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Diabetes Flashcards

1
Q

What is the normal range for blood glucose

A

3.5-8 mmol/L

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2
Q

What is the pathology of T1DM

A

Autoimmune destruction of the B-pancreatic cells leading to decreased insulin release

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3
Q

At what age would you expect someone with T1DM to present with symptoms

A

<15years - normally before puberty

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4
Q

Is the development of symptoms in T1DM fast or gradual

A

Acute onset of severe symptoms so fast

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5
Q

What is the presentation of T1DM

A 
Polyuria
Polydipsia 
Decrease weight 
Increased urinary ketones 
Diabetic ketoacidosis 
Ketones on the breath 
Ketones in the urine
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6
Q

What is T1DM associated with

A

HLA-D3 and D4

Autoimmune conditions including Addisons, coeliac disease and hypothyroidism

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7
Q

What antibodies might you expect to find in someone with T1DM

A

Anti-GAD

Anti-islet

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8
Q

What is the pathology of T2DM

A

Insulin insulin resistance and B cell dysfunction leading to impaired insulin secretion

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9
Q

At what age would you expect someone with T2DM to present with symptoms

A

Older than 30

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10
Q

Would you expect the onset of symptoms in someone with T2Dm to be fast or gradual

A

Gradual

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11
Q

What is the presentation of T2DM

A

Polydipsia
Polyuria
Complications

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12
Q

What is the concordance rate for T2DM in monozygotic twins

A

80%

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13
Q

What are the associations with T2Dm

A 
Obesity 
Lack of exercise 
Calorie Excess 
EtOH excess 
Family history 
Middle East or SE Asian Ethnicity
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14
Q

What is the diabetic diagnostic criteria for someone who is symptomatic

A

Polyuria, polydipsia, weight loss and lethargy

Increased venous plasma glucose once either
Fasting >7mM
Random >11mM

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15
Q

What is the diabetic diagnostic criteria for someone who is asymptomatic

A

Increased venous plasma glucose on two different occasions or a 2Hr OGTT >11.1mM

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16
Q

What specific diagnostic criteria might you look for in someone with T1 diabetes

A

Increased urinary ketones
Decreased arterial pH
Decreased plasma bicarbonate

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17
Q

What are the specific diagnostic criteria you might look for in someone with T2DM

A

Elevated HbA1c

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18
Q

What are the three categories of potential secondary causes for diabetes mellitus

A
  1. Drugs
  2. Pancreatic
  3. Endo
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19
Q

What drugs are potential secondary causes of diabetes mellitus

A
  1. Steroids
  2. Anti-HIV
  3. Atypical neuroleptics
  4. Thiazides
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20
Q

What pancreatic diseases are potentially secondary causes of diabetes mellitus

A

CF

Chronic Pancreatitis

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21
Q

What other endocrinological conditions are potential causes of secondary diabetes mellitus

A
  1. Phaeochromocytoma
  2. Cushings
  3. Acromegaly
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22
Q

What are the lifestyle modifications that can be made by diabetic patients? (Remember DELAYS)

A

Diet (Reduced calorie intake, refined CHO, Fats and sodium and binge drinking)

Exercise

Lipids (prevent hyperlipidaemia with statins)

ABP (Reduce Na+ and EtOH in order to keep blood pressure <130/80 - Can use ACEi’s)

Yearly/6 monthly check ups

Smoking cessation

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23
Q

What is the first step in the oral hypoglycaemic management approach for diabetics

A

Life style modifications (DELAYS)

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24
Q

What is the second step in the oral hypoglycaemic management approach for diabetics

A

Start the patient on metformin (Increases insulin sensitivity and reduces liver glucose production)

500mg after evening meal

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25
What are the Side effects and contraindications for metformin
SE - Nausea, Diarrhoea, Abdominal pain and lactic acidosis CI - GFR <30, tissue hypoxia (Sepsis) or morning before general anaesthetic
26
What is the third step in the oral hypoglycaemic management approach for diabetics
Add Sulfonylureas (release insulin from the pancreas) to metformin
27
Name an example of a sulfonylurea
Gliclazide
28
What are the Side effects and contraindications of Sulfonylureas
SE - hypoglycaemia and Wt gain CI - Omit on morning of surgery
29
What is the third step in the oral hypoglycaemic management approach for diabetics
Additional therapy 1st line is to add insulin to metformin and Sulfonylureas 2nd line DPP4 inhibitor if insulin is unacceptable due to obesity/employment/social issues 3rd line = add subcutaneous exenatide if insulin is unacceptable 4th line = add acarbose
30
Name a DPP4 inhibitor
Sitagliptin or pioglitazone
31
How do DPP4 inhibitors work
Incretins are released following a meal which decrease blood glucose by stimulating the release of insulin and inhibiting the release gf glucose Incretins are inhabited by DPP4 so DPP4 inhibitors can be used to prevent this
32
What are the 3 most common regimes for insulin administration
1. Biphasic Regime 2. Basal Bolus regime 3. Long acting before bed
33
Describe the principles of the biphasic insulin administration regime and which diabetic individuals is this suitable for
Insulin administered 30mins before breakfast and dinner - Rapid acting (Actrapid) - Intermediate (Insulatard) Suitable for T2 or T1 with regular lifestyles (Children and older pTs)
34
Describe the principles of the basal-bolus regime and which diabetics is it suitable for
Bedtime long acting (Glargine) and short acting before each meal (Lispro) Need to adjust dose according to meal size Best for T1Dm to enable a flexible lifestyle
35
What are the three main side effects seen in patients on insulin regimes
1. Hypoglycaemia 2. Lipohypertrophy (need to rotate injection site) 3. Wt gain in T2DM
36
Describe the pathogenesis of diabetic ketoacidosis
1. Decreased insulin 2. Increased glucagon 3. Decreased glucose utilisation 4. Increase fat oxidation in liver 5. Increased fatty acid production 6. Increased generation of ketone bodies
37
What are the three major signs of diabetic ketoacidosis
1. Ketoacidosis 2. Dehydration 3. K+ imbalance
38
Describe why you get dehydration in patient with DKA
Decreased insulin leads to severe hyperglycaemia. This leads to glycosuria which causes an osmotic diuresis, drawing water into the urine thus leading to dehydration
39
Describe why you get K+ imbalance in patients with DKA
insulin normally drives the storage of K+ into cells however in diabetes insulin is deficient so K+ is not stored leading to hyperkalaemia
40
What are the common presentation of DKA
``` Abdominal Pain hypotension tachycardia Vomiting breath smells of ketones Gradual drowsiness Sighing Kussmaul hyperventilation Dehydration Ketotic breath ```
41
What is the diagnostic criteria for DKA
Arterial pH <7.3 (HCO3- <15mM) Hyperglycaemia (>11.1mM) Ketonaemia (>3mM)
42
What investigations would you carry out to determine if an individual has DKA
Urine (Ketones and glucose) Capillaries (Glucose and ketones) VBG (Acidosis and increased K+) Bloods (U and E, FBC and glucose)
43
What are the common complications of diabetic ketoacidosis
Cerebral oedema due to exces fluid accumulation Aspiration pneumonia Hypokalaemia
44
What is the management approach for DKA | FIGPICK
Fluid resuscitation (normal saline, 1L stat then 4L with K+ over 12hr Insulin - Actrapid 0.1u/kg/hr IVI Glucose - monitor blood glucose and add dextrose Potassium - Monitor serum K+ Infection - treat the underlying causes Chart - fluid balance Ketones - monitor blood ketones
45
What criteria is used to determine that DKA has been resolved?
Ketones <0.3mM Venous pH >7.3 HCO3- >18mM
46
What is Whipple's triad for hypoglycaemia
Low plasma glucose <3mM Symptoms consistent with hypoglycaemia Symptoms relieved by administration of glucose
47
At what point do autonomic hypoglycaemic symptoms develop
Blood glucose between 2.5-3
48
At what point do neuroglycopenic hypoglycaemic symptoms develop
Blood glucose <2.5
49
What are the autonomic symptoms of hypoglycaemia
``` Sweating Anxiety Tremor Palpitations Hunger ```
50
What are the neuroglycopenic symptoms of hypoglycaemia
``` Confusion Dizziness Personality changes Seizures Coma (<2.2) Visual changes ```
51
What are the causes of hypoglycaemia (Remember EXPLAIN)
Exogenous drugs (Insulin, oral hypoglycaemics, alcohol) Pituitary insufficiency Liver failure Addison's disease Insulinoma (Islet cell tumour)/Immune (Insulin receptor Abs: Hodgkins) Non-pancreatic neoplasms (Fibrosarcomas)
52
What investigations would you carry out in someone with hypoglycaemia
72hr fasting monitoring
53
Describe the treatment for T1DM.
1. EDUCATION - make sure the patient understands the benefits of good glycaemic control. 2. Healthy diet - low in sugar, high in carbohydrates. 3. Regular activity, healthy BMI. 4. BP and hyperlipidaemia control. 5. Insulin.
54
Give 4 potential complications of insulin therapy.
1. Hypoglycaemia. 2. Lipohypertrophy at ejection site. 3. Insulin resistance. 4. Weight gain. 5. Interference with life style.
55
Why do you rarely see diabetic ketoacidosis in T2DM?
Insulin secretion is impaired but there are still low levels of plasma insulin. Even low levels of insulin can prevent muscle catabolism and ketogenesis.
56
Describe the treatment pathway for T2DM.
1. Lifestyle changes: lose weight, exercise, healthy diet. 2. Metformin. 3. Metformin + sulfonylurea. 4. Metformin + sulfonylurea + insulin. 5. Increase insulin dose as required.
57
How does metformin work in treating T2DM?
Metformin increases insulin sensitivity and inhibits glucose production.
58
How does sulfonylurea work in treating T2DM?
Sulfonylurea stimulates insulin release.
59
Give a potential consequence of taking Sulfonylurea for the treatment of T2DM
Hypoglycaemia. | Wt gain
60
Give 3 microvascular complications of diabetes mellitus.
1. Diabetic retinopathy. 2. Diabetic nephropathy. 3. Diabetic peripheral neuropathy.
61
Give a macrovascular complication of diabetes mellitus.
CV disease and stroke.
62
What is the main risk factor for diabetic complications?
Poor glycaemic control!
63
Give a potential consequence of acute hyperglycaemia?
Diabetic ketoacidosis and hyperosmolar coma.
64
Give a potential consequence of chronic hyperglycaemia?
Micro/macrovascular tissue complications e.g. diabetic reinopathy, nephropathy, neuropathy, CV disease etc.§§
65
What is the commonest form of diabetic neuropathy?
Distal symmetrical polyneuropathy
66
Give 3 major clinical consequences of diabetic neuropathy.
1. Pain. 2. Autonomic neuropathy. 3. Insensitivity.
67
Describe the pain associated with diabetic neuropathy.
- Burning. - Paraesthesia. - Nocturnal exacerbation.
68
Diabetic neuropathy clinical consequences: what is autonomic neuropathy?
damage to the nerves that supply body structures that regulate functions such as BP, HR, bowel/bladder emptying.
69
give 5 signs of autonomic neuropathy
1. Hypotension. 2. HR affected. 3. Diarrhoea/constipation. 4. Incontinence. 5. Erectile dysfunction. 6. Dry skin.
70
What are the consequences of insensitivity as a result of diabetic neuropathy?
Insensitivity -> foot ulceration -> infection -> amputation.
71
Describe the distribution of insensitivity as a result of diabetic neuropathy?
Insensitivity starts in the toes and moves proximally. Glove and stocking distribution.
72
Give 5 risk factors for diabetic neuropathy.
1. POOR GLYCAEMIC CONTROL. 2. Hypertension. 3. Smoking. 4. HbA1c. 5. Overweight. 6. Long duration of DM.
73
Describe the treatments for diabetic neuropathy
1. Improve glycaemic control. 2. Antidepressants. 3. Pain relief.
74
PVD is a potential complication of Diabetes. Give 6 signs of acute ischaemia.
1. Pulseless. 2. Pale. 3. Perishing cold. 4. Pain. 5. Paralysis. 6. Paraesthesia.
75
Give 5 ways in which amputation can be prevented in someone with diabetic neuropathy.
1. Screening for insensitivity. 2. Education. 3. MDT foot clinics. 4. Pressure relieving footwear. 5. Podiatry. 6. Revascularisation and abx.
76
Would there be increased or decreased pulses in a diabetic neuropathic foot?
There would be increased foot pulses.
77
Give 5 risk factors for diabetic retinopathy.
1. Long duration DM. 2. Poor glycaemic control. 3. Hypertension. 4. Insulin treatment. 5. Pregnancy. 6. High HbA1c.
78
Describe the pathophysiology of diabetic retinopathy
Micro-aneurysms -> pericyte loss and protein leakage -> occlusion -> ischaemia
79
How can diabetic retinopathy be sub-divided?
- Proliferative - evidence of neovascularisation in retina. | - Non-proliferative.
80
What is the treatment for diabetic retinopathy?
People with diabetes are offered regular screening to assess visual acuity. - Laser therapy treats neovascularisation
81
What is the hallmark of diabetic nephropathy?
Development of proteinuria and progressive decline in renal function
82
What happens to the glomerular basement membrane in someone with diabetic nephropathy?
On microscopy there is thickening of the glomerular basement membrane.
83
Give one way in which the presentation of diabetic nephropathy differs between T1 and T2DM.
T1 DM: microalbuminuria develops 5-10 years after diagnosis. T2 DM: microalbuminuria is often present at diagnosis.
84
Describe the treatment for diabetic nephropathy.
1. Glycaemic and BP control. 2. ARB/ACEi. 3. Proteinuria and cholesterol control.

Phase 2 (16 decks)

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