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Baz Y2 Semester 2 > Week 6 Diabetes Mellitus > Flashcards

Week 6 Diabetes Mellitus Flashcards

1
Q

Where does the pancreas release insulin into?

A

The portal vien

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2
Q

What is significant about the production of insulin and free c-peptide?

A

Free c-peptide can be used to measure levels of endogenous insulin production in someone who is taking exdogenous insulin

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3
Q

What is true about beta cells, insulin secretion and glucose levels?

A

Insulin secretion by beta cells is directly coupled to glucose influx

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4
Q

What are the phases of insulin secretion?

A

Intially you get a large release of stored insulin in response to food.

You then get a secondary release of newly synthesised insulin a bit later.

This is known as biphasic release

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5
Q

What is GLUT 4?

A

It is a glucose transporter which is prensent in insulin target tissue. Insulin promotes the translocation of GLUT 4 to cell membranes enabling insulin dependent glucose uptake

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6
Q

Why is drowsyness one of the first symptoms of hypoglycemia?

A

The brain has no stores of glucose and depends entirely on blood glucose

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7
Q

What are the three genetic cause of insulin resistance where there are genes missing involved in the receptor cells?

A
  • Leprechaunism
  • Rabson-Mendenhall syndrome
  • Type A insulin resistance
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8
Q

What is different about genetic insulin resistance

A

It is extremely severe compared to aquired

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9
Q

What is distinguishing clinical feature of severe autosomal insulin resistance?

A

Dark skin folds

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10
Q

What is more likely to lead to insulin resistance, visceral fat or subcataineous fat?

A

Visceral fat.

It is more metabolically active.

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11
Q

Are men or women more suceptable to insulin resistance?

A

Men have a stronger tendency to deposit visceral fat (central obesity) whereas women subcataineous. This makes men more like to develop diabetes

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12
Q

What are osme endocrine causes of insulin resistance?

A

Any disorder that results in the overproduction of hormones which aim to increase blood sugar and therefore supress insulin.

Pheochromacytoma
Acromegly
Cushing’s

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13
Q

What are the dianostic cutoffs for diabetes blood tests?

A
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14
Q

What fasting plasma glucose level signifies pre-diabetic?

A

6

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15
Q

What are the HbA1c levels for pre-diabetic and diabetic?

A
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16
Q

What is HbA1c?

A

Represents a lng term average of blood glucose levels as measure the amount of glycated haemaglobin.

This is a long term average as an erythrocyte has a lifespan of 120 days

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17
Q

In what situations should HbA1c not be used as a diagnosis?

A

Any situation where diabetes may have a rapid onset and glucose levels rise rapidly:

  • Suspected type 1 diabetes
  • Pregnancy
    This will result in false nagative

Any situation where red cells survival is reduced:

  • Haemoglobinopathy
  • Haemolytic anaemia
  • Severe blood loss
  • Splenomegaly
  • Antiretroviral drugs
    False negative

Red cell survival increased:

  • Splenectomy
    False positive

Anything where redcell turnover is high:

  • Dialysis
    False negative

Not enough red cells:

  • Iron and vitamin B12 deficiency
    False negative
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18
Q

How does an oral glucose tolerance test work?

A

Patient fasts overnight

In morning they are 75g oral glucose.

Blood glucose then measured 0h and 2h

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19
Q

What levels of a glucose tolerance test define pre-diabetes?

A

Having a fasting plasma glucose of < 7

But oral tolerance reveals 7.8-11.0

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20
Q

What are the levels for all three pre-diabetic states?

A
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21
Q

What is the treatment for someone who is pre-diabetic?

A
  • Advise on weight loss/healthy lifestyle
  • Check HbA1c annually
  • Consider more aggressive cardiovascular risk reduction
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22
Q

Why does type 2 diabetes get worse with age?

A
  • Obesity increases with age
  • Beta cell function reduces with age hence there is also some insuficiency making it worse
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23
Q

What is the pathogenesis of type 1 diabetes?

A
  • Genetic predispostion
  • Environmental trigger e.g. infection/ toxin
  • Autoimmune mechanism activated (can detect antibodie in blood)

A combination of these results in the destruction of pancreatic beta cells

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24
Q

What antibodies can be detecte in type 1 diabetes?

A

GAD, IA2 and/or ZnT8

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25
What are the three stages of type 1 diabetes development?
26
What is a geographical prevelence pattern to type 1 diabetes?
It is more prevelent the further north you go
27
Autoimmune disorders ascosiated with Type 1 diabetes?
* Thyroid disease * Pernicious anaemia * Coeliac disease * Addison’s disease * Vitiligo
28
What is an Exocrine Pancreas Disorder – Type 3c diabetes
Any insulin deficiency caused by damage to the pancreas as a whole * Pancreatectomy * Trauma * Tumours Also causes pancreatic exocrine problems
29
What drug can lead to insukin resistance?
Prednisolone/ Other glucocorticoids Same reason why cushing's can lead to insulin resistance. Glucocorticoids aim to increase blood sugar and can lead to the liver developing insulin resistance.
30
What are the forms of monogenic diabetes?
Maturity Onset Diabetes of the Young (MODY) Neonatal diabetes Mitochondrial diabetes Don't need to know too much. Just remember that MODY happens in teen years, neonatal happens as a baby, mitochondrial diabetes happens in teenage years also but with neurological features
31
32
What is the protocol for diabetic keto acidosis?
* Insulin * Fluids
33
Treatments for hypoglyceamia?
Normally oral glucose If very severe can give glucagon injection
34
Limit for blood glucose you can drive with?
< 4 and you can't drive
35
How long do you need to wait after a severe hypo before driving?
48hours
36
What happens if you have two severe hypos in close succession?
Can't drive for a month
37
When do you have to informt he DVLA of your diabetes?
If your insulin therepy last (or is predicted to last) for more than 3 months
38
What is the diagnosis of a hyperglycaemic hyperosmolar state?
* Marked hyperglycaemia (normally >30mmol/L * Osmolality >320 mOsm/kg * 10% of body weight lost in water (hypovolaemic)
39
Treatment for hyperglycaemic hyperosmolar state?
* Fluids
40
What differentiates HHS form DKA?
HHS is the extreme end of a spectrum of dehyration and hyperglycaemia. There tends not to be ketosis because this is a insulin sufficient state, however, morbidity/mortality is high. If ketones/ acidosis present then treat under DKA protocol instead
41
Why does hyperglycaemia lead to macrovascular disease?
High blood sugar has various mechanisms that damge vessel endothelium leading to atherosclerosis
42
Things that contribute the diabetic retinopathy
- Intracellular polyol pathway : conversion of glucose into sorbitol (glucose alcohol) - Hyperglycaemia promotes formation of advanced glycosylated end products (AGEs) that damage basement membanes and blood vessel wall components - Oxidative stress - Growth factors, including vascular endothelial growth factor (VEGF), play a role in development of retinopathy Highlight: * Sorbitol * AGEs * Oxidative stress * Endothelial growth factor
43
What is the appearence of stage 1 diabetic retinopathy? WHat do it mean for function?
* Micro haemhorrages and micro aneurisms appear as small red dots * Retinal oedema can result from microvascular leakage and compromise of blood-retinal barrier – appears as grayish retinal areas Function: Sight is not affected and you don’t need treatment - 1 in 4 chance that it could progress to other stages in next 3 years
44
What is stage 2 of diabetic retinopathy? What does it mean for function?
Stage 2: Pre-proliferative - Bleeding into the retina - High risk vision could be affected - More frequent appointments (3-6 months) to check retina
45
What is stage 3 diabetic retinopathy? What does it mean for function?
- Stage 3: Proliferative - Formation of new blood vessels on surface of retina -> vitreous haemorrhage - White areas on retina (”cotton wool spots”) can be sign of impending proliferative retinopathy - Blindness can occur through vitreous haemorrhage and traction retinal detachment - Treatment will be offered to stop vision getting worse but not possible to retore any vision lost
46
When does screening start for diabetic retinopathy? How regular is screening?
For those with type 1 it starts at age 12 For those with type 2 it starts at diagnosis If no retinopathy present screen every 2 years If retinopathy present screen every year
47
Two procedural treatments for diabetic reitinopathy?
Treatment * Laser photocoagulation: - All diabetes patients with new vessels * Vitrectomy: - Persistent vitreous haemorrhage - Retinal detachment threatening macula
48
Two pharmacological treatments for diabetic retinopathy?
Pharmacological Therapy: - Fenofibrate: reduce risk of progression of retinopathy and need for laser in T2DM - Anti-VEGF intravitreal injections for macular oedema
49
What is the earliest sign of diabetic renal disease?
Microalbuminuria : urinary albumin excretion 30-300 mg/day
50
What is the definition of Proteinuria/Nephropathy
Proteinuria/Nephropathy: urinary albumin excretion > 300 mg/day with or without raised serum creatinine level
51
What changes happen in the kidney is diabetic kidney disease?
* Increased glomerular basement membrane thickness * Microaneurysm formation * Mesangial nodule formation (KimmelsteilWilson bodies)
52
What levels of glycaemic control and blood pressure should you aim for when screening for diabetic kidney disease?
Screening and Prevention - Glycaemic control : HbA1c < 53 mmol/mol - Blood pressure: BP < 130/80
53
What drugs help with diabetic kidney disease?
* Always ACEi/ARBs regardless of blood pressure * SGLT2 inhibitors
54
What ACR levels indicate nephropathy?
- Urine ACR > 2.5 mg/mmol in men indicates microalbuminuria - Urine ACR > 3.5 mg/mmol in women indicates microalbuminuria - Urine ACR > 30 mg/mmol indicated nephropathy/proteinuria
55
Two types of neuropathy you can get in diabetes
- Distal symmetric polyneuropathy - CV autonomic neuropathy
56
Symptoms of autonomic neuropathy in diabetic patients?
* Hypoglycaemia unawareness * Postural hypotension * Gastroparesis * Bowel changes including faecal incontinence * Erectile dysfunction
57
Problems that present in the feet of someone with diabetes?
* Foot ulcer - neuropathy, can become infected. Loss of sesation makes it harder to look after foot injury. * Ischaemia leading to wet necrosis
58
Three types of diabetic microvascular problems?
- Retinopathy - Nephropathy and CKD - Neuropathy and diabetes foot ulcer
59
Though note that sulphonylureas aren't used much due to weight gain and gypo risk so probs don't need to know too much about them except that they encourage insulin reslease
60
What is the general diagnostic criteria for diabetes?
Osmotic symptoms + 1 blood test +ve OR Two blood tests +ve

Baz Y2 Semester 2 (25 decks)

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