes in the fasting state?

A

Stimulates break down of triglycerides into glycerol and NEFA
Used as an alternative energy source once in liver -lipolysis stimulation

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

In the fasting state what happens to glycerol taken up by liver?

A

Converted into glucose (gluconeogenesis)
Increasing hepatic glucose output

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

I’m the fed state what happens to glycerol taken up by liver?

A

Converted into triglycerides

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

What can the brain use as fuel?

A

Glucose
Ketone bodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

In the fed state, what does insulin do once NEFA is uptake by liver?

A

NEFA converted into Acyl-CoA
Insulin inhibits conversion of fatty Acyl-CoA into ketone bodies, preventing it from being used as an alternative metabolic substrate to glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

In the fasting state, what does insulin do once NEFA is uptake by liver?

A

NEFA converted into fatty Acyl-CoA
Converted into ketone bodies

22
Q

What does a high level of ketones and glucose indicate?

A

Issue with insulin secretion

23
Q

In the fed state what happens to glucose in the liver?

A

Converted into glucose-6-P
Then converted to glycogen (stimulated by insulin)

24
Q

In the fasting state what happens to glycogen in the liver?

A

Glycogen broken down (stimulated by glucagon) - glycogenolysis

25
Q

In the fed state what happens to glucose in myocytes?

A

Glucose converted into glycogen and stored
Used when:
myocytes require energy
Aerobic respiration

26
Q

What effect does glucagon and GH have on the GLUT-4 transporters in myocytes?

A

Inhibits uptake of glucose via GLUT-4 to allow more glucose to remain in circulation and increase the blood glucose levels

27
Q

In the fasting state why is amino acid concentration increased initially and then decreased when prolonged?

A

Increased due to increased proteolysis and then decreased due to more gluconeogenesis to increase hepatic glucose output

28
Q

What is the insulin spike after a meal called?

A

First phase insulin release

29
Q

What 4 tests can be carried out to make a diagnosis of diabetes?

A

Fasting glucose > 7.0mmol/L
Random glucose > 11.1 mmol/L
Oral glucose tolerance test
HbA1c >48mmol/L

30
Q

How many tests are required to diagnose diabetes?

A

2 positive tests
Or 1 positive test and symptoms

31
Q

Desribe the pathophysiology of Type 1 Diabetes Mellitus (T1DM)

A

Autoimmune condition that eventually leads to a T-Cell mediated destruction of the insulin-producing beta cells in the pancreas, leading to absolute insulin deficiency

32
Q

How does T1DM lead to osmotic diuresis?

A

Increased glucose in blood so more glucose in urine
Lowering water potential of urine, water enters urine via osmosis, leading to major water loss

33
Q

How does diabetic ketoacidosis occur ?

A

Less insulin present to down-regulate the breakdown of triglycerides in adipocytes

So more triglycerides are broken down into NEFA and Glycerol

NEFA are then converted into ketone bodies in the liver (which would also normally be inhibited by insulin), leading to a build up of ketones

34
Q

4 symptoms present in patients with T1DM

A

Weight loss

Hyperglycaemia

Glycosuria → polyuria, nocturia, polydipsia

Ketones in blood and urine

-

35
Q

3 diagnostic tests for T1DM over T2DM

A

Antibodies: GAD, IA2

C-Peptide (usually not present)

Presence of ketone bodies

36
Q

What 4 hormones induce a counterregulatory response to hypoglycaemia?

A

Glucagon
Catecholamines
Cortisol
Growth hormone

37
Q

What is the counterregulatory response to hypoglycaemia?

A

Increased HGO with glycogenolysis and gluconeogenesis
Increased lipolysis

38
Q

4 autonomic signs and symptoms of hypoglycaemia

A

Sweating
Pallor
Palpitations
Shaking

39
Q

5 neuroglycopenic symptoms of hypoglycaemia?

A

Slurred speech
Poor vision
Confusion
Seizures
Loss of consciousness

40
Q

What is severe hypoglycaemia?

A

Episode where a person needs third party assistance for treatment

41
Q

After insulin binds to its receptor, in which pathway does insulin resistance reside?

A

PI3K-Akt pathway which leads to metabolic actions

42
Q

Which pathway is followed alternatively since insulin resistance prevents the other?

A

MARK Pathway, leading to growth and proliferation of structures such as arterioles → increasing blood pressure

-

43
Q

What effect does insulin resistance have on Triglyceride and HDL concentration?

A

High Triglyceride concentration in plasma as insulin function is lacking and so LPL cannot breakdown TG into Glycerol and NEFA

Low HDL concentration - overproduction of VLDL leading to increased TG plasma levels which results in lower levels of HDL

44
Q

3 consequences of insulin resistance?

A

Hypertension
Weight gain
High fasting glucose (>6.0mmol/L)

45
Q

6 signs and symptoms of T2DM

A

Hyperglycaemia
Overweight
Dyslipidaemia
Less osmotic symptoms
Insulin resistance
Later insulin deficiency

46
Q

5 risk factors of T2DM

A

Age
High BMI
Ethnicity
Family History
Inactivity

47
Q

5 dietary recommendations could be given to a patient with T2DM?

A

Reduce calories as fat or refined carbohydrate
Increase calories as complex carbohydrate
Increase soluble fibre
Decrease sodium
Total calories control

48
Q

4 management strategies made for patients with T1DM

A

Exogenous insulin (basal-bolus regime) - 1 long acting insulin injection once or twice a day and then quick injections just before meals

Self-monitoring of glucose - fingerprick testing

Structured education

Technology

49
Q

4 management strategies for patients with T2DM

A

Diet
Oral medication
Education
May need insulin later - if loss of B cell function later on in life

50
Q

4 long term diabetes complications that can be avoided through certain management strategies

A

Retinopathy

Neuropathy

Nephropathy

Cardiovascular

BRS 4: Endocrinology (10 decks)

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