Brainscape's Knowledge GenomeTM

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


See full index

Semester 4 > case 6 - diabetes review > Flashcards

case 6 - diabetes review Flashcards

1
Q

what is the WHO diagnosis for diabetes in the fasting state

A

normal: fasting; less than 6.1mmol/L
Impaired fasting glycaemia: 6.1-6.9mmol/L
Diabetes: greater than 7mmol/L

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

what is the WHO diagnosis for diabetes 24 hours post prandial

A

impaired glucose tolerance: greater than 7.8-11mmol/L
Diabetes: greater than 11 mmol/L

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

what is the value of HbA1c that confirms type 2

A

HbA1c greater than 48mmol/mol

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

describe the physiology of the beta cells

A

islet: beta cells
pancreatic beta cells express GLUT2 glucose transporters, which permit rapid glucose uptake regardless of the extracellular sugar concentration

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

what happens in type 1 diabetes

A

beta cells get destroyed which leads to no or very little insulin produced

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

what are the effects of insulin on the liver

A

increased glucose uptake and glycogen synthesis

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

what are the effects of insulin on the muscle

A

increased glucose uptake and glycogen synthesis

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

what are the effects of insulin on adipose tissue

A

increased glucose uptake and storage as fat
decreased breakdown to fatty acids

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

what are the effects of insulin on blood

A

glucose levels fall

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

what are the effects of lack of insulin on the liver

A

decreased glucose uptake
Increased glycogen breakdown and gluconeogenesis
Conversion of fatty acids to ketone bodies

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

what are the effects of lack of insulin on the muscle

A

decreased glucose uptake via GLUT4

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

what are the effects of lack of insulin on adipose

A

decreased glucose uptake and storage
increased breakdown of fat and release of fatty acids

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

what are the effects of lack of insulin in the blood

A

glucose levels rise

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

what are the pathophysiology steps of diabetes;

A

low utilisation of glucose and increased endogenous production of glucose by the liver

hyperglycaemia

loss of glucose in the urine

increased urination - polyuria, nocturia

dehydration - increased thirst-polydipsia

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

what happens when there is loss of glucose in the urine

A

osmotic drag of glucose on water
water and glucose lost in urine
electrolytes lost along with water

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

what are the specific tests used to diagnose type 1 diabetes - there are 5

A

GAD65 antibodies - around 80% at diagnosis
Islet cell antibodies - around 69-90% at diagnosis
ZnT8 antibodies
Insulin antibodies (IAA)
C-peptide/insulin/glucose levels

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

what are markers of beta cell autoimmunity in type 1 diabetes

A

autoantibodies

islet cell antibodies (ICA, against cytoplasmic proteins in the beta cell), antibodies to glutamic acid decarboxylase (GAD-65), insulin autoantibodies (IAA), and IA-2A, to protein tyrosine phosphatase
Autoantibodies against GAD 65 are found in 80% of patients with type 1 diabetes at clinical presentation
Presence of ICA and IA-2A at diagnosis for type 1 diabetes range from 69-90% and 54-75%, respectively

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

what does IAA prevalence correlate with

A

correlates inversely with age at onset of diabetes; it is usually the first marker in young children at risk for diabetes and found in approximately 70% of young children at the time of diagnosis

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

what are the features of type 2 diabetes

A

due to insulin resistance
less acute onset compared to type one
progressive decline in beta cell function

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

describe in more detail, the progressive decline in beta cell functionn

A

may have up to 50% beta cell loss at the time of diagnosis

4-6% decline per year thereafter

21
Q

what does the progressive decline in beta cell function in type 2 diabetes lead to

A

a gradual loss of effectiveness for anti hyperglycaemic therapies that lower blood glucose levels via the action of endogenous insulin

22
Q

what are the modifiable risk factors for type 2 diabetes

A

overweight and obesity
Sedentary lifestyle
Previously identified glucose intolerance
Metabolic syndrome
Hypertension
Decrease HDL cholesterol
Increased triglycerides
dietary factors
Intrauterine environment
Inflammation

23
Q

what are the non modifiable risk factors for type 2 diabetes

A

ethnicity
Family history of type 2 diabetes
Age
History of gestational diabetes
Polycystic ovary syndrome

24
Q

what is first line treatment for diabetes type 2

A

metformin

25
Q

what is 2nd line for diabetes type 2

A

NICE - SU

26
Q

what is 3rd line for type 2 diabetes

A

in obese overweight, if HbA1c is 64 (8%) e.g SGLT2i/DPP4 inhibtors/ GLP-1 receptor agonists

27
Q

what happens in HbA1c is ober 80

A

need to add insulin

28
Q

what is the dosage of metformin

A

start at 500mg, increase to max 2.5 - 3g/day

29
Q

what is the BMI used for metformin

A

BMI greater than or equal to 18kg/m2

30
Q

when do you avoid metformin

A

–eGFR <30; caution with eGFR 45
–Severe hepatic impairment
–Stop with intercurrent illness

31
Q

what do you use if there is GI intolerance

A

metformin MR

32
Q

what kind of onset is metformin

A

slow onset - for rapid control consider SU therapy

33
Q

what are the advantages of metformin

A

safe and effective
Over 50 years of use
Weight neutral
Reduce CV morality
Can be used in pregnancy

34
Q

what does metformin do to glucose

A

it decreases hepatic glucose production, decreases intestinal glucose absorption and improves insulin sensitivity in peripheral tissues

35
Q

does metformin cause hypoglycaemia

A

not when used alone except in starvation, excessive exercise without food or use with alcohol intoxication

36
Q

what are examples of GLP-1 receptor agonists

A

Exenatide, Exenatide Weekly, Lixisenatide, Liraglutide, Albiglutide & Dulaglutide

37
Q

when are GLP-1 therapies used

A

as 3rd line

38
Q

what does GLP-1 receptor agonists lead to

A

weight loss, reduction in SBP

39
Q

what is a hypo episode

A

3.9mmol/L and below

40
Q

what are the symptoms and signs of a hypo episode

A

Sympathetic:
*(Warning signs) Sweating, tremulousness, palpitations, blurring, hunger, pins & needles
–Neuroglycopenic
*Confusion, incoordination, drowsiness, seizures, coma,

41
Q

what is the treatment of a hypo episode

A

glucose - rule of 15

42
Q

what is DKA

A

diabetic ketoacidosis

43
Q

when does DKA happen

A

in type 1 DM, new diagnosis, long standing type 2 rarely

44
Q

what is hyperglycaemia

A

greater than 11mmol/L

45
Q

what are the ketone measurements in DKA

A

*Ketones >=3 mmol/L , Urine >2+ ketones

46
Q

what are the treatments for DKA

A

*IV Fluids
*Potassium replacement
*Insulin replacement
*Replacement of electolytes
LMWH, Antibiotics

47
Q

what is the difference between HHS and HONK

A

HHS is a potentially life-threatening emergency

It does not usually lead to the presence of ketones in the urine, as occurs in diabetic ketoacidosis (DKA), which is why it was previously referred to as HONK (hyperglycaemic hyperosmolar non-ketotic coma).

48
Q

what are the features of HHS and what are the treatments

A

*Poorly controlled Type 2
*Osmolality >320
*Treatment:
–IV Fluids, IV Fluids, IV Fluids
–Replace electrolytes
–IV insulin may be needed
–LMWH

Semester 4 (80 decks)

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