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Met 3b > Diabetes > Flashcards

Diabetes Flashcards

1
Q

How many people diagnosed with diabetes in UK

A

3 million

4.9% of population

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2
Q

How much does DM lower life expectancy by

A

7 years

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3
Q

Insulin effect on liver

A

Inhibits gluconeogenesis

Promotes glycogen storage

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4
Q

Insulin effect on muscle

A

Glucose uptake

Promotes glycogen storage

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5
Q

Insulin effect on adipose tissue

A

Inhibits lipolysis

Increases fat synthesis

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6
Q

Type 1 onset

A

Usually juvenile onset (before 35)

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7
Q

Type 2 onset

A

Mainly after 35

More common in males

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8
Q

Which diabetes is prone to ketosis

A

Type 1

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9
Q

Which diabetes is prone to weight loss

A

Type 1

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10
Q

Type 1 Insulin

A

Insulin deficiency
Ketoacidosis
ALWAYS need insulin

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11
Q

Type 2 insulin

A

Insulin resistance - may have deficiency
Partial insulin deficiency initially and hyperosmolar state
Need insulin when Beta cells fail over time

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12
Q

Type 1 + autoimmune

A

GAD and ICA antibodies

Attack B cells

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13
Q

Type 2 + autoimmune

A

Non autoimmune

Associated with metabolic syndrome

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14
Q

Type 1 + HLA

A

HLA-DR3 and HLA-DR4 in more than 90%

Islet cell antibodies

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15
Q

Type 2 + HLA

A

No HLA relation

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16
Q

MZ Twins + Diabetes

A

50% concordance Type 1

100% concordance Type 2

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17
Q

Symptom duration

A

Type 1- weeks

Type 2- months/years

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18
Q

Ethnicity Type 1

A

Higher risk Northern European

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19
Q

Ethnicity Type 2

A

Higher risk Asian, African, poylnesian, native american

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20
Q

C peptide

A

Disappears in Type 1

Persists in Type 2

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21
Q

LADA

A

Latent autoimmune diabetes of adults

Type 1B DM

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22
Q

MODY

A

Maturity onset diabetes of the young

Rare autosomal form of T2DM

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23
Q

Secondary Diabetes- Pancreatic disease (diseases of exocrine pancreas)

A 
Acute + chronic pancreatitis
Trauma
Pancreatectomy
Neoplasia
Cystic Fibrosis
Haemochromatosis
Thalassaemia
Fibrocalculous pancreatopathy
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24
Q

Secondary Diabetes- Endocrine disease (diseases of endocrine pancreas)

A 
Acromegaly
Cushing's
Glucagonoma
Phaeochromocytoma
Hyperthyroidism
Conn's disease
Aldosteronoma
Somatostatinoma
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25
Q

Drug-induced Diabetes

A 
Immunosuppressive agents- glucocorticoids, cyclosporin, tacrolimus, sirolimus
Beta blockers
Beta adrenergic agonists
Atypical antipsychotics (clozapine, olanzapine)
Thiazide diuretics
Phenytoin
Levothyroxine
Interferon alpha
HIV treatment
Niacin (B3)
Pentamidine
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26
Q

Secondary diabetes- Genetic defects of:

A 
Beta cell function
Insulin action (receptor mutations)
Genetic syndromes- Down's, Friedreich's ataxia, Huntington's chorea
Klinefelter syndrome
Prader- Willi
Turner
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27
Q

Secondary diabetes- Infections

A

Congenital rubella

CMV

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28
Q

Secondary diabetes- uncommon forms f immune mediated diabetes

A

Stiff person syndrome

Anti-insulin receptor antibodies

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29
Q

Diabetes Investigations

A

Fasting plasma glucose (FPG)
Random plasma glucose (RPG)
75g oral glucose tolerance test (OGTT)
HbA1c

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30
Q

75g Oral glucose tolerance test

A

Fast for 9 hours
Check fasting plasma glucose
Give 75g of glucose
Check 2 hour plasma glucose

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31
Q

HbA1c

A

Measure for average glucose control over 3 month period
Normal- below 42 mmol/mol
Generally below 53 indicates well controlled diabetes

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32
Q

Investigating with symptoms

A

1 diagnostic test

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33
Q

Investigating without symptoms

A

2 diagnostic tests OR 1 abnormal OGTT

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34
Q

Type 1 Aetiology

A

Polygenic
Autoantibodies against pancreatic islets
Pancreatic beta cell destruction –> absolute insulin deficiency

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35
Q

LADA

A

diagnosed in adulthood
Usually non-acute –> can be diagnosed as T2DM
ICA or GAD +ve
Require insulin

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36
Q

T1DM environmental influences

A

Peak age onset 5-7 years
Puberty
Seasonal variation
Predominantly European population

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37
Q

T1DM Genetic susceptibility

A

HLA genes on chromosome 6q (MHC)-HLA DR3/4

Genes on chromosomes 2q, 15q and 11q

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38
Q

Pathogenic sequence of T1DM

A

Genetic susceptibility
Environmental insult (virus)
Development of insulitis (infiltration of activated T lymphocytes)
Activation of autoimmunity
Immune attack on Beta vells
Development of DM (when more than 90% of Beta cells are destroyed)

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39
Q

When do you develop T1DM

A

When more than 90% of Beta cells are destroyed

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40
Q

Glucose toxicity

A

Beta cells have decreased functionality when exposed to high levels of glucose
–> lowering glucose may increase beta cell function and promote greater insulin secretion

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41
Q

Alpha cells in T2DM

A

Increased

Leads to increased glucagon/insulin ratio

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42
Q

Classic Osmotic Symptoms

A 
Polyuria
Polydipsia
Weight loss
Nocturia
Fatigue
Pruritis
Blurred Vision
Recurrent UTI or GU infections
DKA
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43
Q

HHS

A

Hyperosmolar Hyperglycaemic Syndrome

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44
Q

Diabetes complications

A 
Skin infections
Foot problems
Retinopathy 
Erectile dysfunction
Arterial disease
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45
Q

Factors in obesity contributing to insulin resistance

A

Adipokines
Inflammation
Lipids

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46
Q

Insulin resistance

A

Diminution in the response of the body’s tissues to insulin, so that higher concentrations of serum insulin are required to maintain normal circulating glucose levels; eventually the islet cells can no longer produce adequate amounts of insulin for effective glucose lowering, resulting in hyperglycaemia

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47
Q

Metabolic syndrome

A 
Cluster of conditions that together increase risk of heart disease, stroke + T2DM
Central obesity
Dyslipidaemia
Hypertension
Impaired fasting glucose
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48
Q

Metabolic syndrome: Central obesity

A 
BMI > 30 or Waist circumference of:
Caucasian men- >94
Caucasian women- >80
South Asian men- >90
South Asian women- >80
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49
Q

Metabolic syndrome: Dyslipidaemia

A

Increased Triglycerides >150mg/dL

Decreased HDL-cholesterol: <40mg/dL women, <50mg/dL men

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50
Q

Metabolic syndrome: Hypertension

A

Systolic >130

Diastolic>85

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51
Q

Metabolic syndrome: Impaired fasting glucose

A

Fasting glucose >6.1mmol/L

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52
Q

Self monitoring blood glucose aims

A

Pre-prandial: 4-7mmol/L

Post-prandial (2hrs): 5-9mmol/L

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53
Q

Fructosamine

A

Another glycated protein- lasts around 2 weeks
Can be used if HbA1c invalid e.g. haemoglobinopathy, increased RBC turnover
Useful in glucose control in pregnancy

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54
Q

First line T2DM

A

Diet
Physical activity- 3x30mins
3-5% weight reduction
Smoking cessation

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55
Q

Smoking in diabetes

A

1 cigarette is equal to 5 cigarettes for non-diabetic

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56
Q

Diabetic BP control

A

Aim 140/80

If CVD or renal disease too, 130/80

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57
Q

Diabetic cholesterol control

A

Diabetic>40 or Diabetic<40 + 1 risk factor= statin

Aim total cholesterol <4, LDL <2

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58
Q

Biguanides

A

Metformin

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59
Q

Biguanides function

A

1st line T2DM
Decreases hepatic glucose production (gluconeogenesis and glycogenolysis)
Improve insulin sensitivity in liver + muscle
Doesn’t affect insulin secretion, doesn’t induce hypoglycaemia and doesn’t predispose to weight gain

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60
Q

Biguanides SEs

A 
Nausea
Diarrhoea
Abdominal pain
Anorexia
Hypoglycaemia
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61
Q

Biguanides STOP IF

A

Tissue hypoxia e.g. sepsis or MI
General anaesthesia
Before contrast medium containing iodine –> renal failure + subsequent lactic acidosis
Restart no earlier than 48hr after test of renal function shows no deterioration

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62
Q

Insulin Secretagogues

A

Sulfonylureas

Meglitinides

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63
Q

Biguanides Contraindictions

A

Severe hepatic disease
Severe renal disease (CKD stage 4 or eGFR<36ml/min)
–> can cause lactic acidosis

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64
Q

Sulfonylureas examples

A 
Gliclazide
Tolbutamide
Glibenclamide
Glipizide
Glimepiride
Chlorpropamide
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65
Q

Sulfonylureas function

A

Oral hypoglycaemic
Increases insulin release from pancreas
Opens K+ channels in beta cells

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66
Q

Sulfonylureas side effects

A

Hypoglycaemia

Weight gain

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67
Q

Meglitinides examples

A

Repaglinide

Nateglinide

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68
Q

Meglitinide function

A

Opens K+ channels in Beta cells to increase insulin release

Short acting agents that promote postprandial release of insulin- Prandial Glucose Regulators (PGRs)

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69
Q

Thiazolidinediones (TZDs)/Glitazones example

A

Pioglitazone

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70
Q

TZDs MOA

A

PPAR-gamma agonist
Modulates gene transcription of regions controlling lipid metabolism in the muscle, adipose tissue and liver –> decreases insulin resistance peripherally + increases insulin sensitivity

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71
Q

TZDs SEs

A 
Hypoglycaemia
Weight gain
Fluid retention
Heart failure
Liver impairment
Bladder cancer
Mild anaemia
Osteoporosis/fractures
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72
Q

TZDs contraindications

A

Past/present HF

Osteoporosis

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73
Q

Glucagon like peptide - 1 (GLP-1)

A

Incretin
Gut peptide that augments insulin release when glucose is detected + decreases glucagon secretion
Slows gastric emptying + induces satiety
Stimulate + preserve Beta cells

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74
Q

GLP 1 receptor analogues examples

A

Exenatide
Liraglutide
Lixisenatide

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75
Q

GLP1 receptor analogues

A

Injected not oral

Only used in overweight patients (BMI > 35) with poor glucose control

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76
Q

GLP1 receptor analogues SEs

A

Nausea
Diarrhoea
Pancreatitis
Pancreatic cancer

77
Q

DDP4 inhibitors/gliptins examples

A 
Sitagliptin
Vildagliptin
Alogliptin
Linagliptin
Saxagliptin
78
Q

DDP inhibitors/gliptins

A

Oral 1x day
Inhibit GLP1 breakdown
Well tolerated, SEs uncommon

79
Q

Alpha-glucosidase inhibitors examples

A

Acarbose

80
Q

Alpha-glucosidase inhibitors

A

Decrease breakdown of starch into glucose

81
Q

Alpha-glucosidase inhibitors SEs

A

Flatulence
Diarrhoea
Abdo pain/distension

82
Q

Diabetes medication Prescribing Pathway

A

Step 1: Lifestyle, try and keep <48
Step 2: Metformin if gone above 48
Step 3: Metformin + Sulfonylurea if gone above 58, try and keep at around 53
Step 4: Triple therapy- metformin, SU + DDP4 inhibitor/insulin/pioglitazone
Step 5: if not better, intensify insulin or add pioglitazone

83
Q

Metformin dose CIs

A

Careful with dose if eGFR <45, if below 30 then stop
Not tolerated if patient not overweight
–> SUs instead

84
Q

Sulfonylurea CIs

A

If hypoglycaemia a problem

–> DPP4 inhibitor/pioglitazone instead

85
Q

If metformin is CI or not tolerated

A
  1. SU/DPP4 inhibitor/pioglitazone
  2. Combination of 2 of SU/DPP-4 inhibitor/Pioglitazone
  3. Consider insulin regime
86
Q

T2DM indications for insulin therapy

A

Inadequate glycaemic control on tablets or CI to tablets
Symptomatic hyperglycaemia
Pregnancy
Infection/foot ulcers

87
Q

Types of Insulin

A

Human

Analogue

88
Q

Human Insulin types

A

Short acting
Intermediate acting
Biphasic

89
Q

Humulin S

A

Short acting human insulin

90
Q

Humulin I

A

Intermediate acting human insulin

91
Q

Humulin M3

A

Biphasic human insulin (mixture of short and intermediate)

92
Q

Analogue Insulin types

A

Rapid acting
Long acting (basal insulin)
Biphasic

93
Q

Novorapid, Lispro

A

Rapid acting analogue insulin

94
Q

Lantus, Levmir

A

Long acting analogue insulin (basal insulin)

95
Q

Novomix 30

A

Biphasic analogue insulin

96
Q

Insulin Injection Sites

A

Subcutaneous
Abdomen
Thighs
Buttocks

97
Q

Insulin Regimes

A

Once daily basal insulin
Premixed insulin twice daily/biphasic
Basal bolus/QDS regimen

98
Q

Once Daily basal insulin

A

Once daily intermediate or long-acting insulin
Given with tablets in T2DM
Usually given before bed or 1st thing in morning

99
Q

Premixed insulin twice daily/biphasic

A

30% short acting and 70% long acting
Breakfast and lunch
If once daily fails in T2DM

100
Q

Basal bolus/QDS regimen

A

1 long acting injection + 3 short acting injections with each meal
Mimics normal physiology
Used primarily in T1DM

101
Q

Sick Days

A 
Illness causes stress and usually requires more insulin
Drink lots of fluids (3L)
Sugary fluids if unable to eat
Regular glucose monitoring
Never stop tablets or insulin
102
Q

Diabetic Ketoacidosis

A

State of absolute or relative insulin deficiency resulting in hyperglycaemia and an accumulation of ketoacids in the blood with subsequent metabolic acidosis

103
Q

Hyperosmolar hyperglycaemic state (HHS)

A

Hyperglycaemia resulting in high osmolarity without significant ketoacidosis

104
Q

Hypoglycaemia

A

Below 3.6mmol/L

105
Q

Hypoglycaemia causes

A

Imbalance between carb intake and insulin/oral hypoglycaemics
Exercise with too much insulin/not enough carbs
Alcohol
Vomiting
Breast feeding

106
Q

Hypoglycaemia medical causes

A 
Liver disease
Progressive renal impairment
Hypoadrenalism (T1DM)
Hypothyroidism
Hypopituitarism
Insulinoma
107
Q

Hypoglycaemia Autonomic Symptoms

A 
Glucose around 3.6mmol/L
Sweating
Shaking
Anxiety
Palpitations
Hunger
Nausea
108
Q

Hypoglycaemia Neuroglycopenic symptoms

A 
Glucose around 2.7mmol/L
Confusion
Slurred speech
Visual disturbance
Drowsiness
Aggression
109
Q

Mild hypoglycaemia management

A

Conscious, lucid, able to self-treat
Sugary drink
5-7 glucose tablets or 3-4 heaped tsp sugar

110
Q

Moderate hypoglycaemia management

A

Conscious but can’t self-administer and needs help
Glucogel (1-2 tubes) or jam, honey, treacle
IM Glucagon

111
Q

Severe hypoglycaemia treatment

A

Unconscious- don’t put anything in mouth + recovery position
0.5-1mg IM Glucagon
In hospital, IV Glucose

112
Q

Severe hypo treatment IV glucose

A

75ml of 20% glucose or 150ml of 10% glucose over 15 mins

50ml of 50% glucose may be given with care as may cause extravasation leading to chemical burns

113
Q

Post-hypo treatment

A

When glucose above 4mmol/L

Longer acting carbs needed- biscuits, bread, milk

114
Q

Hypo + driving

A

Inform DVLA

Licence revoked following 1 or more severe hypos during driving

115
Q

Nocturnal Hypo diagnosis

A

Rebound hyperglycaemia
Headaches/hangover sensation
3am BM or CGMS (continuous glucose monitoring sensor) over 5 days

116
Q

Nocturnal Hypo management

A

Analogue insulins
Pre-bed snack
Change of timing of insulin
Insulin pump therapy

117
Q

DKA MOA

A

Ketosis is pathway use in starvation states
Acetone produced as by-product
Cells can’t take up glucose for metabolism
Cells end up in starvation-like state –> ketoacidosis only form of energy production –> FFAs metabolised via Krebs cycle producing ketone bodies

118
Q

DKA stands for

A

Severe acidosis
Hyperglycaemia
Ketones present

119
Q

DKA triggers

A 
Infection e.g. UTI
Surgery
MI
Pancreatitis 
--> all 4 have glucocorticoid response, increasing levels of cortisol + blood glucose
Chemo
Antipsychotics
Wrong insulin dose
High exogenous steroids
120
Q

DKA presentation

A 
Abdominal pain
Kussmaul respiration
Drowsiness + confusion
Polyuria
Polydipsia
Vomiting
Ketones on breath
Dehydration + tachycardia
Severe- Na, Cl, K, Ca, Mg + phosphate losses due to osmotic diuresis
121
Q

DKA Diagnosis

A

Acidosis- pH<7.30
Hyperglycaemia (usually >14mmol/L)
Ketosis (serum + urine)

122
Q

DKA investigations

A

Pregnancy test
ECG, CXR
Urine dip + MSU culture
Bloods- CBG/biochem profile, plasma ketones, ABG/VBG, amylase, osmolality, FBC, blood culture, HbA1c

123
Q

Plasma osmolality

A

2(Na) + urea + glucose

124
Q

Assessing DKA severity

A 
If one or more on admission, ITU:
Blood ketones >6
Venous bicarb < 5
pH <7.1
K+<3.5
GCS<12
O2 sats<92% on air
SBP<90
Pulse>100 or <60
Anion gap >16
125
Q

DKA monitoring

A 
Consciousness
BP
Pulse
Temp
Glucose
Urine output
K+
Acidosis
126
Q

DKA Fluid therapy

A

2 large bore cannulas
NaCl 0.9%
5% or 10% glucose

127
Q

DKA NaCl 0.9%

A 
1L start until SBP>90
1L in 1hr
1L in 2hrs (+20mmol KCl)
1L in 4hrs (+KCl)
1L in 4hrs (+KCl)
128
Q

DKA 5/10% glucose

A

Start when CBG <12mmol/L and continue at 125ml/hour
If using 10% glucose increase insulin infusion as needed
Increase insulin infusion rate if glucose <6mmol/L

129
Q

DKA K+

A

Do not give in first 2 bags because delivery ratio is too rapid
On each subsequent bag of NaCl or glucose, add KCl dependent on serum levels
<3.5- may need additional K+ and delay insulin
3.5-5.5- 20-40mmol/L
>5.5- none

130
Q

Normal DKA deficits

A

Typical fluid deficit= 100ml/kg

Typical K+ deficit= 3-5mmol/kg

131
Q

Insulin during DKA

A

If known diabetic, continue
Insulin infusion by IV syringe pump
–> 50 units Actrapid made up to 50ml with 0.9% NaCl

132
Q

DKA insulin infusion

A

50 units Actrapid made up to 50ml with 0.9% NaCl
Fixed rate IV infusion
–> 0.1units/kg/hr (around 6-8 units/hr)
Aim for bicarb rise of 3mmol/hr and glucose fall 3mmol/L
If not achieved, increase rate by 1 unit/hr

133
Q

DKA treatment outcomes

A

Ketones <0.3mmol/L- use blood as urinary ketones persist after resolution
Venous pH>7.3
Venous bicarb>18mmol/L

134
Q

DKA complications

A 
Aspiration pneumonia
Hypo K+
Hypo Mg+
Hypo PO4-
VTE
Cerebral oedema
135
Q

Most common cause of DKA death in children

A

Cerebral oedema
Indicated by sudden CNS decline
Treatment- dexamethasone or mannitol

136
Q

DKA features

A 
Increased plasma glucose
Increased WBC
Infection often apyrexial
Increased creatinine
HypoNa+- common due to osmolar compensation of hyperglycaemia, if increased or normal suspect severe
Ketonuria
Recurrent ketoacidosis
Acidosis
Serum amylase increased
Non-specific abdo pain
137
Q

Hyperosmolar Hyperglycaemic Syndrome (HHS)

A 
Severe hyperglycaemia without significant acidosis
Typically seen in T2DM
Subacute history (1 week) with marked dehydration and hyperglycaemia
138
Q

HHS and age

A

Old people experience thirst less acutely + become more dehydrated more readily
Mild renal impairment associated with age
–> increased urinary losses of fluid + electrolytes

139
Q

HHS Features

A 
Hyperglycaemia >40mmol/L
Osmolality >420 
Patient often hypernatraemic
May or may not be ketonuria
No ketoacidosis
Severe dehydration
140
Q

Normal osmolality

A

275-295

141
Q

Calculating Osmolality

A

2(Na+K) + Ur + Glu

142
Q

HHS clinical features

A

Dehydration –> stupor –> coma

143
Q

HHS precipitating factors

A

Consumption of glucose-rich fluids
Concurrent medication e.g. thiazide diuretics or steroids
Intercurrent illness

144
Q

HHS Complications

A

Occlusive events- stroke, MI, DIC, leg ischaemia/rhabdomyolysis, DVT/PE
Give LMWH as prophylaxis

145
Q

HHS Management

A

Rehydrate slowly over 48 hours with 0.9% NaCl IV
No insulin bolus
Replace K+ when urine starts to flow

146
Q

HHS Rehydration

A

Typical deficit 110-220ml/kg

Avoid 0.45% NaCl

147
Q

HHS Insulin

A

Only use insulin if blood glucose not falling by 5mmol/L/hr with rehydration or ketonuria
Slow infusion of 0.05units/kg/hr (max 1unit/hr)
Avoid in first 12 hours
Rapid shifts in glucose should be avoided due to risk of rapid fluid/Na+ shifts and central pontine myelinosis

148
Q

HHS K+

A

Replaces when urine starts to flow
May need CVP monitoring
K+ reduces rapidly
Keep plasma glucose at 10-15mmol/L for 1st 24hrs to avoid cerebral oedema
Look for cause, e.g. bowel infarct, drugs etc.

149
Q

When choosing, giving + monitoring medication- BRAIN + AIMS

A 
Benefits
Risks
Adverse effects
Interactions
Necessary prophylaxis
Susceptible groups
Administering
Informing
Monitoring
Stopping
150
Q

Diabetic mortality rate

A

Increased (x2-2.5) due to cardiovascular complications

80% die of CVD

151
Q

Long term hyperglycaemia leads to

A

Vessel closure- decreased supply of O2 and nutrients

Vessel permeability- damaged vessels dilate and leak unwanted substances

152
Q

Diabetes chronic complications- Macrovascular (atherosclerosis)

A

Coronary Heart disease–> MI, CCF
Cerebrovascular disease –> stroke
Peripheral vascular disease –> ulceration, gangrene, amputation

153
Q

Diabetes chronic complications- Microvascular

A

Nephropathy
Retinopathy
Neuropathy (peripheral sensorimotor, autonomic)

154
Q

Diabetes chronic complications- Other

A

Skin
Rheumatological
Hepatic

155
Q

Complications of Diabetes Risk Factors

A

Smoking- most potent
Hypertension
Dyslipidaemia
Hyperglycaemia- least potent

156
Q

Diabetic retinopathy

A

Common

Around 50% of people with diabetes for more than 10 years have it

157
Q

Non-proliferative Retinopathy

A

Microaneurysms
Dot and blot haemorrhages
Hard exudates (lipid deposits) and soft exudates (cotton wool spots=retinal ischaemia- only in pre-proliferative- REFER)
Macular oedema (leakage of macular blood vessel- main cause vision loss in this case)
Mild, moderate, severe

158
Q

Proliferative Retinopathy

A

Ischaemia of retina –> production of growth factors (GF) –> neovascularisation producing fragile vessels
New vessels on disc and other places
Vitreous haemorrhage
–> vessels prone to haemorrhage, lead to fibrosis/scarring leading to loss of vision

159
Q

Diabetic Maculopathy

A

Suspect if visual acuity decreased
Occurs if retinopathy within 1 disc diameter of the macula
Leads to oedema + vision loss
Refer for laser photocoagulation, intravitreal steroids or anti-angiogenic agents

160
Q

Focal or exudative maculopathy

A

Hard exudates around macula which leads to macular oedema and visual loss

161
Q

Ischaemic maculopathy

A

Due to retinal vessel closure

162
Q

Diff types of diabetic maculopathy

A

Focal or exudative
Diffuse
Ischaemic

163
Q

Diabetic Maculopathy Pathophysiology

A

Capillary endothelial damage –> vascular leak –> microaneurysm –>

164
Q

Diabetic Maculopathy Pathophysiology

A

Capillary endothelial damage –> vascular leak –> microaneurysm –> capillary occlusion –> local hypoxia and ischaemia –> neovascularisation

Occurs due to increased blood flow in hyperglycaemia
New vessels form on disc or ischaemic areas, proliferate, bleed, fibrose + can detach retina

165
Q

Microvascular occlusion

A

Cotton wool spots

166
Q

Maculopathy screening

A

Annual digital retinal screen
BP, cholesterol, glycaemic control
Laser photocoagulation

167
Q

Diabetic Nephropathy

A

Most common cause of end-stage renal failure in UK
25-30% of T2DM have some degree of nephropathy
Associated with atherosclerosis

168
Q

Kidneys damaged in 3 main ways

A

Glomerular damage
Ischaemia- resulting from hypertrophy of afferent and efferent arterioles
Ascending infection

169
Q

Diabetic Nephropathy RFs

A 
Duration of diabetes
Hypertension
FH of hypertension
Poor glycaemic control
Smoking
Gender-male
Ethnicity- South Asians, Afro-Caribbeans
170
Q

Diabetic Nephropathy Clinical Triad

A

Hypertension
Albuminuria (preceded by microalbuminuria)
Declining renal function
–> on renal biopsy: “Kiemmelstein-Wilson” lesion

171
Q

Microalbuminuria screening

A

Void urine in morning + measure urine albumin:creatinine ratio (ACR)
Normal men <3.5mg/mmol, normal women <2.5mg/mmol
If elevated, repeat twice- of 2 out of 3 positive, microalbuminuria present

172
Q

Diabetic Nephropathy management

A 
Maintain BP <130/80
HbA1c<53
Stop metformin eGFR <30
Refer to specialist eGFR<45
Consider renal replacement therapy
Consider simultaneous pancreas and kidney transplant for T1DM
173
Q

Diabetic Neuropathy

A

Peripheral neuropathy- injury or infection at pressure points (e.g. metatarsal heads)
Ischaemia- critical toes and loss of pulses

174
Q

Peripheral sensory neuropathy

A

Glove and stocking distribution
High risk ulceration + amputations if blood supply poor
Numbness, pins and needles, burning and shooting pain
Loss sensation fine touch + proprioception
Loss ankle reflexes, reduced muscle bulk, neuropathic deformity (pes cavus, claw toes, loss transverse arch, rocker bottom sole)
Hands subject to median neuropathy/carpal tunnel

175
Q

Autonomic Neuropathy- Genitourinary

A 
ED
Atonic bladder (difficulty voiding or incontinence) --> self catheterisation
176
Q

Autonomic Neuropathy- GI

A

Gastroparesis (recurrent vom + early satiety due to poor gastric flow)- anti emetics, erythromycin, gastric pacing
Chronic constipation/diarrhoea
Gustatory sweating

177
Q

Autonomic Neuropathy- Cardiovascular

A

Postural hypotension- fludrocortisone or alpha agonist midodrine
Reduced cerebrovascular autoregulation
Loss of respiratory sinus arrhythmia

178
Q

Mononeuropathy

A

CN palsies
Median nerve palsies –> carpal tunnel
–> treat with immunosuppression

179
Q

Proximal motor neuropathy

A

Painful atrophy of quads + pelvifermoal muscles

180
Q

CV complications

A

Manage CV risks

  • smoking cessation
  • BP control
  • cholesterol control
  • glycaemic control
181
Q

BP management

A

ACEI
CCB
Thiazide
Alpha blocker or Beta

182
Q

Cholesterol control

A

Total cholesterol <4

Treat with statins- all diabetics > 40, all diabetics <40 +1 other RF

183
Q

Acute MI - complication

A

4x increased risk
May be silent because autonomic neuropathy
Treatment- aspirin, angioplasty, glucose-insulin infusion, 2ndary prevention

184
Q

Cerebrovascular disease- complication

A

If within 3 hours, consider thrombolysis

Aspirin, statins, glucose insulin infusion

185
Q

Peripheral vascular disease complication

A

Intermittent claudication, rest pain, buttock pain

Aspirin, vasodilators

186
Q

Skin complications

A 
Oral/genital candidiasis
Skin abscesses
Diabetic dermopathy
Necrobiosis Lipoidica diabeticorum
Granuloma annulare
acanthosis nigricans
fungal nail infection
187
Q

Rheumatological complications

A

Charcot neuropathy
Adhesive capsulitis
Diffuse idiopathic skeletal hyperostosis
Flexor tendinopathy

188
Q

Hepatic complications

A

NAFLD
–> non alcoholic steatohepatitis/fibrosis/cirrhosis
Increases ALT and AST more than 2x upper limit needs investigation
Pioglitazone in reducing cirrhosis progression

Met 3b (21 decks)

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