Diabetes mellitus Flashcards

1
Q

what percentage of all diabetes sufferers have diabetes type 1?

a) 5%
b) 10%
c) 50%
d) 100%

A

b) 10%

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2
Q

which gene is diabetes type 1 associated with?

A

HLA

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3
Q

what occurs to the pancreas in type one diabetes?

A

beta cell destruction

absolute insulin deficiency

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4
Q

how do DMT1 patients normally first present?

A

Diabetic ketoacidosis

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5
Q

Presenting symptoms of T1DM? (4)

A

Polyphagia
Polydipsia
Polyuria
Glycosuria

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6
Q

Pathophysiology of T1DM?

A

Destruction of b cells so less insulin released. This means that there is less glucose taken up from the blood into tissues. There is a high level of glucose in the blood causing many symptoms

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7
Q

What age does T1DM affect?

A

Before puberty

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8
Q

what 2 substances will be present in the urine of a patient with DMT1?

A

ketones

glucose

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9
Q

give 2 risk factors for diabetes type 1

A

family history

other autoimmune conditions

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10
Q

what enzyme is used in diagnostic antibody testing for DMT1?

A

Glutamate acid dehydrogenase

The level will be low because in T1DM» there are anti GAD antibodies that attack GAD

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11
Q

Main complication of T1DM and describe it

A

DKA
Adipocytes are not receiving enough food because of a lack of glucose in cells» lots of glucose in blood but not in cells.

Fats are metabolised by the adipocytes to form fatty acids.
Fatty acids are converted to ketones by the liver through ketosis.
Ketones are converted to keto acids which accumulate in the blood.
Blood acidity increases which causes many symptoms

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12
Q

Presentation of DKA? (4)

A

Kussmaul breathing
hyperkalaemia» tall tented t wave
Sweet breath
nausea and vomiting

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13
Q

Why does metabolic acidosis from DKA cause hyperkalaemia?

A

Because every cell needs at least H+ or K+ inside it.
In acidosis, there is lots of H+ in the blood so it’s pumped into the cells through the H+/K+ transporter so lots of K+ is pumped out of the cells into the blood» HYPERKALAEMIA

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14
Q

what will be present to smell on the breath of someone with DMT1?

A

ketones on breath

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15
Q

dx of T1DM (3)

A

Venous glucose is high on 2 measurements
Fasting glucose is >7
Urinalysis shows high glucose

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16
Q

Mx of T1DM? (4)

A

1) educate about glycaemic control
2) short acting and long acting insulin
3) Regular capillary blood glucose testing
4) Hba1c every 3-6 months

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17
Q

what would be first line treatment for a DKA and DMT1 in general?

A

insulin

18
Q

why would you give potassium in treatment for a DKA?

A

to prevent rebound hypokalaemia in response to hyperkalemia in DKA

19
Q

why don’t DMT1 patients get AKI as soon as expected in a DKA?

A

polyuria is a protective factor for the kidney

20
Q

why does caution have to be exercised in giving fluids in a DKA?

A

to avoid cerebral overload as brain hydration is maintained

21
Q

Define T2DM

A

Body is producing insulin but the receptors are insensitive to insulin»> blood glucose is very high as a result

22
Q

Cause of t2dm?

A

Prolonged poor diet» too much sugar intake for a long time

23
Q

App Ix of T2DM (4)

A

Fasting glucose
non fasting glucose
oral glucose tolerance test
Hba1c» greater than 6.5% is diabetes

24
Q

Presentation of t2dm?

A

Polyuria
Polydipsia
Blurred vision
Complication symptoms» e.g. macro and microvascular

25
Q

what is first line treatment for DMT2?

A

metformin

26
Q

what time of drug is metformin?

A

biguanide

27
Q

how does metformin work?

A

increases insulin sensitivity

28
Q

give 2 side effects of metformin

A

anorexia (can be good thing in obese patients)
D&V
reduced B12 absorption

29
Q

what is second line treatment for DMT2?

A

sulfonylureas

30
Q

how do sulphonylureas work?

A

increase insulin secretion from beta cells

31
Q

give 2 examples of sulphonylureas

A

gliclazide
glibenclamide
tolbutamide

32
Q

give a side effect of sulfonylureas

A

weight gain and hypoglycaemia

33
Q

what is third line treatment for diabetes?

A

thiazolidinedione (glitazone)

34
Q

what does glitazone do?

A

increases insulin sensitivity

35
Q

4 microvascular complications of T2DM?

A

HHS
Retinopathy
Nephropathy
Neuropathy

36
Q

What is HHS?

A

Hyperglycaemic hyperosmolar state
This is because there is a high amount of glucose in the blood so a high level of osmolarity in the blood» this makes your cells more dehydrated as water moves out of the cells to try and compensate

37
Q

How to check for retinopathy

A

Fundoscopy

Hard exudates, microaneurysms= background retinopathy

Cotton wool spots and angiogenesis= pre-proliferative retinopathy

38
Q

Mx for background and pre-proliferative retinopathy?

A
Background= improve glucose control
Pre-proliferative= pan-retinal photo coagulation
39
Q

Lifestyle Mx for DM?

A

delays

Diet
Exercise
Lipids
ABP
Yearly check up for 4Cs
Smoking cessation
40
Q

What are the 4 Cs for check up?

A

Complications» macro and micro

Control (glycaemic)

Competency» checking injection sites etc

Coping

41
Q

Macrovascular complications of t2dm? (3)

A

Pulses
BP
Cardiac auscultation