Brainscape's Knowledge GenomeTM

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


See full index

Endocrine > Diabetes 2 > Flashcards

Diabetes 2 Flashcards

1
Q

What is DIDMOAD (Wolfram Syndrome)?

A

Diabetes Insipidus, DM, Optic atrophy, Deafness, neuro anomalies

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

How does Bardet-Biedl Syndrom usually present?

A

Very obese, polydactyly, hypogonadal, visual impairment, hearing impairment, mental retardation, DM, consanguineous parents

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

What are some associated AI conditions of T1DM?

A

Thyroid disease, coeliac, pernicious anaemia, addison’s, IgA deficiency. Rare-AI polyglandular syndrome (Type 1 and 2), AIRE mutations, IPEX syndrome

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

What is Type 2 Polyglandular Endocrinopathy?

A

Most common polyglandular failure syndrome. Can include conditions such as T1DM, addisons, vitiligo, primary hypogonadism/thyroidism, coeliac

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

What is Type 1 Polyglandular Endocrinopathy?

A

Polyglandular syndrome in which multiple endocrine glands dysfunction. Autosomal recessive condition, associated with mild immune deficiency (Muco-cutaneous candidiasis), any associated condition in Type 2, primary hypoparathyroidism, pernicious anaemia, alopecia

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

What causes insulin resistance?

A

Ectopic fat accumulation and increase FFA circulation, increase inflammatory mediators, reduction in insulin-stimulated glycogen synthesis due to reduced glucose transport

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

What occurs due to insulin resistance leading to a decline in beta cell function?

A

Glucotoxicity and lipotoxicity (due to elevated FFA, TG)

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

Does an apple or pear weight distribution have a higher risk of T2DM and CVD?

A

Apple

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

What is the therapy staircase in T2DM?

A

Diet and exercise, oral monotherapy, oral combination, injectable and oral therapy

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

What are some traditional oral anti-hyperglycaemic agents?

A

Biguanides-metformin. Sulphonylureas-glicazide, glibenclamide, glimeparide. Thiazolidinediones-pioglitazone

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

What are some of the effects of metformin?

A

Hyperglycaemia management-reduces HbA1c by 15-20mmol/l, hypoglycaemia (not when monotherapy), weight effect (can reduce it), prevention of micro/macrovascular complications

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

What are some adverse effects of metformin?

A

GI S/Es-anorexia, nausea, vomiting, diarrhoea, abdo pain, taste disturbance. Interference with vitB12 and folic acid absorption, lactic acidosis (can be fatal), liver failure/toxcity, rash, renal toxicity

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

What is the 1st line agent for T2DM?

A

Metformin

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

What is a sulphonylurea?

A

An insulin secretagogue. 1st gen (rarely used)-chlorpropramide, tolbutamide. 2nd gen (shorter acting)- glicazide, glipizide, glibenclamide/glyburide, glimepiride

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

What are the effects of the SUs?

A

Hyperglycaemia management-reduces HbA1c, results in more rapid reduction in hyperglycaemia than insulin sensitisers, (concern with beta cell demise acceleration). Prevention of microvascular complications, not macrovascular

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

What are the adverse effects of the SUs?

A

Hypoglycaemia, wt gain, GI upset, headache, rarely hypersensitivity, blood dyscrasias and liver dysfunction. Avoid in severe renal/hepatic failure

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

When should SUs be considered?

A

After metformin or in those intolerant of metformin

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

What kind of drug are the Thiazolidinediones (TZDs)?

A

PPAR gamma agonists

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

What are the effects of the TZDs?

A

Hyperglycaemia management-reduces HbA1c. Hypoglycaemia (not if used without SU). Wt increase, heart failure, improvement in microalbuminuria, prevention of macrovascular complications

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

What are therapies based on incretins?

A

GLP-1 receptor agonists- exenatide, exendin, liraglutide, lixisenatide, DPP-IV inhibitors-vildagliptin, sitagliptin, saxagliptin, linagliptin

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

What are the benefits of GLP-1 receptor agonists?

A

Promote insulin secretion from pancreas without hypoglycaemia, suppress glucagon (increased in T2DM), decrease gastric emptying-early satiety, act on hypothalamus-reduce appetite-resulting wt loss

22
Q

What are the downsides of GLP-1 receptor agonists?

A

Nausea-resolves in most, injectable, pancreatitis, pancreatic cancer

23
Q

What are the benefits of DPP4 inhibitors?

A

Promote insulin secretion from pancreas without hypoglycaemia, suppress glucagon (increased in T2DM), weight neutral

24
Q

What are the side effects of DPP4 inhibitors?

A

Very limited S/Es, pancreatitis, pancreatic cancer

25
Q

What are some SGLT2 inhibitors?

A

Dapa/cana/empa-gliflozin

26
Q

What do SGLT inhibitors do?

A

Decrease uptake of sugar by about 1/4- increase sugar in urine

27
Q

What are the downsides to SGLT inhibitors?

A

Sugar in urine can lead to thrush, possible increase in UTIs

28
Q

How is insulin given more commonly in T2DM?

A

Basal insulin- insulin is given if people fail on non-insulin therapies. Once daily NPH insulin is added to metformin (+-SU)

29
Q

What inheritance does MODY exhibit?

A

Autosomal dominant

30
Q

Is MODY insulin or non-insulin dependent?

A

Non-insulin

31
Q

What is the common age of onset of MODY?

A

Usually before 25yo

32
Q

What are the types and proportions of different MODY mutations?

A

Glucokinase mutation 14%, transcription factor (HNF1…) 75%, MODY x 11%

33
Q

How do glucokinase mutations causing MODY present and how are they treated?

A

At birth, stable hyperglycaemia, complications are rare. Diet based treatment

34
Q

How do transcriptiion factor mutations causing MODY present and how are they treated?

A

Adolescence/young adult onset, progressive hyperglycaemia, frequent complications. Treatment is 1/3 diet, OHA, insulin

35
Q

Describe transient neonatal dm (TNDM)

A

Type of DM at birth that is not permanent. Considered to be a type of MODY

36
Q

Describe permanent neonatal diabetes (PNDM)

A

Diabetes usually diagnosed 0-6wks. Lifelong insulin treatment

37
Q

To what drug are HNF1alpha mutations causing MODY sensitive to?

A

SU’s

38
Q

What channel mutation can cause neonatal diabetes?

A

Katp channel mutation

39
Q

What are some examples of types of insulin?

A

Rapid, short, intermediate, long acting.Also rapid intermediate/short intermediate mixture

40
Q

What insulin regimen should all/most of T1DM patients be on?

A

Basal bolus

41
Q

What is the disadvantage of twice daily insulin regimen?

A

It does not mimic physiological insulin secretion

42
Q

What is the BG target pre-meal regarding insulin treatment?

A

3.9-7.2mmol/l

43
Q

What is the BG target 1-2hrs after beginning of meal regarding insulin treatment?

A

Less than 8mmol/l

44
Q

What are the key difference between insulin analogues and historic soluble insulin??

A

Faster onset (10-15 mins opposed to 30-60), peak action at 60-90mins rather than 2-4hrs, duration of 4-5 hours rather than 5-8

45
Q

Should T1DM patients be on an analogue or isophane basal insulin usually?

A

Analogue

46
Q

What does an insulin pump do?

A

Provides continuous administration of short acting insulin subcut. Background dictated by basal rate, manually activated bolus to cover meals

47
Q

How is glycated haemoglobin (HbA1c) formed?

A

By non-enzymatic glycation of hg on exposure to glucose

48
Q

Over what period of time is HbA1c a measure of average BG?

A

6-8wks

49
Q

What factors effect insulin absorption/action?

A

Pen accuracy, leakage, temperature, injection site and depth, exercise

50
Q

What checks should be employed to reduce risk in insulin injection?

A

Check site for lipohypertrophy, check needle

Endocrine (14 decks)

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