ENDO: Diabetes Flashcards
1
Q
Random plasma glucose level for diabetes
A
> 11 mmol/L
2
Q
Fasting plasma glucose level for diabetes
A
> 7mmol/L
3
Q
If a person has no symptoms how are they diagnosed as diabetic
A
- GTT (75mg) fasting > 7 or 2h value > 11mmol/L
4
Q
HbA1c level for diabetes
A
> 48 mmol/mol
5
Q
Clinical presentation of diabetes
A
- Thirst
- Polyuria
- Weight loss + fatigue
- Hunger
- Pruritis vulvae and balanitis
- Blurred vision
6
Q
What causes polyuria
A
Osmotic diuresis
7
Q
Why is there weight loss ann fatigue in diabetes
A
Lipid and muscle loss due to unrestrained gluconeogenesis
8
Q
What causes pruritus vulvae
A
Vaginal candidiasis (fungal infection)
9
Q
Why is vision blurred in diabetes
A
Altered acuity due to uptake of glucose/water into the lens
10
Q
When does type I diabetes present
A
Childhood
11
Q
Suggestive features of type I diabetes
A
- Lean body habitus
- Acute onset of osmotic symptoms
- Prone to ketoacidosis
- High levels of islet autoantibodies
12
Q
What factor does type I diabetes presentation depend on
A
Rate of beta-cell destruction
13
Q
What three features indicate type I diabetes and immediate insulin treatment for any age
A
- Weight loss
- Short history of severe symptoms
- Large urinary ketones
14
Q
Suggestive features of type II diabetes
A
- Presents in over 30
- Gradual onset
- Familial hypercholesterolaemia positive
- Identical twins
15
Q
What autoantibodies would I find in someone with type I diabetes
A
- Anti GAD (glutamate decarboxylase)
- Anti Pancreatic islet cell antibody
- Anti Islet antigen-2 Ab
16
Q
What there autoimmune conditions are associated with diabetes mellitus
A
- Hypothyroidism
- Addisons
- Coeliac’s
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
18
Q
How do free fatty acids damage the body
A
- Impair glucose uptake
- Transported to the liver where they undergo gluconeogenesis
- Oxidised to form ketone bodies
19
Q
What ketone bodies are produced from free fatty acids
A
- Beta hydroxybutyrate
- Acetoacetate
- Acetone
20
Q
What is ketoacidosis
A
- Absence of insulin causes hyperglycaemia and rising ketones
- Glucose and ketones escape in urine but lead to osmotic diuresis and falling blood volume
- Increasing dehydration, hyperglycaemia and acidosis = circulatory collapse and death
21
Q
Clinical presentation of ketoacidosis
A
Ketone sin the body cause anorexia and vomiting
22
Q
Define Diabetic Ketoacidosis
A
- Hyperglycaemia
- Raised plasma ketones
- Metabolic acidosis
23
Q
What value is hyperglycaemia
A
<50mmol/L
24
Q
What value is raised ketones
A
> 2+
25
What value defines metabolic acidosis
Plasma HCO3- < 15mmol/L
26
What causes Diabetic Ketoacidosis
1. Idiopathic
2. Infection/MI
3. Treatment errors (stoping insulin dose)
4. Previously unknown diabetes
27
The triad features of DKA
1, Hyperglycaemia
2. Ketones
3. Acidosis
28
Symptoms of DKA
1. Polyuria
2. Polydipsia
3. Nausea + vomiting
4. Weight loss
5. Weakness
6. Abdo pain (confused with surgical abdomen)
7. Drowsiness and confusion
29
Signs of DKA
1. Kussmaul breathing
2. Dehydration (loss of 5-6 litres)
3. Hypotension
4. Tachycardia
5. Coma
30
What is Kussmaul breathing
Initially in DKA, breathing is rapid and shallow but deep, laboured gasping occurs when it gets worse - this pattern is Kussmaul breathing
31
How does Kussmaul breathing effect blood constituents
1. Low CO2 and low HCO3-
32
Diagnostics of DKA
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
33
Why is K+ initially high on presentation of DKA
Acute shift of K+ out of the cell due to acidosis but will fall with rehydration
34
How is DKA managed
1. Rehydration (3L in first 3 hours)
2. Insulin
3. Replacement of electrolytes (K+)
4. Treat underlying cause
5. Immediate treatment start!
35
Why is insulin given in DKA
1. Inhibits lipolysis
2. Inhibits vetogenesis
3. Lowers acidosis
4. Reduces gluconeogenesis
5. Increase tissue glucose uptake
36
Complications of DKA
1. Cerebral oedema
2. Adult respiratory distress syndrome
3. Thromboembolism
4. Aspiration pneumonia
5. Death
37
what there microvascular complications of diabetes do we get
1. NEPHROPATHY (leads to chronic renal failure)
2. RETINOPATHY
3. NUEUROPATHY
4. Cardiomyopathy
5. Erectile dysfunction
38
What neuropathy is seen in diabetics
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)
39
What happens in diabetic retinopathy
1. Damage blood vessels are replaced buy weaker, poor-quality vessels in the retina.
2. Causes macular oedema (vision loss and blindness)
40
How is type I diabetes treated
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
41
What microvascular diseases are caused by diabetes
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
42
Why does insulin levels have to be closely monitored
Too high and this can cause hypoglycaemia
43
What part of the body is susceptible to hypoglycaemia
BRAIN - cerebral dysfunction (loss of concentration, confusion and coma)
44
What are two physiological defences against hypoglycaemia
1. Release of glucagon, adrenaline
45
What symptoms are seen in hypoglycaemia
1. Sweating, tremor, palpitations
| 2. Hunger and loss of concentration
46
At what glucose level is sweating, tremor and palpitations seen (autonomic symptoms)
3.8-2.8mM
47
What is seen at glucose levels of less than 2.8mM
Confusion, drowsiness, speech difficulty (neuroglycopenic symptoms)
48
What is seen at 1.5 mM glucose level
CONVULSIONS
COMA
HEMIPARESIS
49
What is HbA1c
1. Haemoglobin that is covalently bonded to glucose
50
Over how long is HbA1c monitored
3 months
51
Why is the HbA1c test limited to 3 months
RBC lifespan is 120 days
52
What is the normal range of Hb1Ac
6.7 - 7.6%
53
What is DAFNE
Dose adjustment For Normal eating
54
What can DAFNE prevent
DKA and hypos
55
What is the most common type of monogenic diabetes
MODY (Maturity-onset diabetes of the young)
56
At what age is MODY diagnosed
Less than 25
57
What kind of inheritance is MODY
Autosomal dominant
58
How does MODY cause diabetes
Single gene defect altering beta cell function
59
What types of MODYs are tehre
They are subdivided into Hepatic nuclear factor mutations: HNF1A (MODY 3) and HNF4A (MODY 1)
60
How is HNF1A mutation caused diabetes treated
VERY SENSITIVE to sulphonylureas treatment so no need for insulin
61
Clinical presentation of HNF4A mutation
1. Non-obese, Familial Hypercholesterolaemia
2. MACROSOMIA
3. Neonatal hypoglycaemia
62
What define macrosomia
Greater than 4.4kg at birth
63
What is MODY 2
1. Mutation in Glucokinase gene
64
Role of GCK
Glucose-sensor in beta cells, RATE DETERMINING STEP in glucose metabolism controlling release of insulin
65
How is MODY 2 controlled
1. Tight glycemic control in mild diabetes
| 2. More insulin is given to patients with MODY 2
66
What is MODY typically misdiagnosed as
Type I or younger onset Type II
67
Do MODY patients depend on insulin therapy
No
68
How do we distinguish MODY from TYPE I and TYPE II
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
How does C-peptide help distinguish between Type II and MODY from type I
1. C-peptide is negative within 5 years (completely destroyed)
2. Stilll persists in type II and MODY
70
AT what age is permanent Neonatal Diabetes diagnosed
Less than 6 months
71
Clinical presentation of Permenant Neonatal diabetes
Small Babies
Epilepsy
Muscle Weakness
72
Where do mutations in permanent neonatal diabetes occur
Kir6.2 and SUR1 subunits of the beta cell ATP sensitive potassium channel
73
How does mutation in Kir6.2 and SUR1 cause diabetes
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
How is Permenant neonatal diabetes treated
Sulphonylureas closes K-ATP channel
75
What is Maternally Inherited diabetes and deafness (MIDD
Mutation in mitochondrial DNA causes loss of beta cell mass
76
Clinical presentation of MIDD
Type 2 similarities
77
What is Lipodystrophy
Selective loss of adipose tissue causing increased insulin resistance
78
What other conditions is lipodystrophy associated with
1. Hepatatic steatosis
2. Hyperandrogenism
3. Dyslipidaemia
79
What inflammatory conditions can cause diabetes
1. CHRONIC PANCREATITIS
80
What causes chronic pancreatitis
Alcohol
81
How does chronic pancreatitis cause diabetes
1. Alters secretions, formation of proteinaceous plus that block ducts and act as foci for calculi formation
82
How is chronic pancreatitis caused diabetes treated
STOP ALCOHOL
| Insulin treatment
83
Name an autoimmune condition that can cause diabetes
1. HEREDITARY HAEMOCHROMATOSIS
AMYLOIDOSIS and cystinosis
84
What is Hereditary haemocrhomatosis characterised by
1. Cirrhosis
2. Diabetes
3. Bronze hyper pigmentation
85
Where does iron in hereditary haemochromatosis deposit
1. Liver
2. Pancreas
3. Pituitary
4. Heart
5. Parathyroids
86
How is hereditary haemochromatosis treated
Insulin
87
How does Pancreatic neoplasia cause diabetes
Loss of glucagon function
88
How is diabetes caused by pancreatic neoplasia treated
1. Require SC insulin
2. Frequent small meals
3. Enzyme replacement
4. Insulin pumps
5. PANCREATIC RESECTIONS
89
How does Cystic Fibrosis cause diabetes
1. Viscous secretions lead to duct obstructions and fibrosis (no glucagon production)
2. Ketoacidosis
3. Insulin treatment required
90
How do we treat diabetic caused CF
1. INSULIN:
- Body weight
- reduces infections
- lung function improves
91
How does Acromegaly cause diaetes
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
How does Cushing syndrome cause diabetes
1. Glucocorticoids excess causes increased glycerol and NEFA in fat
2. Glucocorticoid excess causes proteolysis and AA
2. Gluconeogenesis = increased hepatic glucose output
3. Less glucose intake due to increased NEFA
93
How does Pheochromocytoma cause diabetes
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
What drugs cause diabetes
1. GLUCOCORTICOIDS (increase insulin resistance)
| 2. Thiazides/protease inhibitors (HIV) and antipsychotics
95
What autonomic neuropathies are experienced in diabetes
1. Orthostatic hypotension
2. Cardiac AN
3. Gastroparesis
4. Diarrhoea
5. COnstipation
6. Incontinence
7. Erectile Dysfunction
96
What are the consequences of insensitivity in neuropathy
1. FOOT ULCERATION
2. INFECTION
3. GANGRENE
4. Falls
5. Charcot foot
97
What is charcot foot
1. Degeneration of the weight bearing joint in the ankle resulting in ulcers
98
Sensory neuropathy changes
1. Burning
2. Paraesthesia
3. Hyperaesthesia
4. Allodynia (Central pain in response to non-painful stimulation)
99
How is Diabetic neuropathy treated
1. GLYCAEMIC CONTROL
2. SSRIs
3. Gabapentin or Carbamazepine
4. Opioids (Oxycodone)
5. IV lignocaine
6. Capsaicin
--------
Transcutaneous nerve stimulation
Acupuncture
Hypnosis
100
What is Capsaicin
Heating sensation that relives muscle pain
101
What is IV lignocaine
Tissue numbing
102
What diabetic problem commonly lead stop gangrene and amputation
Diabetic Foot Ulceration
103
How does ulcer lead to amputation
Trauma -> Ulcer -> Failure to heal - Infection -> Amputation
104
How do we screen for diabetic peripheral neuropathy
1. Test sensation
2. Vibration perception
3. Ankle reflexes
105
What test sensation do we do
1. 10gm monofilaments
| 2. Neurotips
106
What vibration perception do we do
1. Tuning fork
| 2. Biothesiometer
107
WHya re diabetics likely to be amputated
Due to PERIPEHRAL VASCULAR DISEASE (decreased perfusion to distal sites due to microvascular disease)
108
Clinical presentation of PVD
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
How do we evaluate for peripheral vascular disease
1. DOPPLER PRESSURE STUDIES
2. DUPLEX ARTERIAL IMAGING
Determine need for surgical intervention
Or Doppler ultrasound for non-invasive
110
Where do we do doppler ultrasound
1. Pressure at brachial, pedal and toe arteries
Produces Ankle Brachial Index
111
What is an abnormal ABI
<0.9
| >1,3 is non-compressible
112
How is peripheral vascular disease treated
1. SMOKING CESSATION
2> Walk through pain
3. Surgical intervention
113
How is amputation prevented
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
Risk factors for Diabetic Retinopathy
1. Poor glycemic control
2. Hypertensive
3. Insulin treatment
4. Pregnancy
115
What can give us an indication for retinopathy risk
1. Higher HbA1c = greater rate of retinopathy progression
116
How is retinopathy risk reduced
1. National Screening Programme for those over 11
2. 2 field retinal photography
3, Screeners grade photographs and reports sent to GP
117
Pathophysiology of blindness in diabetes
1. Pericyte loss and smooth muscle cell loss due to micro-aneurysms
2. Basement membrane thickening reduces junctional contact with endothelial cells = leakage
118
How does ischaemia occur in the eye
1. Pericyte loss causes endothelial cells to rapidly multiply = ischaemia
2. Glial cells grow down = occlusion
119
How is diabetic retinopathy graded
1. R0 = none
2. R1 = Background
3. R2 = Pre-proliferative
4. R3 = Proliferative
120
How is diabetic retinopathy treated
1. LASER THERAPY (doe snot Importe sight just stabilises changes)
2. Photocoagulation (cauterises ocular blood vessels)
121
Risk of laser treatment
1. Night vision loss
2. Peripheral vision loss
3. Vitreous haemorrhage
122
Risk factors for diabetic nephropathy
1. Poor BP control
| 2. BG control is poor
123
What characterises diabetic nephropathy
PROTEINURIA
124
How is diabetic nephropathy diagnosed
1. First void midstream collected in 3 to 6 months
| 2. Urine albumin: Creatinine ratio
125
GFR in Grade 1 CKD
90->105
126
GFR in Grade 2
60-89
127
GFR in grade 3
30-59
128
GFR in grade 4
15-29
129
GFR in grade 5
<15 (NEEDS DIALYSIS)
130
Nephropathy in Type I vs Type II
Microalbuminuria develops 5-10 years after diagnosis vs present at time of diagnosis
GFR is normal in some patients with albuminuria
131
How is GFR controlled
1. BP control
2. BG control
3. RAAS blockade (ARB and ACEI)
4. Cholesterol control
