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Year 2 > ENDO: Diabetes > Flashcards

ENDO: Diabetes Flashcards

1
Q

Random plasma glucose level for diabetes

A

> 11 mmol/L

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2
Q

Fasting plasma glucose level for diabetes

A

> 7mmol/L

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3
Q

If a person has no symptoms how are they diagnosed as diabetic

A
  1. GTT (75mg) fasting > 7 or 2h value > 11mmol/L
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4
Q

HbA1c level for diabetes

A

> 48 mmol/mol

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5
Q

Clinical presentation of diabetes

A
  1. Thirst
  2. Polyuria
  3. Weight loss + fatigue
  4. Hunger
  5. Pruritis vulvae and balanitis
  6. Blurred vision
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6
Q

What causes polyuria

A

Osmotic diuresis

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7
Q

Why is there weight loss ann fatigue in diabetes

A

Lipid and muscle loss due to unrestrained gluconeogenesis

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8
Q

What causes pruritus vulvae

A

Vaginal candidiasis (fungal infection)

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9
Q

Why is vision blurred in diabetes

A

Altered acuity due to uptake of glucose/water into the lens

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10
Q

When does type I diabetes present

A

Childhood

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11
Q

Suggestive features of type I diabetes

A
  1. Lean body habitus
  2. Acute onset of osmotic symptoms
  3. Prone to ketoacidosis
  4. High levels of islet autoantibodies
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12
Q

What factor does type I diabetes presentation depend on

A

Rate of beta-cell destruction

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13
Q

What three features indicate type I diabetes and immediate insulin treatment for any age

A
  1. Weight loss
  2. Short history of severe symptoms
  3. Large urinary ketones
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14
Q

Suggestive features of type II diabetes

A
  1. Presents in over 30
  2. Gradual onset
  3. Familial hypercholesterolaemia positive
  4. Identical twins
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15
Q

What autoantibodies would I find in someone with type I diabetes

A
  1. Anti GAD (glutamate decarboxylase)
  2. Anti Pancreatic islet cell antibody
  3. Anti Islet antigen-2 Ab
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16
Q

What there autoimmune conditions are associated with diabetes mellitus

A
  1. Hypothyroidism
  2. Addisons
  3. Coeliac’s
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17
Q

What is the effect of reduced insulin in the body

A

Leads to fat breakdown and formation of glycerol (a gluconeogenic precursor) and free fatty acids

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18
Q

How do free fatty acids damage the body

A
  1. Impair glucose uptake
  2. Transported to the liver where they undergo gluconeogenesis
  3. Oxidised to form ketone bodies
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19
Q

What ketone bodies are produced from free fatty acids

A
  1. Beta hydroxybutyrate
  2. Acetoacetate
  3. Acetone
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20
Q

What is ketoacidosis

A
  1. Absence of insulin causes hyperglycaemia and rising ketones
  2. Glucose and ketones escape in urine but lead to osmotic diuresis and falling blood volume
  3. Increasing dehydration, hyperglycaemia and acidosis = circulatory collapse and death
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21
Q

Clinical presentation of ketoacidosis

A

Ketone sin the body cause anorexia and vomiting

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22
Q

Define Diabetic Ketoacidosis

A
  1. Hyperglycaemia
  2. Raised plasma ketones
  3. Metabolic acidosis
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23
Q

What value is hyperglycaemia

A

<50mmol/L

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24
Q

What value is raised ketones

A

> 2+

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25
Q

What value defines metabolic acidosis

A

Plasma HCO3- < 15mmol/L

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26
Q

What causes Diabetic Ketoacidosis

A
  1. Idiopathic
  2. Infection/MI
  3. Treatment errors (stoping insulin dose)
  4. Previously unknown diabetes
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27
Q

The triad features of DKA

A

1, Hyperglycaemia

  1. Ketones
  2. Acidosis
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28
Q

Symptoms of DKA

A
  1. Polyuria
  2. Polydipsia
  3. Nausea + vomiting
  4. Weight loss
  5. Weakness
  6. Abdo pain (confused with surgical abdomen)
  7. Drowsiness and confusion
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29
Q

Signs of DKA

A
  1. Kussmaul breathing
  2. Dehydration (loss of 5-6 litres)
  3. Hypotension
  4. Tachycardia
  5. Coma
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30
Q

What is Kussmaul breathing

A

Initially in DKA, breathing is rapid and shallow but deep, laboured gasping occurs when it gets worse - this pattern is Kussmaul breathing

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31
Q

How does Kussmaul breathing effect blood constituents

A
  1. Low CO2 and low HCO3-
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32
Q

Diagnostics of DKA

A
  1. Hyperglycaemia (<50 mol/L)
  2. K+ high on presentation despite total body K+ deficit
  3. HCO3- <15 mol/L
  4. Urea and creatinine raised due to pre-renal failure
  5. Urinary ketones > 2+
  6. Blood ketones >3.0
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33
Q

Why is K+ initially high on presentation of DKA

A

Acute shift of K+ out of the cell due to acidosis but will fall with rehydration

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34
Q

How is DKA managed

A
  1. Rehydration (3L in first 3 hours)
  2. Insulin
  3. Replacement of electrolytes (K+)
  4. Treat underlying cause
  5. Immediate treatment start!
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35
Q

Why is insulin given in DKA

A
  1. Inhibits lipolysis
  2. Inhibits vetogenesis
  3. Lowers acidosis
  4. Reduces gluconeogenesis
  5. Increase tissue glucose uptake
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36
Q

Complications of DKA

A
  1. Cerebral oedema
  2. Adult respiratory distress syndrome
  3. Thromboembolism
  4. Aspiration pneumonia
  5. Death
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37
Q

what there microvascular complications of diabetes do we get

A
  1. NEPHROPATHY (leads to chronic renal failure)
  2. RETINOPATHY
  3. NUEUROPATHY
  4. Cardiomyopathy
  5. Erectile dysfunction
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38
Q

What neuropathy is seen in diabetics

A
  1. Glove in stocking distribution which starts in the feet and moves into the hands
  2. Autonomic neuropathy
  3. Diabetic amyotrophy (muscle weakness due to neuropathy)
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39
Q

What happens in diabetic retinopathy

A
  1. Damage blood vessels are replaced buy weaker, poor-quality vessels in the retina.
  2. Causes macular oedema (vision loss and blindness)
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40
Q

How is type I diabetes treated

A
  1. Insulin twice daily (short/medium acting insulin)
  2. Basal bolus pumps (once or twice daily + pre-meal quick acting insulin)
  3. Ability to judge JHO intake
  4. Exercise
  5. Monitoring with blood glucose pens
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41
Q

What microvascular diseases are caused by diabetes

A
  1. Angina and MI
  2. Diabetic myonecrosis (muscle wasting in thigh due to infarcted muscle tissue)
  3. Peripheral vascular disease causing intermittent claudication
  4. Diabetic foot
  5. Female infertility
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42
Q

Why does insulin levels have to be closely monitored

A

Too high and this can cause hypoglycaemia

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43
Q

What part of the body is susceptible to hypoglycaemia

A

BRAIN - cerebral dysfunction (loss of concentration, confusion and coma)

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44
Q

What are two physiological defences against hypoglycaemia

A
  1. Release of glucagon, adrenaline
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45
Q

What symptoms are seen in hypoglycaemia

A
  1. Sweating, tremor, palpitations

2. Hunger and loss of concentration

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46
Q

At what glucose level is sweating, tremor and palpitations seen (autonomic symptoms)

A

3.8-2.8mM

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47
Q

What is seen at glucose levels of less than 2.8mM

A

Confusion, drowsiness, speech difficulty (neuroglycopenic symptoms)

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48
Q

What is seen at 1.5 mM glucose level

A

CONVULSIONS
COMA
HEMIPARESIS

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49
Q

What is HbA1c

A
  1. Haemoglobin that is covalently bonded to glucose
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50
Q

Over how long is HbA1c monitored

A

3 months

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51
Q

Why is the HbA1c test limited to 3 months

A

RBC lifespan is 120 days

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52
Q

What is the normal range of Hb1Ac

A

6.7 - 7.6%

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53
Q

What is DAFNE

A

Dose adjustment For Normal eating

54
Q

What can DAFNE prevent

A

DKA and hypos

55
Q

What is the most common type of monogenic diabetes

A

MODY (Maturity-onset diabetes of the young)

56
Q

At what age is MODY diagnosed

A

Less than 25

57
Q

What kind of inheritance is MODY

A

Autosomal dominant

58
Q

How does MODY cause diabetes

A

Single gene defect altering beta cell function

59
Q

What types of MODYs are tehre

A

They are subdivided into Hepatic nuclear factor mutations: HNF1A (MODY 3) and HNF4A (MODY 1)

60
Q

How is HNF1A mutation caused diabetes treated

A

VERY SENSITIVE to sulphonylureas treatment so no need for insulin

61
Q

Clinical presentation of HNF4A mutation

A
  1. Non-obese, Familial Hypercholesterolaemia
  2. MACROSOMIA
  3. Neonatal hypoglycaemia
62
Q

What define macrosomia

A

Greater than 4.4kg at birth

63
Q

What is MODY 2

A
  1. Mutation in Glucokinase gene
64
Q

Role of GCK

A

Glucose-sensor in beta cells, RATE DETERMINING STEP in glucose metabolism controlling release of insulin

65
Q

How is MODY 2 controlled

A
  1. Tight glycemic control in mild diabetes

2. More insulin is given to patients with MODY 2

66
Q

What is MODY typically misdiagnosed as

A

Type I or younger onset Type II

67
Q

Do MODY patients depend on insulin therapy

A

No

68
Q

How do we distinguish MODY from TYPE I and TYPE II

A
  1. Absence of islet autoantibodies
  2. Evidence of non-insulin dependence (no ketosis, good control on low dose insulin, measurable C-peptide)
  3. Sensitive to sulphonylurea
69
Q

How does C-peptide help distinguish between Type II and MODY from type I

A
  1. C-peptide is negative within 5 years (completely destroyed)
  2. Stilll persists in type II and MODY
70
Q

AT what age is permanent Neonatal Diabetes diagnosed

A

Less than 6 months

71
Q

Clinical presentation of Permenant Neonatal diabetes

A

Small Babies
Epilepsy
Muscle Weakness

72
Q

Where do mutations in permanent neonatal diabetes occur

A

Kir6.2 and SUR1 subunits of the beta cell ATP sensitive potassium channel

73
Q

How does mutation in Kir6.2 and SUR1 cause diabetes

A
  1. Rising ATP closes channel as a result of hyperglycaemia, depolarising the membrane and insulin is secreted
  2. Mutations prevent closure of the channel so Beta cells can’t secrete insulin
74
Q

How is Permenant neonatal diabetes treated

A

Sulphonylureas closes K-ATP channel

75
Q

What is Maternally Inherited diabetes and deafness (MIDD

A

Mutation in mitochondrial DNA causes loss of beta cell mass

76
Q

Clinical presentation of MIDD

A

Type 2 similarities

77
Q

What is Lipodystrophy

A

Selective loss of adipose tissue causing increased insulin resistance

78
Q

What other conditions is lipodystrophy associated with

A
  1. Hepatatic steatosis
  2. Hyperandrogenism
  3. Dyslipidaemia
79
Q

What inflammatory conditions can cause diabetes

A
  1. CHRONIC PANCREATITIS
80
Q

What causes chronic pancreatitis

A

Alcohol

81
Q

How does chronic pancreatitis cause diabetes

A
  1. Alters secretions, formation of proteinaceous plus that block ducts and act as foci for calculi formation
82
Q

How is chronic pancreatitis caused diabetes treated

A

STOP ALCOHOL

Insulin treatment

83
Q

Name an autoimmune condition that can cause diabetes

A
  1. HEREDITARY HAEMOCHROMATOSIS

AMYLOIDOSIS and cystinosis

84
Q

What is Hereditary haemocrhomatosis characterised by

A
  1. Cirrhosis
  2. Diabetes
  3. Bronze hyper pigmentation
85
Q

Where does iron in hereditary haemochromatosis deposit

A
  1. Liver
  2. Pancreas
  3. Pituitary
  4. Heart
  5. Parathyroids
86
Q

How is hereditary haemochromatosis treated

A

Insulin

87
Q

How does Pancreatic neoplasia cause diabetes

A

Loss of glucagon function

88
Q

How is diabetes caused by pancreatic neoplasia treated

A
  1. Require SC insulin
  2. Frequent small meals
  3. Enzyme replacement
  4. Insulin pumps
  5. PANCREATIC RESECTIONS
89
Q

How does Cystic Fibrosis cause diabetes

A
  1. Viscous secretions lead to duct obstructions and fibrosis (no glucagon production)
  2. Ketoacidosis
  3. Insulin treatment required
90
Q

How do we treat diabetic caused CF

A
  1. INSULIN:
    - Body weight
    - reduces infections
    - lung function improves
91
Q

How does Acromegaly cause diaetes

A
  1. Excessive GH causes increased insulin resistance

Stops insulin action liver and peripheral tissues

GH cause increased lipolysis which increases NEFA causing B-cell failure

92
Q

How does Cushing syndrome cause diabetes

A
  1. Glucocorticoids excess causes increased glycerol and NEFA in fat
  2. Glucocorticoid excess causes proteolysis and AA
  3. Gluconeogenesis = increased hepatic glucose output
  4. Less glucose intake due to increased NEFA
93
Q

How does Pheochromocytoma cause diabetes

A

Disease of CATECHOLAMINE EXCESS:

Muscle:
Binds to B2 receptors causing increased glycolysis -> lactate (gluconeogenesis)

Decreased glucose uptake and use

Fat:
Binds to B1,2,3 receptors = lipolysis

Increased glycerol + NEFA -> gluconeogenesis

Increases blood glucose overall

94
Q

What drugs cause diabetes

A
  1. GLUCOCORTICOIDS (increase insulin resistance)

2. Thiazides/protease inhibitors (HIV) and antipsychotics

95
Q

What autonomic neuropathies are experienced in diabetes

A
  1. Orthostatic hypotension
  2. Cardiac AN
  3. Gastroparesis
  4. Diarrhoea
  5. COnstipation
  6. Incontinence
  7. Erectile Dysfunction
96
Q

What are the consequences of insensitivity in neuropathy

A
  1. FOOT ULCERATION
  2. INFECTION
  3. GANGRENE
  4. Falls
  5. Charcot foot
97
Q

What is charcot foot

A
  1. Degeneration of the weight bearing joint in the ankle resulting in ulcers
98
Q

Sensory neuropathy changes

A
  1. Burning
  2. Paraesthesia
  3. Hyperaesthesia
  4. Allodynia (Central pain in response to non-painful stimulation)
99
Q

How is Diabetic neuropathy treated

A
  1. GLYCAEMIC CONTROL
  2. SSRIs
  3. Gabapentin or Carbamazepine
  4. Opioids (Oxycodone)
  5. IV lignocaine
  6. Capsaicin

Transcutaneous nerve stimulation
Acupuncture
Hypnosis

100
Q

What is Capsaicin

A

Heating sensation that relives muscle pain

101
Q

What is IV lignocaine

A

Tissue numbing

102
Q

What diabetic problem commonly lead stop gangrene and amputation

A

Diabetic Foot Ulceration

103
Q

How does ulcer lead to amputation

A

Trauma -> Ulcer -> Failure to heal - Infection -> Amputation

104
Q

How do we screen for diabetic peripheral neuropathy

A
  1. Test sensation
  2. Vibration perception
  3. Ankle reflexes
105
Q

What test sensation do we do

A
  1. 10gm monofilaments

2. Neurotips

106
Q

What vibration perception do we do

A
  1. Tuning fork

2. Biothesiometer

107
Q

WHya re diabetics likely to be amputated

A

Due to PERIPEHRAL VASCULAR DISEASE (decreased perfusion to distal sites due to microvascular disease)

108
Q

Clinical presentation of PVD

A
  1. Intermittent Claudication
  2. Rest Pain
  3. Diminished pedal pulses on the foot
  4. Coolness of hands and feet
  5. Poor skin and nails
  6. Absence of hair on feet and legs
109
Q

How do we evaluate for peripheral vascular disease

A
  1. DOPPLER PRESSURE STUDIES
  2. DUPLEX ARTERIAL IMAGING

Determine need for surgical intervention

Or Doppler ultrasound for non-invasive

110
Q

Where do we do doppler ultrasound

A
  1. Pressure at brachial, pedal and toe arteries

Produces Ankle Brachial Index

111
Q

What is an abnormal ABI

A

<0.9

>1,3 is non-compressible

112
Q

How is peripheral vascular disease treated

A
  1. SMOKING CESSATION
    2> Walk through pain
  2. Surgical intervention
113
Q

How is amputation prevented

A
  1. Screening to identify neuropathy risk
  2. Education and providing orthotic shoes to prevent trauma
  3. MDT foot clinic if ulceration occurs
  4. Pressure relieving footwear, podiatry, revascularisation and antibiotics if infection occurs
114
Q

Risk factors for Diabetic Retinopathy

A
  1. Poor glycemic control
  2. Hypertensive
  3. Insulin treatment
  4. Pregnancy
115
Q

What can give us an indication for retinopathy risk

A
  1. Higher HbA1c = greater rate of retinopathy progression
116
Q

How is retinopathy risk reduced

A
  1. National Screening Programme for those over 11
  2. 2 field retinal photography
    3, Screeners grade photographs and reports sent to GP
117
Q

Pathophysiology of blindness in diabetes

A
  1. Pericyte loss and smooth muscle cell loss due to micro-aneurysms
  2. Basement membrane thickening reduces junctional contact with endothelial cells = leakage
118
Q

How does ischaemia occur in the eye

A
  1. Pericyte loss causes endothelial cells to rapidly multiply = ischaemia
  2. Glial cells grow down = occlusion
119
Q

How is diabetic retinopathy graded

A
  1. R0 = none
  2. R1 = Background
  3. R2 = Pre-proliferative
  4. R3 = Proliferative
120
Q

How is diabetic retinopathy treated

A
  1. LASER THERAPY (doe snot Importe sight just stabilises changes)
  2. Photocoagulation (cauterises ocular blood vessels)
121
Q

Risk of laser treatment

A
  1. Night vision loss
  2. Peripheral vision loss
  3. Vitreous haemorrhage
122
Q

Risk factors for diabetic nephropathy

A
  1. Poor BP control

2. BG control is poor

123
Q

What characterises diabetic nephropathy

A

PROTEINURIA

124
Q

How is diabetic nephropathy diagnosed

A
  1. First void midstream collected in 3 to 6 months

2. Urine albumin: Creatinine ratio

125
Q

GFR in Grade 1 CKD

A

90->105

126
Q

GFR in Grade 2

A

60-89

127
Q

GFR in grade 3

A

30-59

128
Q

GFR in grade 4

A

15-29

129
Q

GFR in grade 5

A

<15 (NEEDS DIALYSIS)

130
Q

Nephropathy in Type I vs Type II

A

Microalbuminuria develops 5-10 years after diagnosis vs present at time of diagnosis

GFR is normal in some patients with albuminuria

131
Q

How is GFR controlled

A
  1. BP control
  2. BG control
  3. RAAS blockade (ARB and ACEI)
  4. Cholesterol control

Year 2 (155 decks)

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