Diabetes

Question 1

Are all new-onset Diabetes in older people is type 2

Answer 1

No, if ketotic +/- poor response to oral hypoglycaemics and patient is slim or has a family/PMH of autoimmunity

THINK OF LATENT AUTOIMMUNE DIABETES IN ADULTS (LADA)

Measure Islet cell antibodies

Nevertheless it is a form of type 1 DM

Question 2

Define Type 1 diabetes Mellitus

Answer 2

Usually occurs in adolescents or at any age.

It is the autoimmune destruction of pancreatic B cells causing in no insulin production.

patients must have insulin

prone to ketoacidosis (can present with it) and weight loss

Associated with HLADR3 or DR4 and can be with other autoimmune diseases

Question 3

Define Type 2 diabetes Mellitus

Answer 3

It is the gradual resistant to insulin or the fail of secretion of enough insulin from pancreatic B cells or BOTH.

Formally non-insulin dependent DM (NIDDM)

usually in Asian men and the elderly

most are over 40s, but now many teenagers get it too

Stronger environmental association compared to T1DM

Question 4

Cuases of Type 2 diabetes Mellitus

Answer 4

Obesity

Lack of exercise

calorie and alcohol excess

Question 5

Maturity onset diabetes of the young (MODY)

Answer 5

A rare from of type 2 DM of autosomal dominant form.

Affects young people with +ve Fx

Question 6

Investigations of Diabetes

Answer 6

Diabetic if:

Fasting plasma glucose >7mmol/L

Random plasma glucose (+ Symptoms) >11.1mmol/dL

Glycated Hemoglobin HbA1c >6.5% (48mmol)

Question 7

What is impaired glucose tolerance test

Answer 7

fasting plasma glucose of <7mmol/L

and at 2h after oral glucose load –> 7.8-11 mmol/L

plasma glucose at 2h: >11.1mmol/L

Question 8

Impaired fasting glucose

Answer 8

plasma glucose 5.6-6.9mmol/L

Question 9

Other causes of DM

Answer 9

very important

Steroids

Anti-HIV drugs

newer antipsychotics

Thiazides

others:

Pancreatic: -itis, malignancy, surgery (90% otomy), trauma

Cushing’s disease

Congenital

Question 10

Presentation of diabetes

Answer 10

T1DM				T2DM
Polydipsia			Asymptomatic
Polyuria			        complications - MI
Reduced weight
ketosis

Question 11

Conservative treatment of DM

Answer 11

T1 and T2 the same

Diet
Exercise
Smoking cessation
is
BMI
A HbA1c and blood glucose monitoring
Decrease alcohol

Question 12

Type 1 Medical treatment

Answer 12

Insulin thassss it

Question 13

Type 2 Medical treatment

Answer 13

Metformin (biguanide) 1st line

Question 14

What does Metformin do

Answer 14

Increases insulin sensitivity and helps weight

SE: Nausea, diarrohoea, abdominal pain, not hypoglycaemia

Question 15

When to avoid Metformin

Answer 15

If eGFR <36mL/min

stop if
tissue hypoxia (MI, Sepsis)

Morning before GA

Iodine contrast

Question 16

When do you start adding more treatment for T2 diabetes

Answer 16

When HbA1c >53mmol/L at 16 weeks

Question 17

Additional treatments for T2DM at 16 weeks

Answer 17

Sulfonylurea (gliclazide)

increases insulin secretion

SE: increases weight, hypoglycaemia (monitor glucose),

Question 18

Additional treatments for T2DM at 6 months

Answer 18

If HbA1c >57mmol/L at 6 months consider

Insulin

Glitazone

sulfonylurea receptor binders

Glucagon like peptide analogues

a-glucosidase inhibitors

Question 19

Complications of DM

Answer 19

Macrovascular - prevalent in the West as a whole
• Stroke - ↑ x2
• MI - ↑ x3-5
• Amputation for foot gangrene - ↑ x50

Microvascular - specific to DM; manifest 10-20 years after diagnosis:
• Diabetic retinopathy - ~1/3 pts develop eye problems; commonest cause of blindness in <65yo
• Diabetic nephropathy
• Diabetic neuropathy
• Diabetic foot ulcers
Diabetic ketoacidosis
Cataracts - changes in blood sugar cause osmotic changes in the lens

Question 20

What is diabetes insipidus

Answer 20

A disorder cause by low levels of or insensitivity to antiduretic hormone (ADH) leading to polyuria

Question 21

Glucose and the liver

Answer 21

The liver is the principal organ of glucose homeostasis which absorbs and stores glucose as glycogen

Question 22

What is the major consumer of glucose

Answer 22

The brain and is not dependent to insulin

brain only uses glucose and ketones for energy, but prefers glucose

Question 23

What does insulin do

Answer 23

promotes uptake of glucose by cells by activating glucose transporters (GLUT)

Question 24

What happens to glucose in muscles

Answer 24

Stored as glycogen or metabolised to lactate or CO2 and water

Question 25

Effects of insulin in the postprandial state

Answer 25

There will be increased insulin levels, therefore it will inhibit production of glucose from liver and promote entry of glucose to peripheral cells.

Question 26

What is postprandial

Answer 26

After food

Question 27

Where dose glucose come from

Answer 27

When you eat gut breakdown food into glucose in small intestine

Question 28

Effects of insulin in the fasting state

Answer 28

The insulin levels will be low, therefore it will excite the liver to produce more glucose

Question 29

What are hypoglycaemia symptoms

Answer 29

Confusion

Dizziness

Fainting

Coma

Question 30

Factors that affect glucose levels

Answer 30

The WHALE factors
Weigh
Health - MH
Age
Level of activity
Eating habits - diet

Question 31

Define hypoglycaemia

Answer 31

Reduced levels of glucose in blood stream

Question 32

Symptoms of hyperglycaemia

Answer 32

Thirsty

Polyuria - kidneys trying to flush glucose

Dehydration

increased apetite

weight gain may be

Question 33

Define hyperglycaemia

Answer 33

Increased levels of glucose in blood stream

Question 34

What is Diabetic ketoacidosis

Answer 34

acute emergency of T1DM
it is when the body is at stress (infection maybe) so more energy is required but not enough insulin (because of T1DM) therefore there could be hyperglycaemia but no uptake by cells, no insulin, and result in what is called starvation metabolism
to compensate the body starts breaking protein from muscles for amino-acids (proteolysis) and adipose for glycerol and free fatty acids (lipolyisis) all of these products are to taken to the liver for Gluconeogenesis (formation of new glucose). Then glucose is formed which is good, but a by-product is produced by gluconeogensis is Acetyl-COa. Acetyl-COa promotes ketogenesis which produces ketones. Ok ketones are good they give the brain energy, however too much ketones in the blood alter the bloods Ph causing metabolic acidosis (ketoacidosis)
glycogenolyisis also takes place independent of the above factors, here glycogen is broken down for glucose which is good as well.
However, although we were successful in producing more glucose, we cant use the glucose because of the lack of insulin, therefore we have hyperglycaemia.
Now, for the clinical presentation of diabetic ketoacidosis. One will have abdominal pain, nausea, and vomiting. These are caused by the release of inflammatory cytokines (released after lipolysis) causing irritation of the gut. After this vomiting dehydration occurs, but in ketoacidosis dehydration is severe. This is made worse with hyperglycaemia. Why? Because, with hyperglycaemia will not be able to reabsorb all of the glucose, causing glucosuria. When there is glucoseuria, glucose is osmosmotically active therefore it will suck more water with it and releasing it in the urine, thus less water levels in the body, thus dehydration (osmotic diuresis). Dehydration causes altered mental status, which is made worse with metabolic acidosis caused by increased ketone levels in the blood. Metabolic acidosis, if severe enough, can cause cardiac arrhythmias or abnormal heart rhythms that can be fatal.

Question 35

Patient with MI and is found to have hyperglycaemia

Answer 35

Give insulin infusion then consider management of diabetes