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Met 3b > Diabetes > Flashcards

Diabetes Flashcards

1
Q

What percentage of UK adults have diabetes?

A

4.9 percent

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2
Q

What percentage of DM cases are type 2?

A

85 to 95 percent

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3
Q

Is type 1 DM acute onset?

A

yes

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4
Q

What can be said about the onset of type 2 DM?

A

Subacute and insidious

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5
Q

What is the name given to the type of symptoms of T2DM?

A

Osmotic

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6
Q

Which infections are more common amongst DM patients?

A

Staph aureus

Oral and genital candidiasis

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7
Q

What macrovascular complications can occur in DM?

A

Stroke

Myocardial infarction

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8
Q

What eye change is commonly seen on retinoscopy with DM?

A

Diabetic retinopathy

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9
Q

What is the gold standard test for DM?

A

OGTT

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10
Q

What is the normal value for HbA1c?

A

Less than 42mmol/l

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11
Q

What is the target HbA1c for DM patients?

A

Less than 53mmol/l

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12
Q

How can a diagnosis of DM be definitively made?

A
  1. Two abnormal blood tests
  2. One abnormal blood results with symptoms
  3. One abnormal OGTT
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13
Q

What is the aetiology of T1DM?

A

Autoimmune destruction of beta cells in the pancreas leading to dysfunction

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14
Q

Which antibodies are positive in T1DM?

A

ICA and GAD

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15
Q

What is idiopathic T1DM?

A

no antibodies present

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16
Q

What are the features of latent autoimmune diabetes in adults?

A
  1. Diagnosed in adulthood
  2. Usually non-acute (can be often misdiagnosed as T2DM)
  3. Give insulin soon after diagnosis
  4. GAD and ICA antibody positive
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17
Q

What is the peak age of onset for T1DM?

A

5 to 7 years

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18
Q

Which pathogens are linked to the causation of T1DM?

A

Cocksackie

Parvovirus

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19
Q

Which environmental factors influence T1DM?

A

Puberty
European
Season
? Cows milk protein

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20
Q

Which genes increase the susceptibility of T1DM?

A

HLA genes on 6q-HLA DR3/DR4 (high risk)

Genes on chromosomes 2q, 15q, 11q

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21
Q

Which lymphocytes attack beta cells in T1DM?

A

T lymphocytes

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22
Q

What percentage of beta cells are destroyed before symptoms develop?

A

90 percent

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23
Q

What is the pathogenic sequence of T1DM?

A

genetic susceptibility > environmental insult > insulitis > immune attack of beta cells

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24
Q

How often should a diabetic review take place?

A

Every 2 years

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25
Q

What should be checked in the diabetic review?

A 
Symptoms
HbA1c
BP, cholesterol, urine dip, ACR
Eyes, feet, kidney function
Discuss targets
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26
Q

What is the first step in management for DM?

A

Lifestyle advice
Stop smoking
BP control

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27
Q

What is the target BP in DM?

A

140/80

130/80 in cardiovascular or renal disease

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28
Q

What should be given to reduce blood pressure in DM patients?

A

ACE-I

CCBs

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29
Q

What is the cholesterol target in DM?

A

Total

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30
Q

How should eyes be checked for diabetic changes?

A

Annual digital retinal photography

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31
Q

How often should feet be checked in DM?

A

Yearly

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32
Q

How often should ACR/GFR be checked in DM?

A

Yearly

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33
Q

What is the pre prandial glucose target in DM?

A

4-7 mmol/l

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34
Q

What is the post prandial 2 hour target in DM?

A

5-9 mmol/l

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35
Q

When are fructosamine levels useful?

A

To look at long term glycemic control in haemoglobinopathy or pregnancy

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36
Q

What dietary/lifestyle advice is useful in DM?

A

Low salt/fat/sugar
Low GI carbs
30 mins exercise 3 times a week
Weight loss

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37
Q

What is the target weight reduction in DM?

A

3-5 percent

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38
Q

On average, how long does lifestyle work for?

A

One year

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39
Q

What is the second line treatment in T2DM?

A

Oral hypoglycaemic drugs

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40
Q

What are insulin secretagogues?

A

Stimulate insulin secretion from beta cells

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41
Q

How do sulfonyureas work?

A

They stimulate insulin secretion

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42
Q

Give an example of a sulfonylurea?

A

Gliclazide

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43
Q

What are the side effects of sulfonylureas?

A

Risk of hypo

Weight gain

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44
Q

Give an example of a biguanide?

A

metformin

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45
Q

how do biguanides work?

A

increase glucose uptake in liver and muscle cells by improving sensitivity to insulin
decrease gluconeogenesis

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46
Q

What are the side effects of biguanides?

A

Nausea and vomiting

Lactic acidosis if eGFR

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47
Q

What type of drug is acarbose?

A

Alpha glucosidase inhibitor

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48
Q

How do alpha glucosidase inhibitors work?

A

Reduce intestinal glucose absorption by inhibiting alpha glucosidase

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49
Q

What are the side effects of alpha glucosidase inhibitors?

A

Diarrhoea and flatulence

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50
Q

Give examples of glitazones

A

Poiglitazone

Thiazolidinediones

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51
Q

How do glitazones work?

A

PPAR GAMMA agonists that stop FFA binding
Improve insulin sensitivity in the muscle and adipose tissue to increase glucose uptake and put less stress on the beta cells in the pancreas

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52
Q

What are the side effects of glitazones?

A 
Weight gain
Oedema
Heart failure
Post menopausal bone fractures
Bladder cancer
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53
Q

How does a prandial glucose regulator work?

A

Increase insulin secretion from beta cells

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54
Q

Give an example of a prandial glucose regulator?

A

(linides) - repaglinide

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55
Q

How do gliptins work?

A

Stop GLP-1 breakdown by inhibiting DPP-IV

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56
Q

Which enzyme does a gliptin inhibit?

A

DPP-IV

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57
Q

Give an example of a gliptin?

A

Sitagliptin

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58
Q

When should a gliptin be used?

A

3rd line

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59
Q

Are gliptins well tolerated?

A

Yes

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60
Q

Which cells normally make GLP-1?

A

L cells mainly in the ileum

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61
Q

What is the precursor to GLP-1?

A

Proglucagon

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62
Q

What naturally causes the release of GLP-1?

A

Meal ingestion

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63
Q

Which family of hormones does GLP-1 belong to?

A

Incretins

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64
Q

What is the function of GLP-1?

A

Delays gastric emptying so promotes satiety
Increases insulin secretion
Reduced glucagon secretion
Preserves beta cell mass

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65
Q

How does GLP-1 effect beta cells?

A

Promotes insulin secretion

Preserves mass

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66
Q

Give examples of GLP-1 analogues?

A

Liraglutide
Exanantide
Lixsenatide

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67
Q

How many amino acids in GLP-1?

A

31

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68
Q

How do gliptins work?

A

By inhibiting DPP-IV enzyme that normally breaks down GLP-1

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69
Q

What are the side effects of gliptins?

A

Nasopharyngitis

Pancreatitis

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70
Q

What are the side effects of GLP-1 analogues/agonists?

A

Nausea and diarrhoea
Pancreatitis
Pancreatic cancer

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71
Q

Why must GLP-1 analogues be given as an injection?

A

Peptide so will be digested in the gut

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72
Q

What does a GLP-1 analogue do in relation to DM?

A

Increase insulin secretion

Suppresses appetite

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73
Q

When should a GLP-1 analogue be given?

A

BMI>35 and poor glycemic control

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74
Q

How do gliflozins work?

A

Stop reabsorption of glucose in the kidney by inhibiting SGLT2

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75
Q

When should insulin be given in T2DM?

A

When oral glycemic drugs fail

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76
Q

Where is glucose normally absorbed?

A

Small intestine

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77
Q

What hormone stimulates insulin release from the pancreas?

A

Incretins

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78
Q

In which tissues does insulin stimulate glucose uptake?

A

Liver
Muscle
Adipose

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79
Q

When should you give insulin in T1DM?

A

Always

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80
Q

When is insulin given in T2DM?

A 
Poor glycemic control
Pregnancy
Symptomatic hyperglycaemia
Infection
Foot ulcers
Intolerance to drugs
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81
Q

If blood glucose is high in the morning, what adjustment should be made to insulin therapy?

A

Reduce night time long acting insulin

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82
Q

How is endogenous insulin usually secreted?

A

Basal bolus (baseline insulin with increased secretion at meal times)

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83
Q

What are the types of insulin?

A

Human

Analogue

84
Q

What types of human insulin are available?

A

Short acting
Immediate acting
Biphasic (Short and immediate acting)

85
Q

What types of analogue insulin are available?

A

Rapid acting
Long acting - basal
Biphasic (Long and rapid acting)

86
Q

Where should insulin be injected?

A

Into subcutaneous fat
Thigh
Abdomen
Buttocks

87
Q

Which site of insulin injection has the fastest absorption?

A

Abdomen

88
Q

What type of insulin is given with once or twice daily therapy?

A

Long acting

89
Q

What should once to twice daily therapy be used with?

A

Oral hypoglycaemics

90
Q

When is the insulin normally taken in once/twice daily therapy?

A

Before bed or in the morning

91
Q

When should pre mixed (biphasic) insulin be taken?

A

Once before breakfast and again before dinner

92
Q

Which insulin regimen mimics regular physiology?

A

Basal bolus therapy

93
Q

When is the long acting insulin taken in basal bolus therapy?

A

In the morning or before bed

94
Q

When should rapid acting insulin be used?

A

Before main meals

95
Q

Should the units of insulin be included in prescriptions?

A

No

96
Q

For which conditions does DM increase mortality by 2.5x?

A

Cardiovascular disease
Coronary heart disease
Cerebrovascular disease

97
Q

What is the most common complication at the time of diagnosis of DM?

A

Retinopathy

98
Q

Where some other complications of DM?

A

Erectile dysfunction

Abnormal ECG

99
Q

How does DM cause vascular disease?

A

Long term exposure to hyperglycaemia causes full/partial vessel closure and increased vessel permeability

100
Q

What are the risk factors for DM complications?

A

Smoking
Hypertension
Dyslipidaemia
Hyperglycaemia

101
Q

What is the biggest risk factor for DM complications?

A

Smoking

102
Q

What is the least potent risk factor for DM complications?

A

Hyperglycaemia

103
Q

Is diabetic retinopathy common?

A

Yes

104
Q

What is the most common reason for blindness in the UK?

A

Diabetic retinopathy

105
Q

What percentage of people who have had diabetes for 10 years get diabetic retinopathy?

A

50 percent

106
Q

Does proliferative retinopathy involve the macula?

A

No

107
Q

How does severe diabetic retinopathy appear?

A

Cotton wool spots (soft exudates indicating retinal ischaemia)

108
Q

What does fundoscopy show in mild to moderate diabetic retinopathy?

A

Microaneurysms
Dot haemorrhages
Hard exudates (lipid deposits)

109
Q

What is proliferative retinopathy?

A

Retinal ischaemia leading to the production of growth factors and new vessel formation

110
Q

In proliferative retinopathy, where do the new vessels appear?

A

On the disk (NVD)

Elsewhere (NVE)

111
Q

What is diabetic maculopathy?

A

Retinopathy within 1 disc diameter around the macula

112
Q

What types of diabetic maculopathy are there?

A

Focal or exudative

113
Q

What can exudative diabetic maculopathy lead to?

A

Oedema

114
Q

How is diabetic retinopathy monitored?

A

Yearly digital retinal screen

115
Q

How is diabetic retinopathy treated?

A

HbA1c less than 53
Good BP and cholesterol control
Laser photocoagulation

116
Q

What are the types of diabetic neuropathy?

A

Peripheral sensory
Autonomic
Proximal motor (amyotrophy)
Mononeuropathy (cranial nerve palsy)

117
Q

What distribution is often seen in peripheral neuropathy?

A

Glove and stocking

118
Q

What are common complications of peripheral neuropathy?

A

Ulceration and amputation

119
Q

What symptoms are seen in peripheral neuropathy?

A

Numbness
Pins and needles
Burning
Shooting

120
Q

What is the most common cause of neuropathic ulceration?

A

Diabetic neuropathic ulceration

121
Q

Which 3 systems can autonomic neuropathy affect?

A

Genitourinary
GI
Cardiovascular

122
Q

How does autonomic neuropathy affect the genitourinary system?

A

Erectile dysfunction

Atonic bladder leading to urinary incontinence and difficulty voiding

123
Q

Which GI symptoms are seen in autonomic neuropathy?

A

Gustatory sweating
Gastroparesis
Constipation or diarrhoea

124
Q

Which cardiac symptoms are seen is autonomic neuropathy?

A

Postural hypotension

125
Q

What is the most common cause of end stage renal failure in the UK?

A

Diabetic nephropathy

126
Q

Which ethnicities are at greater risk of diabetic nephropathy?

A

South Asians and Afro Carribeans

127
Q

Which histological lesion is seen in on biopsy of diabetic nephropathy?

A

Kimmelstein - Wilson Lesion

128
Q

Which 3 criteria are needed to diagnose diabetic nephropathy?

A

Declining renal function
Hypertension
Albuminuria

129
Q

Which factors need to be controlled in diabetic nephropathy?

A

BP

130
Q

How should blood pressure be controlled in diabetic nephropathy?

A

ACE-I

131
Q

When should metformin be stopped in diabetic nephropathy?

A

eGFR less than 30ml/min

132
Q

When should you refer to nephrology with diabetic nephropathy?

A

eGFR

133
Q

When may a simultaneous kidney and pancreas transplant be needed?

A

T1DM

134
Q

When is HbA1c acceptable at 58mmol/l?

A

Diabetes longer than 10 years

135
Q

How should an MI be treated in diabetic vascular disease?

A

Aspirin, primary angioplasty, IV glucose and insulin

136
Q

What is the 2 year mortality in those that present with peripheral neuropathy?

A

20 percent

137
Q

In a stroke, when can can thrombolysis be used?

A

Within 4h

138
Q

What should be given acutely with ischaemic stroke in diabetic vascular disease?

A

ACE-I, statins, aspirin, glucose and insulin infusion

139
Q

What are the complications of peripheral vascular disease?

A

Intermittent claudication
Rest pain
Buttock pain

140
Q

How is peripheral vascular disease managed?

A

Aspirin and vasodilators

141
Q

Which surgical interventions are available in peripheral vascular disease?

A

Angioplasty/reconstructive surgery

Amputation

142
Q

What are the musculoskeletal manifestations of diabetes?

A 
Charcots neuroarthropathy
Diffuse idiopathic skeletal hyperostosis
Flexor tendniopathy
Diabetic osteoarthropathy
Diabetic cheiroarthropathy (due to limited joint mobility)
143
Q

Which liver condition is more common in DM?

A

NAFLD

144
Q

How can NAFLD progress?

A

NASH

Cirrhosis and fibrosis

145
Q

What do LFTs show with NAFLD?

A

Raised ALT and AST

146
Q

When should a raised ALT and AST prompt further investigation?

A

When more than 2x normal limit

147
Q

What liver disease needs to be excluded with raised ALT and AST?

A

Haemochromatosis

148
Q

Which investigations should be carried out in NAFLD?

A

LFTs
Liver biochemistry
USS
Ferritin

149
Q

How is poiglitazone useful in NAFLD?

A

Stops progression to cirrhosis

150
Q

How can the progression to cirrhosis be halted in NAFLD?

A

Poiglitazone

Rigorous glycemic and diabetic risk factor control

151
Q

When do patients start to experience symptoms of hypoglycaemia?

A

Blood glucose less than 3.6mmol/l

152
Q

What is false hypoglycaemia?

A

if patients are constantly hyperglycaemic they begin to exhibit hypoglycaemia symptoms when in normoglycemia

153
Q

Which function tumour can cause hypoglycaemia?

A

Insulinoma

154
Q

Which renal condition is associated with hypoglycaemia?

A

CKD

155
Q

Which endocrine conditions cause hypoglycaemia?

A

Hypothyroid
Hypoadrenalism
Hypopituarism
Insulinoma

156
Q

Which diabetic treatments are most likely to cause hypoglycaemia?

A

Sulphonylureas

Insulin

157
Q

What autonomic symptoms are seen in hypoglycaemia?

A 
Nausea
Hunger
Anxiety and palpitations
Sweating
Tremor
158
Q

When do neuroglycaemic symptoms begin to occur in hypoglycaemia?

A

Glucose less than 2.7mmol/l

159
Q

What percentage of T1DM may not recognise a hypo?

A

25 percent

160
Q

What are the risk factors for a hypo in T1DM?

A

Autonomic neuropathy
Very tight glycemic control
Duration of diabetes

161
Q

Are there any restrictions on insulin users and driving?

A

Not if they are compliant with treatment and have not had a hypo whilst driving

162
Q

What is the first line management of a hypo?

A

Give carbs

Relax glycemic control

163
Q

What is the second line treatment of a hypo?

A

Switch to analogue insulin

Continuous subcutaneous insulin infusion therapy

164
Q

When may a driving licence be revoked in relation to a hypo?

A

Severe hypo that needed 3rd party assistance

165
Q

How may nocturnal hypoglycaemia present?

A

Rebound hyperglycaemia

Headaches

166
Q

How can nocturnal hypoglycaemia be diagnosed?

A

3am blood glucose

Subcutaneous glucose monitor for 5 days

167
Q

What is the management of nocturnal hypoglycaemia?

A

Pre bed snack
Reduce night time insulin
Insulin pump
Switch to analogue insulin

168
Q

What is DKA?

A

Relative or absolute insulin deficiency resulting in hyperglycaemia and accumulation of ketoacids in the blood

169
Q

What type of acidosis is seen in DKA?

A

Metabolic

170
Q

What capillary glucose is often seen in DKA?

A

Over 14 mmol/l

171
Q

How is ketosis diagnosed?

A

Elevated blood or urine ketones

172
Q

What bicarbonate level is often seen in DKA?

A

Less than 15mmol/l

173
Q

How does insulin deficiency lead to DKA?

A

Insulin normally inhibits gluconeogenesis

174
Q

How does catecholamine excess promote the pathogenesis of DKA?

A

Promotes triglyceride breakdown to FFA and glycerol which stimulates gluconeogenesis

175
Q

Where do the ketones come from in DKA?

A

FFA metabolism

176
Q

Which ketones are usually present in DKA?

A

3-OH-butyric acid

Acetoacetic acid

177
Q

Which type of respiration is seen in DKA?

A

Kaussmauls

178
Q

What signs and symptoms are seen in DKA?

A 
Kaussmauls respiration
Reduced GCS
Ketones on breath
Abdominal pain and vomiting
Dehydration and tachycardia
179
Q

What can precipitate DKA?

A

MI, infection, pregnancy, insulin admission

180
Q

How is DKA initially diagnosed?

A

VBG showing acidosis
Capillary blood glucose greater than 14
+/- raised urea/creatinine
+/- raised urea/plasma ketones

181
Q

Which level of care should DKA patients be admitted to?

A

HDU

182
Q

How is DKA managed?

A

Fluids (plus potassium), glucose and insulin

183
Q

How is normal saline given in DKA?

A

1l stat and 1l over 1hour

Then 1l over 2 hours and 1l over 4 hours both with 20mmol potassium

184
Q

When should glucose (5 percent) be given in DKA?

A

When the blood glucose drops below 12

185
Q

At what rate should the glucose be given in DKA?

A

125ml/hour

186
Q

When should 10 percent glucose be given in DKA?

A

When insulin infusion has started

187
Q

How should insulin be given in DKA?

A

If know diabetic continue long acting insulin on admission
Commence stat IV insulin infusion with 50u actrapid (in 50ml NaCl)
Insulin 0.1kg/hour after

188
Q

When should the insulin infusion be given at an increased rate in DKA?

A

When the glucose falls below 6mmol/l

189
Q

What is the desired bicarb in DKA?

A

3mmol/hour

190
Q

How can the insulin infusion be changed to raise bicarbonate at a faster rate in DKA?

A

Raise the rate of infusion by 1u/hour

191
Q

What complication of DKA especially arises in children?

A

Cerebral oedema

192
Q

How is cerebral oedema in DKA treated?

A

Dexamethasone or mannitol

193
Q

When can a patient be returned to their normal insulin regime following DKA?

A

When eating and drinking reliably

194
Q

In which type of diabetes does HHS occur?

A

T2DM

195
Q

What capillary blood glucose is often seen in HHS?

A

over 40 mmol/l

196
Q

What is the osmolality of blood in HHS?

A

Over 340

197
Q

In HHS, are patients often hypernatremic?

A

yes

198
Q

When are ketones seen in HHS?

A

If the patient is not eating

199
Q

What type of acidosis is present in HHS?

A

Lactic acidosis (metabolic)

200
Q

How is HHS treated?

A

No insulin for first 12 hours then give 1u/hr (DO NOT GIVE INSULIN BOLUS)

201
Q

What is the maximum rate the glucose should be corrected at in HHS?

A

2mmol/l/hour

202
Q

What complication arises when glucose levels are fixed too rapidly in HHS?

A

Cerebral pontine myelinolysis - due to sodium shifts

203
Q

How is fluid administered in HHS?

A

1l stat and 1l over 1hr

Then 1l over 2 hours and 1l over 4 hours both with potassium

204
Q

Why should normal saline, and not 0.45 percent saline be used in correcting HHS?

A

Sodium declines rapidly with insulin

205
Q

What consideration must be made when giving IV fluids?

A

If the patient is elderly or in congestive heart failure

206
Q

Should we accept normal biochemistry for a couple of days after correcting HHS?

A

Yes

207
Q

What are the sick day rules for patients with DM?

A 
Glucose checked more regularly
Give insulin to those on oral therapy
Go to hospital if vomiting
More fluid and sugary food/fluid
Increased insulin if on insulin therapy

Met 3b (5 decks)

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