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Year 3 - Medicine > Week 11 - Diabetes Mellitus > Flashcards

Week 11 - Diabetes Mellitus Flashcards

1
Q

When is the peak incidence of diagnosis of T1DM?

A

6m - 5yr

50% are diagnosed before 18

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2
Q

What percentage of Ps with T1DM have a FHx of this disease?

A

15%

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3
Q

Which region of which chromosome is predominantly affected in T1DM?

A

HLA region on Chromosome 6

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4
Q

What do the following cells of the pancreas produce?
- α cells
- β cells
- δ cells
- γ cells
- epsilon cells

A
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5
Q

What is the pathophysiology of T1DM?

A

AI destruction of insulin-secreting pancreatic β cells - means they are unable to produce insulin. Cannot regenerate.

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6
Q

Which are the main ABs that we look for in T1DM?

A

GAD
IA2
ZnT8

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7
Q

What happens to the pancreas in T1DM?

A

Loses mass, get atrophy / hypertrophy - loss of β cells.

In healthy pancreas - get lots of β cells filling the space

In T1DM - β cells are destroyed = lots of spaces within the pancreas

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8
Q

What is the honeymoon period in T1DM?

A

Thought that there is a genetic predisposition towards T1DM. When an environmental trigger occurs - this kicks the body into attacking the pancreas = inflammation and necrosis.

However, it may take time for Sx to be noticeable as the body is still able to produce some insulin = honeymoon period (insulitis & pre diabetes).

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9
Q

Which other AI diseases are associated with T1DM?

A

Coeliac
Hypothyroidism
Grave’s
Addison’s
Hypogonadism
Pernicious Anaemia
Vitiligo
AI Polyglandular syndromes

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10
Q

What are the Sx of T1DM?

A
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11
Q

What are ketones?

A

They are produced as a result of FA breakdown - and are used peripherally as an energy source if glucose is not available.

Ketones cause acidosis of the blood to rise.

Can measure ketone levels in blood or urine.

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12
Q

What is C-peptide? How is it used to detect DM?

A

Proinsulin = broken into insulin and C-peptide.

If the body is producing insulin, you will get good C-peptide levels.

If the body is not producing insulin (DM) then you cannot detect C-peptide.

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13
Q

What does it mean if the C-peptide levels are
- low
- intermediate
- high?

A

Low - think T1DM

Intermediate - favours T2 over T1. Consider rarer genetic forms of diabetes

High = T2DM (insulin resistance)

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14
Q

What is the first line choice of Rx for T1DM in the UK?

A

Basal-bolus regime of insulin

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15
Q

Which Ps should be offered insulin pump therapy in the UK?

A

Those who suffer disabling hypoglycaemia or have HbA1c >69

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16
Q

Which insulins are long acting (once-daily)?

A

Lantus
Levemir

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17
Q

Which insulins are ultra-long acting?

A

Tresiba
Toujeo

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18
Q

What are biphasic insulins?

A

A mixture of short acting and intermediate acting insulin

e.g. Novomix 30 (30% short and 70% intermediate)

Rarely used in T1DM

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19
Q

What is the basal-bolus regime of insulin?

A

Have a basal injection at the start of the day and then add bolus injections 15-20 mins before each meal time of short-acting insulin.

Is called multi daily injection therapy

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20
Q

When are Ps more insulin resistant?

A

In the morning

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21
Q

What are ultra strength insulins?

A

Ps are told to inject with them each day but actually covers a little bit longer - which means they are good for teenagers.

Used for Ps with recurrent DKAs.

However can get areas of lipohypertrophy over time.

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22
Q

What is a continuous insulin pump?

A

Delivers continuous insulin via a cannula in both basal and bolus patterns

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23
Q

What do you need to be cautious of with continuous insulin pumps?

A

If they get disconnected there is only 2-3 hours before the P goes into DKA

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24
Q

Who can have continuous insulin pumps?

A

12+
T1DM
+ multiple episodes of disabling hypoglycaemia
+ HbA1c has remained high despite other Rx

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25
Q

What is DAFNE?

A

Dose Adjustment for Normal Eating
- adjusting dose of bolus insulin depending on the carb amount you are eating

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26
Q

What is the insulin to carb ratio?

A

1 : 10g carbs

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27
Q

How much does 1 unit of insulin bring the BS down on average?

A

On average it will reduce the BS by 3

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28
Q

What are the warning signs of hypoglycaemia?

A

Shaky, dizzy
Blurry vision
Sweaty
Weak or tired
Upset or nervous
Headache
Hungry

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29
Q

What are the warning signs of hyperglycaemia?

A

Dry skin
Extreme thirst
Hungry
Freq urination
Blurred vision
Drowsy
Wound healing slow

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30
Q

What are sick day rules?

A

How and when you should adjust insulin amounts during periods of illness

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31
Q

Who needs to inform the DVLA about diabetes?

Who should not drive with diabetes?

A

Anyone using insulin therapy must inform the DVLA.

Anyone who has had impaired awareness of hypoglycaemia, or 1 episode of severe hypoglycaemia in the last 12 months should not drive. (Severe = did they need 3rd party assistance to recover)

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32
Q

Which score can be used to assess whether Ps are coping with living with their diabetes?

A

Diabetes Distress Score

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33
Q

What are the possible methods being investigated to fix T1DM in the future?

A

Artificial pancreas

Islet cell transplantation

Allogeneic pancreatic islet cell transplantation involves the removal of cells called islet cells, which are responsible for the production of insulin, from human donors. These cells are inserted into the patient’s liver to restart insulin production within the body. However, patients who have this procedure will need to take medications to help their bodies’ immune system to accept the cells.

An artificial pancreas is a man-made device that is designed to release insulin in response to changing blood glucose levels in a similar way to a human pancreas.

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34
Q

What are the microvascular complications of T2DM?

A

Retinopathy
Neuropathy
Nephropathy

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35
Q

What are the microvascular complications of T2DM?

A

IHD
CVD
PVD

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36
Q

How is T2DM diagnosed on bloods?

A

Glucose >11.1 + Sx
or 2 x separate Glucose >11.1

HbA1c = or > 48

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37
Q

What should fasting blood values be for Ps with and without T2DM?

A

<6 = without
6.1-6.9 = impaired tolerance
>7 = DM

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38
Q

What should the blood values for Ps be 2 hours after drinking glucose solution?

A

<7.8 = without
7.9-11.0 = impaired tolerance
>11.1 = DM

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39
Q

What is the pathophysiology of T2DM?

A

dec insulin secretion - due to β cell death
Inc α cells = inc glucagon which causes blood sugars to rise.

Get inc in circulating FAs and high lipids

Get insulin resistance in the muscles and liver

Get impaired incretin effect in the gut (e.g. GLP1) - make the body secrete insulin.

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40
Q

What are the RF for developing T2DM?

A

Age > 45 years increased risk ~ 6 fold
Obesity – BMI > 35 = x5, BMI > 25 = x3
HTN = x3
Hyperlipidaemia = x4
FHx: first degree relative = x3, 2 first degree x6
Genetic upto x10
South Asians - x6 risk
Some meds can inc risk - e.g. steroids, some antipsychotics, beta blockers, statins and diuretics

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41
Q

What are the stages of T2DM

A

Normal glucose tolerance
Impaired glucose tolerance
T2DM

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42
Q

How does ectopic fat cause T2DM?

A

Ectopic fat => inc inflammation = impaired oxidative capacity and triggers insulin resistance

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43
Q

What is metabolic syndrome?

A

Central obesity + 2 of
- inc 3Gs
- dec HDL
- inc BP
- inc fasting plasma glucose

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44
Q

Why is exercise good in combating T2DM?

A
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45
Q

What has been shown to reverse T2DM?

A

Diet or weight changes

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46
Q

What is the most common cause of death amongst diabetic patients?

A

IHD

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47
Q

Why does T2DM cause IHD?

A

It increases atherogenesis (formation of fatty deposits in the arteries).

Does so because fatty acid excess, insulin resistance and hyperglycaemia = inc oxidative stress, inc PKC and AGEs. This in turn causes changes to the endothelium = vasoconstriction, inflammation and thrombogenesis.

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48
Q

How is T2DM managed?

A

Diet
Exercise
Weight loss
Medications
Prevent complications - statins, Anti-HTs, Anti-Plts

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49
Q

At what BMI would the NHS consider bariatric surgery for a P?

A

> 35

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50
Q

What is the first line medication for hypertension with T2DM?

A

ACE1 or ARB

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51
Q

When do you give anti-platelet therapy in Ps with T2DM?

A

Only if there is CVD.

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52
Q

When do you give statins in Ps with T2DM?

A

If the Qrisk score is >10% over the next 10 years.

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53
Q

Is glucose monitoring offered in Ps with T2DM?

A

Not routinely - unless on an agent which causes hypoglycaemia.

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54
Q

What is the emergency presentation of
- T1DM
- T2DM

A

T1 = DKA

T2 = HHS (Hyperosmolar Hyperglycaemic State)

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55
Q

What is the MOA of biguanides?

A
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56
Q

Name one example of a biguanide drug used.

A

Metformin

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57
Q

What are the SEs of biguanides?

A

GI - 5% are intolerant
Headaches
B12 deficiency - dec absorption - troublesome as diabetic pop are at risk of peripheral neuropathy
Hypoglycaemia with combo therapy

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58
Q

When are biguanides contraindicated?

A
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59
Q

What is the MOA of sulphonylureas?

A

Block K+ ATP in β cells of pancreas - simulates insulin secretion.

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60
Q

Give an example of a sulphonylurea

A

Gliclazide
Glimepiride

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61
Q

What are the SEs of sulphonylureas?

A

Hypoglycaemia
Weight gain
Secondary failure

(Secondary failure to oral hypoglycemic agents is defined as a good initial response to oral agents (at least one month) with decreasing effectiveness and eventual failure.)

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62
Q

What are the contraindications of sulphonylureas?

A
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63
Q

What is the MOA of SGLT2 inhibitors?

A

Decrease renal tubular glucose absorption - diuretic effect - pee the glucose out.

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64
Q

What examples of SGLT2 inhibitor drugs are there?

A

Dapagliflozin
Canagliflozin
Empagagliflozin

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65
Q

What are the SEs of SGLT2 inhibitors?

A
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66
Q

When are SGLT2 inhibitors contraindicated?

A

Risk of DKA

Caution - elderly, HF, CKD

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67
Q

What is the MOA of GLP 1 agonists?

A

Stimulate insulin release
Reduce glucose sensitivity
Enhance pancreatic β cells replication
Prevents β cells from decline
Delayed gastric emptying
Inhibit glucagon secretion

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68
Q

What GLP1 agonist drugs are there?

A

Duraglutide
Exanagluitide
Liraglutide
Semaglutide

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69
Q

What are the SEs of GLP1 agonists?

A
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70
Q

When are GLP1 agonists contraindicated?

A
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71
Q

What are the SEs of insulin?

A
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72
Q

What are the different types of insulin that you can get?

A

Short Acting
Mixed
Long Acting

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73
Q

What is the first line Rx for Ps not at high CVD risk?

A

Metformin
Or if GI side effects - Metformin MR

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74
Q

What is the first line Rx for Ps with CHF or atherosclerotic CVD or Qrisk >10%?

A

Metformin (poss MR)
+
SGLT2 inhibitor

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75
Q

If metformin is contraindicated - what drug should be used in diabetic Ps?

A

SGLT2 inhibitors

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76
Q

If metformin or SGLT2 do not adequately control HbA1c - what is the next step?

A

Can switch or add in DPP4 inhibitor, Piogliatzone or Sulfonylureas

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77
Q

What is the definition of hypoglycaemia?

A

Varies
Generally glucose <4mmol

Ps with diabetes - who are used to having high BS much of the time - will get symptomatic at a higher glucose range than this.

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78
Q

Why do Ps get signs of hypoglycaemia?

A

Is an autonomic response via the adrenegeric system.

Adrenal glands and pancreas produce ADR and glucagon in attempt to force the liver to release glucose stores.

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79
Q

What are neurological signs of hypoglycaemia (neuroglycopenia)?

A

Occur when the brain isn’t getting enough glucose

Later sign of hypoglycaemia - <2.8

Slurred speech, slow reactions, disorientation, seizures, loss of concentration, dizziness, confusion, aggression / irrational, COMA

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80
Q

What causes hypoglycaemia unawareness?

A

That neuroglycopenia occurs before autonomic signs - in about 40% if Ps with T1DM

These Ps would qualify for insulin pump therapy

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81
Q

What can precipitate a hypo?

A
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82
Q

Why can impaired renal function cause hypos?

A

Insulin is renally excreted - therefore if there is impaired excretion get a rise in insulin levels = hypo.

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83
Q

How should a hypo be treated?

A

If adult, conscious, orientated and able to swallow - 20g quick / rapid acting carbohydrate

Repeat CBG (capillary blood glucose) 10-15 mins later. If still below <4 then repeat.

Test again - if still below 4 - consider IV dextrose

Once above 4 = ensure slow release carb given - 10-20g.

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84
Q

What can be considered to be 20g or rapid acting carbohydrate?

A
  • 200 ml pure fruit juice e.g. orange
  • 120ml of original Lucozade® (preferable in renal patients) 6-7 Dextrosol® tablets (or 5 Glucotabs®)
  • 4 heaped teaspoons of sugar dissolved in water
  • 3 – 4 Jelly babies
  • 200mls Cola
    Glucojuice is equivalent of 15g of carbs
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85
Q

How should unconscious adults with low BS be treated?

A
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86
Q

When can a glucagon injection be given?

A

If the P is unable to swallow hypo Rx safely

If you have used this - Ps are at risk of further hypos for 24 hours - because the liver has used up all its storage - want to give the liver time to replenish its stores.

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87
Q

How is DKA diagnosed?

A

Hyperglycaemia >11
Ketonaemia >3 (serum) or 2+ (urine)
Acidosis - pH <7.3 + Serum bicarb <15

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88
Q

What is the mortality rate of DKA?

A

4-10%

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89
Q

What is euglycaemic DKA?

A

Meet the criteria for DKA on ketones and acidosis, but have normal glucose values (because the excess glucose is lost in the urine - SGLT2 inhibitors)

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90
Q

What is the pathophysiology behind DKA?

A
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91
Q

What are the signs of DKA?

A
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92
Q

What can precipitate DKA?

A
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93
Q

How is DKA managed by the body?

A

Get hyperventilation - to blow off CO2, renal excretion of H+ (slow), intracellular buffering.

Renal excretion of H+ -> low K+ and Na+, dehydration

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94
Q

What fluids are given in DKA?
How does this affect K+?

A

Usually 100ml per Kg - so 5-7L over 24 hour.

Do a VBG after each bag - check K+

If <3.5 - get senior review
If K is 3.5-5.5 - give 40mmol K+ with each L of fluid
If >5.5 - no K+ given

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95
Q

Which Ps should you be cautious about fluid replacement in?

A

Young (18-25)
Elderly
Pregnant
HF
Renal failure

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96
Q

What is the aim of Rx in terms of ketones, bicarb and blood glucose levels when giving insulin in DKA?

A

Want reduction of

0.5mmol / hr ketones

HCO3 rise of 3mmol / hr

BG fall of 3mmol / hr

Maintain K+ in normal range

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97
Q

What insulin regime is given in DKA?

A

Fixed rate IV insulin

0.1 unit / kg / hr

Also give the Ps usual long acting insulin at usual dose and time - in case the P has a problem with access - otherwise would mean there is no background insulin.

98
Q

What is dextrose used for in DKA?

A

As an add on Rx - NOT REPLACEMENT FLUID or K+

Give 10% dextrose when CBG is <14mmol/L

99
Q

When is a variable rate insulin regime given to a P?

A

If they are not eating and drinking normally

100
Q

What are the possible complications of Rx DKA?

A

Cerebral oedema = from fluid overload
Hypo / hyperkalaemia
Hypoglycaemia
Pulmonary oedema - fluid overload

101
Q

What is the mortality rate of HHS?

A

10-20% - higher than DKA!

102
Q

How does HHS differ from DKA?

A

Get the hyperglycaemia, but do have some insulin so dont get the lipolysis -> ketones & acidosis.

Hyperglycaemia can be going on for quite some time and BS can be quite high for a while before Ps present - dehydration and electrolyte losses are therefore more severe when the P presents.

103
Q

What is the diagnostic criteria for HHS?

A

Hypovolaemia
Hyperglycaemia >30mmol without ketonaemia or acidosis
Osmolality >320

104
Q

How is osmolality calculated?

A

2 (Na + K) + Urea + Glucose

105
Q

What are normal values of blood osmolality?

A

275-295 mmol/kg

106
Q

What does the anion gap show?

A

Whether the anions are out of balance - calculates the difference between the amounts of negative and positive electrolytes in the blood.

Elevated gap - strongly suggests metabolic acidosis

107
Q

How does the diagnostic criteria for HHS and DKA differ?

A

Ps are more dehydrated in HHS and more prone to electrolyte disturbances than DKA - which is why the mortality rate is higher.

108
Q

What are the clinical features of HHS?

A
109
Q

What can precipitate HHS?

A
110
Q

What is the Rx for HHS?

A

Replace fluid loss
Correct electrolytes and osmolality
Reduce glucose
Treat precipitating factor
Prevent complications - e.g thrombosis, cerebral oedema, CPM
Encourage P to eat and drink if safe

111
Q

Which is the best fluid for HHS?

A

0.9% NaCl - 3-6L by 12 hours

112
Q

What reduction of Na and glucose do we aim for when treating HHS?

A

Reduction of Na no more than 10mmol/L in 24 hr

Glucose reducion of no more than 5mmol/L/hr

113
Q

When can you give IV insulin in HHS?

A

If the glucose is not reducing or if ketones are present

114
Q

When is diabetic retinopathy usually observed in Ps with
- Type 1 DM
- Type 2 DM

A

T1 = 3-5 years after diagnosis
T2 = 50-80% have it at 20 years

115
Q

What is the pathophysiology of diabetic retinopathy?

A

Inc glucose => inc oxidative stress -> inc VEGF => inc neovascularitsaion and inc permeability.

116
Q

What are the clinical signs of diabetic retinopathy?

A

Floaters
Blurred vision
Reduced visual acuity
Loss of vision

117
Q

What can be seen on a retina with diabetic retinopathy?

A

Hard exudates
Cotton wool spots
Proliferation of blood vessels
Haemorrhages
Aneurysm

118
Q

What is the general medical Rx for Ps with diabetic retinopathy?

A

Glycemic control
BP control
Antiplatelets
Fibrates

119
Q

What specific Rx exists for diabetic retinopathy?

A
120
Q

What is the term for neovascularisation of the iris?

A

Rubeosis Iridis

121
Q

Why does diabetes cause kidney problems?

A

In diabetes mellitus, there’s an excess of glucose in the blood, because it can’t get into cells, and when blood gets filtered through the kidneys, some of that excess glucose starts to spill into the urine, called glycosuria.
In addition, when there’s a lot of glucose in the blood, it also starts sticking to proteins in the blood — a process called non-enzymatic glycation because no enzymes are involved.
Because glucose can get through the endothelium, this process of glycation can also involve the basement membrane of small blood vessels making it thicken. The process particularly affects the efferent arteriole causing it to get stiff and more narrow - a process called hyaline arteriosclerosis.
This creates an obstruction that makes it difficult for blood to leave the glomerulus, increasing pressure within the glomerulus. At the same time, the afferent arteriole dilates, allowing more blood flow into the glomerulus and increasing pressure further.
High pressure in the glomerulus leads to an increase in the glomerular filtration rate–which is simply the amount of blood filtered through per minute. This is the first stage of diabetic nephropathy, called hyperfiltration.
In response to this high-pressure state, the supportive mesangial cells secrete more and more structural matrix expanding the size of the glomerulus. This matrix deposition and mesangial expansion happen uniformly, or it can result in little nodules within the mesangium called Kimmelstiel-Wilson nodules - which are tiny little balls of protein.
The thickening of the basement membrane counterintuitively makes it more permeable—allowing proteins like albumin through that otherwise would have been filtered out.
It makes sense if you think about our octopus friend once more - as the glomerulus expands, the legs of the octopus naturally have larger gaps between them, in other words the filtration slits widen, making it easier for substances to slip through.
So in the end, the key abnormalities in diabetic nephropathy are a thickened glomerular basement membrane, mesangial expansion, Kimmelstiel-Wilson nodules, and disruption of the podocytes.
Eventually, these changes damage the glomerulus so much that it’s unable to filter blood normally, and the glomerular filtration rate decreases.

122
Q

What is the difference between microalbuminuria and proteinuria?

A

Microalbuminuria is present before proteinuria

30-300mg = albuminuria
300mg + day = proteinuria

123
Q

What histological changes happen to the glomerulus in diabetes?

A

Expansion of mesangium
Glomerular basement membrane thickening
Glomerular sclerosis

Diabetic kidney disease induces structural changes, including thickening of the glomerular basement membrane, fusion of foot processes, loss of podocytes with denuding of the glomerular basement membrane, and mesangial matrix expansion.

124
Q

What is the treatment for diabetic nephropathy?

A

ACEIs
ARBs
BP control
Glycemic control
Lipid management
Protein restricted diet

125
Q

What causes diabetic neuropathy?

A

Inc glucose - inc AGEs, sorbitol = in oxidative stress.

Get impaired peripheral nerve repair

126
Q

What is this called?

A
127
Q

What is this called?

Gets severe pain in 1+ nerve root distribution, usually resolves over 6-12 months

A
128
Q

What is this called?

Affects a single CN or peripheral nerve

A
129
Q

What are the potential autonomic consequences of neuropathy?

A
130
Q

What are the other causes of peripheral neuropathy other than diabetes?

A
131
Q

What Rx can be given for peripheral neuropathy?

A

Lifestyle modification
+
Analgesia - e.g. Duloxetine, TCAs, Gabapentin

132
Q

What risks are associated with PVD?

A

Inc risk of IHD and CV events

133
Q

What are the risk factors for PVD?

A
134
Q

What is peripheral vascular disease?

A

Arterial narrowing due to atheroma deposition

Affects 1/3 of diabetic Ps >50

135
Q

What causes PVD?

A
136
Q

What are the Sx of PVD?

A

Cramp with exertion
Reduced circulation (cold)
Discolouration
Ulcers
Hair loss to extremities

137
Q

What measurement can you take to detect PVD?

A

ABPI

138
Q

What are the Rx options for PVD?

A

Lifestyle modifications
Anti-hypertensives
Lipid lowering meds
Anti-platelets

139
Q

What makes osteomyelitis more likely in an ulcer?

A

Visible bone
Ulcer > 2x2cm and >3mm depth
Longer than 1-2 weeks
ESR >70

140
Q

What is the Rx for foot ulcers?

A

Offloading
Debridement
Abx
Amputation

141
Q

What is Charcot arthropathy?

A

Sudden onset unilateral warmth, redness and oedema over foot/ankle - usually with a Hx of minor trauma

Is a syndrome in patients who have peripheral neuropathy, or loss of sensation, in the foot and ankle. Patients may experience fractures and dislocations of bones and joints with minimal or no known trauma.

142
Q

What are the following called?

A
143
Q

What percentage of pregnancies have diabetic mothers?

A

5%
Most of these = gestational diabetes
Then T1 and T2

144
Q

Why does gestation diabetes occur?

A

More glucose in the blood in pregnancy

Insulin resistance increases in Mum during pregnancy - this is to direct nutrients towards the foetus

Human placental lactogen opposes insulin

Therefore when you have insulin resistance + adaptations in pregnancy to direct nutrients to foetus - get increased lipolysis in adipose and less glucose uptake in the muscle - to direct nutrients to foetus - should lead to increased insulin secretion - and therefore euglycaemia - if glucose is too high, and insulin resistance is already there - mechanism is shifted = hyperglycaemia in pregnancy.

145
Q

How do lipid levels change in pregnancy?

A

They increase during pregnancy

146
Q

What are the risks to the mother of having diabetes in pregnancy?

A

Pre-eclampsia risk inc
Preterm labour risk inc
Worsening of diabetic retinopathy

147
Q

What are the risks to the foetus of diabetes in pregnancy?

A

As diabetes is a vascular disease and the placenta is a vascular organ, the placenta can be in variable condition during pregnancy (both IUGR and macrosomia can occur). Hypoglycaemia at the end of pregnancy can be an indication of less hormonal production and placental failure and necessitate early delivery of the baby by caesarean section.

Risks inc
- congenital malformations
- macrosomia
- birth injury
- perinatal mortality, still birth and miscarriage
- postnatal hypoglycaemia

148
Q

What is it called when the baby’s shoulder gets stuck behind the mother’s pelvic bone during delivery?

A

Shoulder dystocia

149
Q

What is it called when there is increased levels of amniotic fluid?

A

Polyhydraminos

150
Q

What are potential consequences of polyhydraminos?

A

Premature delivery <37w
Waters breaking early
Prolapsed umbilical cord

151
Q

What are the ideal plasma glucose levels (both fasting and throughout the day) that a patient planning pregnancy should aim to maintain?

A

Fasting = 5-7 mmol

Throughout the day = 4-7 mmol

152
Q

At what plasma glucose levels (both fasting and 2-hour) can a diagnosis of GDM be made?

A

Diagnose gestational diabetes if the woman has either:
a fasting plasma glucose level of 5.6mmol/litre or above or
a 2-hour plasma glucose level of 7.8mmol/litre or above

153
Q

When should folic acid be taken in pregnancy?

A

Should be taken preconception until 12 weeks gestation - 5mg/day

154
Q

What should you screen for before a diabetic patient discontinues contraception?

A

Retinopathy screening
Nephropathy screening
Monthly HbA1c - aim <48 without problematic hypoglycaemia

155
Q

At what level of HbA1c should a woman be advised not to get pregnant?

A

If HbA1c is greater than 86mmol

156
Q

Which diabetic medications are safe in pregnancy?

A

Metformin
Insulin

Others are not

157
Q

Which Ps are at risk of GDM?

A

If they have a BMI >30
Previous large baby >4.5kg
Previous gestational diabetes
FHx of diabetes
Minority ethic origin with high prevalence of diabetes in the family

158
Q

How is gestational diabetes managed?

A

Diet and exercise for 2 weeks - if still fasting glucose 5.3-7 - add metformin

2 further weeks - if still 5.3-7 - add insulin

If >7 at diagnosis - add insulin, or if there are complications and FPG is 6-6.9

159
Q

Which is the only sulfonylurea licensed for pregnancy?

When is it prescribed?

A

Glibenclamide

If target not achieved with metformin and insulin, or if metformin cannot be tolerated.

160
Q

When are babies delivered if the mum has
- T1 or T2 DM with no complications
- GDM

A

T1/T2 = between 37 and 39 weeks

GDM = no later than 40+6 week (due to baby size risk)

161
Q

How is diabetes managed during labour?

A

Monitor CBG hourly - ensure between 4-7

Give variable rate insulin infusion in all T1DM at labour onset

Give VRII if CBG is not maintained between 4-7 for other pregnancies

162
Q

How is neonatal hypoglycaemia best avoided?

A

Women should feed their babies as soon as possible after birth (within 30 minutes) and then every 2–3 hours until feeding maintains pre-feed capillary plasma glucose levels at a minimum of 2.0mmol/litre
If capillary plasma glucose values are below 2.0 mmol/litre on 2 consecutive readings despite maximal support for feeding, if there are abnormal clinical signs or if the baby will not feed orally effectively, use additional measures such as tube feeding or intravenous dextrose.
Test blood glucose levels if clinical signs of hypoglycaemia, and treat those who are hypoglycaemic with intravenous dextrose as soon as possible

163
Q

How long do neonates of a diabetic pregnancy need to remain in hospital for following delivery?

A

At least 24 hours - to ensure the BG level is stable and they are feeding well

164
Q

What happens to post-partum women with diabetes?

A

T1/T2 diabetes - back to pre pregnancy care arrangements

GDM - test BG to exclude persisting hyperglycaemia before transferring to community care.
- Check fasting plasma glucose at 6-13 weeks post deliver or HbA1c after 13 weeks. If >7 = T2DM.

Should have annual HbA1c test as well.

165
Q

Neonatal hypoglycaemia is common and will usually resolve within how long?

A

2-3 days of onset

166
Q

What is the most common cause of neonatal diabetes?

A

Monogenic diabetes

167
Q

What age is monogenic diabetes usually diagnosed at?

A

<6 months

168
Q

Is T1 diabetes commonly seen in young children?

A

No - neonatal diabetes and MODY are more common and often misdiagnosed as T1DM

169
Q

What is the common ages for MODY to be diagnosed?

A

6-25 years

170
Q

What percentage of neonatal diabetes will be permanent?

A

40%

171
Q

What are the most common genes that are affected to cause MODY?

A

GCK
HNF1A (HNF4A and HNF1 as well)

172
Q

What is the definition of neonatal DM?

A

Severe hyperglycaemia occurring in the neonatal period

Lasts at least 2 weeks

Requires insulin therapy to control BG

No AI cause

173
Q

When should you suspect MODY?

A

Young person

FHx of diabetes being diagnosed at a young age

Negative AB results for diabetes

Persistently detectable C-peptide

Chronicly mildly elevated fasting blood sugars

174
Q

How do neonatal and MODY differ from T1 DM?

A

because they are caused by gene defects - they may produce insulin (Cpeptide positive) but defective insulin, or a problem with the insulin receptors etc.

They can have less severe hyperglycaemia

Will not have antibodies as no AI cause

May be asymptomatic as a result

175
Q

Which types of diabetes are considered to be polygenic?

A

T1 and T2

176
Q

Will Ps with GCK (glucokinase) MODY require Rx?

A

No - will have lifelong mild stable fasting hyperglycaemia.

May require monitoring in pregnancy and normalisation of BG at this time. Otherwise no Rx needed.

177
Q

How does GCK-MODY affect Ps?

A

It means that they have a fasting BG level higher than the normal population.

178
Q

Are GCK-MODY Ps at risk of micro and macro vascular complications?

A

No - therefore no Rx or screening required

179
Q

What should be a red flag for GCK MODY in pregnancy?

A

Slim Ps with GDM

Ps who have persistent fasting hyperglycaemia between their pregnancies

180
Q

What is the Rx for HNF1A/4A diabetes?

A

Diet

Sulphonylureas

Then add in other meds - metformin and GLP1

Finally progress to insulin.

181
Q

How does HNF1A/4A MODY progress with age?

A

The hyperglycaemia will increase with age - requiring escalation of Rx over time.

182
Q

What is HNF1B MODY linked to?

A

Renal abnormalities
ASD
Pancreatic exocrine deficiency
Neurodevelopmental disorders

183
Q

How can you distinguish between T1 and MODY at diagnosis?

A

Permanent insulin required
DKA
Positive B cell antibodies
= T1DM

MODY - is the opposite of this

184
Q

What is the consequence of insulin resistance?

A

There is reduced glucose uptake by muscle

Is increased hepatic glucose production

Is increased lipolysis in the adipose tissues

185
Q

What factors are linked to insulin resistance?

A

Diet (inc calories, fat, sugars)
Physical inactivity
Genetic conditions (abnormal insulin receptor, signalling, body composition, fat distribution)
Ageing
Medications

186
Q

What syndrome can be caused by insulin resistance?

A

Metabolic syndrome

187
Q

How does metabolic syndrome affect lipid levels?

A

It increases 3Gs, LDL
Reduces HDL
Causes fatty liver

188
Q

Which hormones play a role in metabolism and weight?

A

Thyroxine
Corticosteroids
Growth hormone
Gut hormones - Leptin, Gherkin and GLP1

189
Q

Which is the main appetite stimulating hormone?

A

Ghrelin

190
Q

Which gut hormones are long term regulators of food intake?

A

Insulin
Leptin

191
Q

Which hormone is secreted in response to food consumption, enhances insulin and decreases glucagon secretion and increases satiety?

A

GLP-1

192
Q

What are the two main incretins?

A

GLP-1 and GIP

193
Q

What does DDP4 do to GLP1 and GIP?
How is this used in T2DM?

A

DDP4 degrades GLP1 and GIP

Therefore DDP4 inhibitors are used in T2DM to prevent this from happening.

194
Q

Which syndrome is a rare AR ciliopathy, characterised by retinal dystrophy, obesity, post-axial polydactyl, renal dysfunction, learning difficulties and hypogonadism?

A

Bardet-Biedel Syndrome (BBS)

195
Q

Which syndrome is the commonest cause of syndromic obesity?

A

Prader Willi Syndrome

196
Q

Which Ps qualify for weight loss surgery?

A

BMI >40
or
BMI 35-40 with severe obesity-related comorbidity (e.g. diabetes)

30-35 with poorly controlled diabetes may also be considered.

Remove 2.5 for Ps of Asian descent

197
Q

Why does weight loss surgery cause weight loss?

A

Not just reduced food intake

Also thought to be hormone changes, altered bile acids = poor absorption of nutrients and altered instestinal microbiome

198
Q

What are the systemic benefits of bariatric surgery?

A
199
Q

What are the complications of bariatric surgery?

A
200
Q

What is it called when adults get diagnosed with T1DM later in life?

A

LADA - Latent AI Diabetes in Adults

201
Q

What is the most common medical complication in pregnancy?

A

Gestational diabetes

202
Q

How is insulin affected in T2DM?

A

Is a mix of insulin resistance in cells + reduced insulin output (deficiency)

203
Q

What type of inheritance is found in MODY?

A

Autosomal dominant

204
Q

Apart from neonatal, MODY and T1 & T2 - what other things can cause diabetes?

A

Diseases of the pancreas
Endocrinopahties
Drugs - steriods, thiazides
Immune mediated - rare
Some genetic syndromes

205
Q

Which genetic syndromes are associated with diabetes?

A

Friedreich’s ataxia, Huntington’s disease, myotonic dystrophy, Down’s syndrome, Klinefelter’s syndrome, Turner’s syndrome severe obesity syndromes like Prader Willi, Bardet-Biedl

206
Q

What percentage of Ps are diagnosed with T1DM after 18 years?

A

50%

207
Q

Which antibodies are linked to T1DM?

A

GAD
IA2
ZnT8

208
Q

What BG levels diagnose diabetes?

A

Random plasma glucose >11.1
Fasting plasma glucose >7

Need 2 positive tests on 2 different days

209
Q

What are the glucose thresholds and HbA1c levels for fasting and after 2OGTT

A
210
Q

What are the 4 biggest things that T2DM Ps are at risk of?

A

Microvascular disease
MI
Stroke
HF

211
Q

What has dapagliflozin been proven to be beneficial in?

A

Primary CV prevention
Renal impairment
Established heart failure

212
Q

What are the sick day rules for Ps with T2DM?

A

Temporarily stop
- glucose lowering meds (metformin, SGLT2, GLP-1)

Consider stopping
ACEIs and ARBs
Mineralcorticoid receptor antagonists
Diuretics
Statins (also stop if clarithromycin or erythromycin are prescribed)

213
Q

Why does metformin need to be stopped in illness?

A

Can accumulate in AKI secondary to dehydration - causing lactic acidosis

214
Q

What is the pathophysiology of GDM?

A
215
Q

Which is the only reliable method screening for GDM?

A

OGTT

CBP, FBG, HbA1c, glucose challenge test and urinalysis should not be used.

216
Q

Why is HbA1c not used to identify GDM?

A

Due to the high turn over of RBCs in pregnancy

217
Q

When can pregnant women with GDM stop insulin / metformin?

A

Usually after birth

218
Q

What should you discuss with a pregnant P with GDM at their 36 week appt?

A

Mode and timing of delivery
BG management plan for labour
Inc risk of T2DM after - how to prevent (diet, lifestyle, breastfeeding, metformin)
Benefits of breastfeeding

219
Q

What is more strongly linked to insulin resistance? BMI or central obesity?

A

Central obesity

This is due to more visceral stores of fat

220
Q

How does obesity harm health?

A

4M headings
Mental:-Depression, low self-esteem, Attention deficit disorder( ADHD), Eating disorder, cognitive impairment

Mechanical:-Sleep apnoea , Hypoventilation, Osteoarthritis, Chronic pains, Gastroesophageal reflex(GORD), incontinence, intertrigo, Thrombosis

Metabolic:- Type 2 diabetes, Dyslipidaemia, Hypertension, IHD, Gout, NAFLD,NASH, Cancer-at least 13 types

Monetary:- Lower education achievement, Employment discrimination, Lower income, Chronic disability, Increased health care costs

221
Q

Which staging system is used to score obesity?

A

Edmonton Obesity Staging System (EOSS)

222
Q

Where is ghrelin secreted?

A

Ghrelin(hunger hormone)- secreted in stomach, raised in obesity but reduced by bariatric surgery

223
Q

Where is GLP-1 secreted?

A

Glucagon like peptide-1(GLP-1)- secreted in distal intestine, stimulate insulin secretion and islet cell differentiation & proliferation, reduced in patient with diabetes, levels markedly elevated after bariatric surgery

224
Q

Where is leptin secreted?

A

Leptin – secreted by adipose tissue, decrease food intake and increase energy expenditure by act on hypothalamic receptors

In human obesity, leptin levels are high rather than low suggesting leptin resistance

Congenital leptin deficiency due to mutation of the coding LEP gene causes severe obesity reversed by recombinant leptin replacement

225
Q

Which drugs can cause obesity?

A

Antipsychotics
Glucose-lowering meds - e.g. sulphonylureas and insulin
Recreational drugs - cannabis

226
Q

What is the best approach to discussing a patient’s weight with them?

A

Ask
Assess
Advise
Agree
Assist

227
Q

What is the difference between tier 3 and tier 4 weight loss services in the NHS?

A

Tier 3 services-Structured weight loss programme in the community involving Dietian, obesity physician, psychologist, GP

Tier 4 services in the hospital involving bariatric surgery(obesity physician/endocrinologist, dieticians, diabetes specialist nurse, psychologist , bariatric surgeon) at times hepatologist, cardiologist, sleep physicans

228
Q

What diet principles are good for weight loss in obesity?

A

Deficit of 600 cal per day
Low carb or low fat

229
Q

What dietary change has been linked to remission of recent onset T2DM?

A

Meal replacement approach - 800cal / day for 8-12 weeks

230
Q

How much exercise each week is recommended for weight loss maintenance?

A

225-300 mins / week

231
Q

How does orlistat work?

A

Pancreatic lipase inhibitor - therefore reduces fat absorption.

232
Q

What are the AEs of GLP-1 agonists?

A

N&V, gallstones, pancreatitis

233
Q

Is surgery linked to diabetes remission?

A

Yes at 2 years (72%) but by 10 years 50% had relapsed = 36% remission rate

234
Q

For symptomatic hyperglycaemia, what can be given as rescue therapy?

A

Insulin
Sulfonylurea

235
Q

Following new guidance - what do you have to assess before prescribing Rx for new T2DM Ps?

A

HbA1c
CV risk
Kidney function

236
Q

What is the first line Rx for T2DM Ps?

A

Not at high CV risk = Metformin

CHF or atherosclerotic CVD = Metformin, once tolerated + SGLT2 inhibitor

High risk of CVD (Qrisk 10%+) = Metformin, once tolerated + SGLT2 inhibitor

237
Q

Which drug can be offered if Ps are struggling to tolerate Metformin?

A

Metformin Modified Release

238
Q

If Ps cannot tolerate Metformin or Metformin MR, or they are CI, what drug can be given as a standalone Rx instead?

A

SGLT2 inhibitor

239
Q

If the HbA1c is not well controlled below the individually agreed threshold - what Rxs can be switched or added in to metformin + SGLTi?

A

DDP4 Inhibitor
Sulfonylurea
Pioglitazone

240
Q

When are GLP1 Rxs considered for T2DM?

A

When triple therapy (metformin + 2 other oral drugs) is not effective, tolerated or CI.

Year 3 - Medicine (15 decks)

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