Diabetes and its treatment Flashcards

1
Q

What is type 1 diabetes

A

Insulin deficiency

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2
Q

What is type 2 diabetes

A

Impaired B-cell function and/or loss of insulin sensitivity (insulin resistance)

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3
Q

Symptoms of diabetes

A

Glucosuria (glucose in urine)

Polyuria, thirst (increased volume and frequency of urine)

Fatigue and malaise

Blurred vision

Infections (e.g. candidiasis)

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4
Q

Extra symptoms of type 1

A

Weight loss

Ketoacidosis (N&V, acetone breath)

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5
Q

extra symptoms of type 2

A

Complications (secondary)

altered mental state

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6
Q

What are normal glucose levels (fasting and random)

A

Fasting- <7.0mmol/L

Random <11.1mmol.L

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7
Q

How is diabetes diagnosed

A

If patient is presenting with signs/symptoms and levels of plasma glucose are as below, then positive diagnosis:

  • Fasting>7mmol/L
  • Random>11.1mmol/L
  • Plasma glucose concentration >11.1mmol/L 2h after 75g glucose in an oral glucose tolerance test
  • HbA1c> 48mmol/mol
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8
Q

What does the HbA1c test show

A

Shows glycated haemoglobin

-Indicator of glycemic control during the previous 2-3 months

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9
Q

IF a person is asymptomatic, how is diabetes diagnosed

A

Two abnormal test results are needed (preferably using same test)

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10
Q

What are the test results like when there is impaired glucose tolerance

A

Fasting<7

random or OGTT>7.8<11.1 mol/L (still under the normal range but on the higher end)

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11
Q

What are the test results like when someone has impaired fasting glycaemia

A

Fasting>6.1<7mmol/L

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12
Q

What is the HbA1c like for someone who is pre-diabetic

A

42-47 (do annual screening /give lifestyle advice)

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13
Q

What is ketogenesis

A

Synthesis of ketone bodies by the liver from fatty acid breakdown products

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14
Q

What are the ketone bodies produced during ketogenesis

A
Acetoacetate
which turns into
B-hydroxybutyrate
and
acetone 

(normally a small amount in blood)

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15
Q

When is there increased ketogenesis

A

In starvation and in diabetes mellitus so there is an excess of ketones

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16
Q

What does an excess of ketones do

A

cause metabolic acidosis (decrease in blood pH)

17
Q

What inhibits and stimilates hepatic ketogenesis

A

Inhibited by insulin

Stimulated by glucagon

18
Q

What are the different types of insulins and when would you use them

A

-Short acting (before meals) i.e. analogues

Intermediate-acting (isophane)

Long-acting (insulin zinc suspension and analogues)

Biphasic (pre-mixed) - mix of short and intermediate acting insulins

–> Use them depending on the patient. They are made to suit life-style of patients

19
Q

What is the basal/bolus treatment programme

A

Long acting insulin (Basal) given which lasts for 24h and short acting insulin is given prior to every meal (Bolus)

20
Q

What are the twice daily injections programme

A

Short and intermediate acting insulin injections

21
Q

Where are insulin injections given

A

outer thighs
Lower abdomen
Upper outer arms
Buttocks

22
Q

Why are patients asked to rotate injection sites of insulin

A

To avoid lipodystrophy (which is lipoatrophy and lipohypertrophy) in some sites

23
Q

What are insulin pumps and what do they do (and who can use them)

A

Type 1 only

Continuous subcutaneous insulin infusion

-Continuous basal dose, with patient activated bolus doses at meal times

24
Q

When are insulin injections given

A

(short acting soluble insulin for urgent treatment)
For fine control in serious illness

IN diabetic ketoacidosis

In surgery- peri-operative

25
Q

Secondary causes of diabetes

A

Endocrine- Cushing’s, acromegaly, pheochromocytoma (excess adrenaline)

Pancreatic disease- chronic pancreatitis, surgery, CF, tumour

Genetic disorders- Down’s syndrome, Prader-Willi

Drug induced- steroids, beta blockers, diuretics

26
Q

What is the first step in the treatment of diabetes

A

Diet/ lifestyle interventions trialled for 3 months

27
Q

What is the second step in treatment of diabetes and what are the cautions

A

Metformin (first in line but caution in renal impairment)

or

Sulphonylurea or DDP-4 inhibitor or pioglitazone or SGLT-2 inhibitor

28
Q

What is the third step in treatment of diabetes

A

Dual therapy

29
Q

What is the fourth step in treatment of diabetes and what do you do if this dousing work

A

Triple therapy

-Start insulin- then intensify insulin regime or add drugs

30
Q

action of metformin

A

Decrease gluconeogenesis and increase glucose utilisation

31
Q

Action of sulphonylureas and prandial glucose regulators

A

Stimulate insulin secretion

-Via blockade of islet B cell ATP sensitive K+ channel

32
Q

Mode of action of pioglitazone

A

PPAR y (gamma) agonists which boost the action of insulin

33
Q

What is the incretin release like in type 2 diabetes

A

Slower than a ‘normal’ patient

34
Q

Mode of action of GLP-1

A

Incretin mimetics

35
Q

Mode of action of DDP-4

A

Block enzyme that degrades incretins

36
Q

What do both DDP-4 and GLP-1 mimetic do (they are drugs used in incretin based therapy)

A
Promote insulin release
reduce glucagon secretion
reduce gastric emptying
Promote satiety
Reduce hepatic glucose production
37
Q

What is the sodium glucose co-transporter 2 inhibitor drug (SGLT-2)

Side effects?

A

Inhibits renal glucose reabsorption by inhibits SGLT2 in renal PCT. Increases urinary glucose excretion and decreases blood glucose

Urinary tract infections
POlyuria
Dehydration