diabetes and its treatments

Question 1

Distinguish between the 2 types of diabetes

Which is more common?

Answer 1

Type 1 - insulin deficiency Type 2 - impaired beta-cell function and/or loss of insulin sensitivity (more common)

Question 2

List at least 3 signs and symptoms of DM

An additional 2 more common in T1DM?

Answer 2

DM:
glucosuria 
polyuria, thirst 
fatigue and malaise 
blurred vision 
infections 

T1DM - weight loss
ketoacidosis (N&V, acetone breath)

Question 3

what is the normal fasting, random plasma glucose ranges, and OGTT (oral glucose tolerance test)

Answer 3

fasting <7
random <11.1

OGTT = if above >11.1 diagnosis of diabetes

Question 4

What is the normal range of HBA1C? Above what is diabetes?

Answer 4

normal = 20-42 mmol/mol
diabetes = >48mmol/mol

Question 5

What is HBA1C a measure of?

Answer 5

indicator of glycaemic control during the previous 2-3 months

Question 6

What conditions required for a person to be diagnosed with DM?

Answer 6

presents with signs and symptoms and levels of plasma are not in the normal ranges for fasting, random, OGTT or HbA1c

Question 7

what are the ranges for impaired glucose control? Impaired fasting glycaemia?

Answer 7

Impaired glucose control
normal fasting, random or OGTT >7.8 but <11.1

Impaired fasting glycaemia
fasting >6.1 but <7
so one the high end

they have pre-diabetes and at an increased risk of diabetes and CVD

Question 8

What kind of disease is T1DM? Treatment options?

Answer 8

autoimmune progressive destruction of islet beta-cells 
treatment:
-insulin 
-regular exercise
-healthy diet

Question 9

What’s ketogenesis (what are the ketones)? What are the acidic parts? Why does this happen more commonly in T1DM rather than T2DM?

Answer 9

ketogenesis - synthesis of ketone bodies by the liver, from fatty acid breakdown products
acidic parts are the acetoacetate = beta-hydroxybutyrate part

happens more commonly in T1DM as they lack insulin, the process of ketogenesis isn’t inhibited. As insulin in T2DM insulin is present, ketogenesis is inhibited.

Question 10

How is hepatic ketogenesis usually regulated?

Answer 10

inhibited by insulin

stimulated by glycagon

Question 11

What danger does this pose?

Answer 11

in starvation and T1DM, ketosis can lead to metabolic acidosis (decrease in blood pH)

Question 12

What’s the main principle behind the insulin schedule for T1DM?

Answer 12

based on the lifestyle of patient

Question 13

What is lipodystrophy and how can you avoid it?

Answer 13

complication of subcutaneous insulin injection

avoid by rotating injection areas

Question 14

Explain the natural history of T2DM in terms of insulin levels, glucose levels, and insulin insensitivity

Answer 14

insulin levels increase to compensate for resistance, rise in prediabetes
glucose levels is maintained for a while but then increase when beta-cell starts to struggle
insulin insensitivity can happen years before pre-diabetes

Question 15

What are 4 other causes of T2DM?

Answer 15

secondary:
endocrine: Cushing’s, acromegaly
pancreatic disease: chronic pancreatitis, surgery, cystic fibrosis
genetic disorders: Down’s syndrome, Prader-Willi
drug induced: steroids, beta blockers, diuretics

Question 16

Explain all the steps of treatment of T2DM

Answer 16

diet/lifestyle interventions 
metformin or SU or DPP-4i or pioglitazone 
duel therapy 
triple therapy 
start insulin 
intensify insulin regime or add drugs

Question 17

How do the following drugs work? Metformin, Sulphonylureas, Prandial Glucose regulators, pioglitazone

Answer 17

METFORMIN = might activate AMP kinase, decreases gluconeogensis and increase glucose utilisation
SULPHONYLUREAS and PRANDIAL GLUCOSE REGULATORS - stimulate insulin secretion - via blockade of islet beta-cell and bind to ATP-sensitive K+ channel cells to release insulin
PIOGLITAZONE - promotes lipid met

Question 18

Acarbose? Incretin mimetics? DPP-4 inhibitors?

Answer 18

ACARBOSE - delays digestion and absorption of starch and sucrose
INCRETIN MIMETICS - incretin response to decrease, promotes insulin release, reduce glucagon secretion and reduces gastric emptying and promotes satiety (controls food intake)
DPP-4 INHIBITORS - same as above

Question 19

SGLT-2 inhibitors – how do they work?

Answer 19

Sodium-glucose co-transporter 2 inhibitors

inhibit renal glucose reabsorption to increase urinary glucose excretion

Question 20

Under what circumstances would bariatric surgery be indicated for patients with T2DM?

Answer 20

BMI >40

or BMI >30 (failed to lose weight and failed drug intervention)