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5. Endocrinology > 15. Endocrine Pancreatic disorders > Flashcards

15. Endocrine Pancreatic disorders Flashcards

1
Q

A diagnosis of diabetes can be made by measuring plasma glucose levels.

What would a persons fasting plasma glucose be if they were diabetic?

A

Fasting plasma glucose >7mmol/L.

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2
Q

A diagnosis of diabetes can be made by measuring plasma glucose levels.

What would a persons random plasma glucose be if they were diabetic?

A

Random plasma glucose >11mmol/L.

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3
Q

A diagnosis of diabetes can be made by measuring plasma glucose levels.

What would the results of the oral glucose tolerance test be if someone was diabetic?

A

Fasting plasma glucose >7mmol/L and 2-hour value >11mmol/L.

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4
Q

What might someone’s HbA1c be if they have diabetes?

A

> 48mmol/mol.

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5
Q

Give 5 investigations carried out for diabetes.

A
  1. Urine dip
  2. FPG - fasting plasma glucose
  3. RPG - resting plasma glucose
  4. OGTT - oral glucose tolerance test
  5. HbA1c - glycated haemoglobin

(n.b. this won’t be accurate in anaemic patients)

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6
Q

Criteria for diabetes diagnosis.

A
  1. Symptomatic + one elevated FPG (≥7.0) or RPG (≥11.1)
  2. Asymptomatic + two elevated FPG or RPG
  3. OGTT with 2 hr glucose ≥ 11.1mmol/L
  4. HbA1c ≥ 48mmol/mol or 6.5%

*FPG = fasting plasms glucose
*RPG = resting plasma glucose
*OGTT = oral glucose tolerance test
*HbA1c = glycated haemoglobin

Symptoms of hyperglycaemia with 1 or more of:
o Ketosis
o Rapid weight loss
o Age of onset <5 years old
o BMI < 25 kg/m2
o Personal and/or family history of autoimmune disease

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7
Q

If you take a Resting Blood Glucose (RBG) as part of general monitoring/while testing for something else, and it comes back at 23 mmol/L, what do you need to confirm a diagnosis of diabetes?

A

Repeat the blood glucose test at another time.

One result is enough if the patient is symptomatic.

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8
Q

How would you diagnose T1DM if patient is asymptomatic and to differentiate from T2DM?

A
  1. Autoantibodies against beta cells
    - GADA
    - IA-2A
    - IAA
  2. C-peptide
    - T1DM: low
    - T2DM: high
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9
Q

Explain the origin of T1DM.

A

Beta cells express HLA antigens.
Autoimmune destruction -> beta cell loss -> impaired insulin secretion.
Insulin deficiency.

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10
Q

T1DM is characterised by impaired insulin secretion. Describe the pathophysiological consequence of this in the body.

A
  1. Severe insulin deficiency
  2. Glycogenolysis not suppressed
  3. Gluconeogensis not suppressed
  4. Lipolysis not suppressed
  5. Reduced peripheral glucose uptake
  6. ALL lead to hyperglycaemia and glycosuria
  7. Perceived stress -> cortisol and Ad secretion
  8. Lead to catabolic state -> increased plasma ketones
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11
Q

Give 2 potential consequences of T1DM.

A
  1. Hyperglycaemia.
  2. Raised plasma ketones -> ketoacidosis.
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12
Q

Is type 1 diabetes characterised by a problem with insulin secretion, insulin resistance or both?

A

Type 1 diabetes is characterised by impaired insulin secretion - there is severe insulin deficiency.

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13
Q

At what age do people with T1DM present?

A

Often people with Type 1 diabetes will present in childhood.

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14
Q

Give 3 risk factors for T1DM.

A
  1. Genetic predisposition - HLA DR3/4
  2. Family history
  3. Other AI diseases e.g. Coeliac, AI thyroid, Addison’s, Pernicious anaemia.
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15
Q

Give 3 symptoms of T1DM (the classical triad of symptoms for T1DM).

A

3 Ps:
1. Polyphagia - increase in appetite/eating
2. Polydipsia - extreme thirst
3. Polyuria - excessive urine passing

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16
Q

Other than the 3Ps, give 3 symptoms of T1DM.

A
  1. Unexplained weight loss
  2. Lethargy and fatigue
  3. Blurred vision
  4. Gastroparesis -> constipation
  5. Paresthesis
  6. Recurrent infections (candida)
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17
Q

One symptom of T1DM is polyphagia - rise in appetite and eating. Explain why this happens in T1DM.

A

Decreased insulin -> glucose unable to get into cells -. hyperglycaemia -> cells “starve” due to no glucose for energy generation -> polyphagia + fatigue

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18
Q

One symptom of T1DM is polydipsia - extreme thirst. Explain why this happens in T1DM.

A

Decreased insulin -> glucose unable to get into cells -. hyperglycaemia -> glucose gets above renal threshold -> glycosuria -> osmotic diuresis -> polyuria -> hypovolemia -> increased serum osmolality -> polydipsia.

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19
Q

One symptom of T1DM is polyuria - excessive urine passing. Explain why this happens in T1DM.

A

Decreased insulin -> glucose unable to get into cells -. hyperglycaemia -> glucose gets above renal threshold -> glycosuria -> osmotic diuresis -> polyuria.

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20
Q

Describe the treatment for T1DM.

A
  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 therapy.
  6. Frequent self-monitoring of blood glucose + long-term monitoring of HbA1c.
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21
Q

What are the different types of insulins available for insulin therapy?

A
  1. Human insulins
    - Produced by recombinant DNA technology
    - Have the same AA sequence as endogenous human insulin.
  2. Human insulin analogues
    - Produced in the same way as human insulins
    - But the insulin is modified to produce a specific desired kinetic characteristic (E.G. an extended duration of action or faster absorption and action)
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22
Q

Describe the different insulin categories in terms of time-action profiles.

A
  1. Rapid acting insulins
    - Quick onset of action: 15 mins
    - Short duration of action: 2-5 hrs
    - E.G. Humalog® (insulin lispro) and Novorapid® (insulin aspart)
  2. Short-acting insulins (regular or neutral)
    - Quick onset of action: 30-60 mins
    - Short duration of action: up to 8 hrs
    - E.G. Actrapid® and Humulin S®
  3. Intermediate-acting insulins (isophane)
    - Slow onset of action: 1-2 hrs
    - Maximal effects: 3-12 hrs
    - Long duration of action: 11-24 hrs
    - E.G. Humulin I®, Insuman Basal®, and Insulatard®
  4. Long-acting insulins
    - Duration of action of up to 24 hours
    - Steady-state level achieved after 2–4 days
    - To produce a constant level of insulin
    -E.G. Lantus® (insulin glargine), Levemir® (insulin detemir), and Tresiba® (insulin degludec)

Rapid- and short-acting insulins have a quick onset of action and a short duration of action. They are used to replicate the insulin normally produced by the body in response to glucose absorbed from a meal or sugary drink.

Intermediate- and long-acting insulins have a slow onset of action and a long duration of action. They mimic the effect of endogenous basal insulin (insulin that is secreted continuously throughout the day).

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23
Q

What is the difference between rapid/short acting insulins AND intermediate/long acting insulins in terms of their effects?

A
  1. Rapid/short acting insulins
    - Used to replicate the insulin normally produced by the body in response to glucose absorbed from a meal or sugary drink.
  2. Intermediate/long-acting insulins
    - Mimic the effect of endogenous basal insulin (insulin that is secreted continuously throughout the day).
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24
Q

What is the difference between rapid/short acting insulins AND intermediate/long acting insulins in terms of onset + duration of action?

A
  1. Rapid- and short-acting insulins have a quick onset of action and a short duration of action.
  2. Intermediate- and long-acting insulins have a slow onset of action and a long duration of action.
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25
Q

Explain the 3 different insulin therapy regimes for T1DM.

A
  1. 1st line:
    Multiple daily injection (MDI) basal-bolus insulin regimen
    -> Long or intermediate at bedtime AND rapid/short before meals
  • Long-acting Basal: twice-daily insulin detemir
  • Bolus: rapid-acting insulin analogue (Humalog or Novorapid)
  1. Mixed (biphasic) regimen (the person has 1/2/3 insulin injections per day)
    -> Once daily: Long or int at bedtime - only suitable T2DM
    -> Twice daily human mixed insulin: Pre breakfast/evening meal
  2. Continuous insulin infusion (insulin pump) therapy
    -> If very poor control
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26
Q

How is insulin administered in someone with T1DM?

A

Injected into SC fat.

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27
Q

Give examples of possible injection sites for insulin. Why is it important they are rotated regularly?

A

Outer thigh, abdomen, arm.

Rotating reduces risk of infection and lipohypertrophy.

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28
Q

Other than SC injections, how else can insulin be administered?

A

Insulin pump.

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29
Q

Give 4 potential complications of insulin therapy.

A
  1. Hypoglycaemia.
  2. Lipohypertrophy at ejection site.
  3. Insulin resistance.
  4. Weight gain.
  5. Interference with life style.
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30
Q

What is a hypoglycaemic coma?

A

Rapid onset of hypoglycaemia preceded by aggression, sweating, high pulse, seizures - leading to loss of consciousness.

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31
Q

Give 5 symptoms of hypoglycaemia.

A
  1. Hunger.
  2. Sweating.
  3. Tachycardia/Palpitations
  4. Anxious.
  5. Shaking/Tremor
  6. Dizziness
  7. Confusion
  8. Visual trouble
  9. Seizures
  10. Coma
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32
Q

How would you treat hypoglycaemia?

A

Oral sugar and long-acting starch (e.g. toast).
IV glucose if can’t swallow.

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33
Q

Give 3 complications a T1DM may present with.

A
  1. Staphylococcus skin infections
  2. Retinopathy
  3. Polyneuropathy
  4. Erectile dysfunction
  5. Arterial disease e.g. MI
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34
Q

What are the differences in onset between T1DM and T2DM?

A

Type 1 - adolescent onset usual.
Type 2 - onset usually >40yrs.

Type 1 is linked to HLA D3 and D4.
Type 2 has no HLA association.

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35
Q

What is the difference in the investigation of C-peptide between T1DM and T2DM?

A

C-peptide: low @ T1, high @ T2

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36
Q

What are the differences in T1DM and T2DM presentations?

A

Type 1 will present with polydipsia, polyuria, weight loss, ketonuria etc.

Type 2 presents asymptomatically (picked up on blood test), or with complications e.g. MI.

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37
Q

Explain the pathophysiology of T2DM.

A
  1. Insulin resistance develops
  2. Pancreatic beta cells hyperplasia + hypertrophy
  3. Increases beta cell secretion of insulin -> hypersecretion
  4. Beta cell exhaustion, dysfunction, atrophy
  5. Decreases insulin secretion
  6. Hyperglycaemia

Impaired insulin secretion and resistance -> IGT (impaired glucose tolerance) -> T2DM -> hyperglycaemia and high FFAs (free fatty acids)

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38
Q

Give 3 endocrine diseases that can cause diabetes.

A
  1. Cushing’s.
  2. Acromegaly.
  3. Phaeochromocytoma.
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39
Q

Give 5 risk factors for T2DM.

A
  1. Obesity / central adiposity
  2. Lack of exercise / physical inactivity
  3. Poor diet
  4. Asian background
  5. Age > 40 yrs
  6. Family history
  7. Gestational diabetes
  8. Medications/drugs e.g. glucocorticoids, thiazides diuretics, atypical psychotics
  9. PCOS
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40
Q

What class of drugs can cause diabetes?

A
  1. Steroids.
  2. Thiazides.
  3. Anti-psychotics.
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41
Q

Is type 2 diabetes characterised by a problem with insulin secretion, insulin resistance or both?

A

Type 2 DM is characterised by impaired insulin secretion AND insulin resistance.

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42
Q

What happens to insulin resistance, insulin secretion and glucose levels in T2DM?

A
  • Insulin resistance increases.
  • Insulin secretion decreases.
  • Fasting and post-prandial glucose increase.
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43
Q

Why is insulin secretion impaired in T2DM?

A

Impaired insulin secretion is thought to be due to lipid deposition in the pancreatic islets.

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44
Q

Is insulin secretion or insulin resistance the driving force of hyperglycaemia in T2DM?

A

Hepatic insulin resistance is the driving force of hyperglycaemia.

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45
Q

Describe the treatment pathway for T2DM.

A

1) Monotherapy
- Lifestyle changes: healthy eating, weight control, increased physical activity, diabetes education
- Metformin

2) Dual therapy
- Add DPP-4 inhibitor (gliptin) / sulfonyurea / TZD (glitazone) / SGLT-2 inhibitor / GLP-1R agonist

3) Triple therapy
- Add any of the above not used

4) Start insulin therapy alongside other medications

*3-month monitoring between each stage
*Move onto next if HbA1c >58 mmol/L

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46
Q

In what class of drugs does metformin belong?

A

Biguanide.

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47
Q

How does metformin work?

A

Reduces rate of gluconeogenesis -> reducing hepatic glucose output.
Increases insulin sensitivity.
Decreases absorption of glucose in GI tract.

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48
Q

When can metformin not be used?
Give 3 contraindications.

A
  1. Renal impairment -> eGFR < 30
  2. Congestive heart failure / Heart failure
    (due to the risk of lactic acidosis side effect of metformin)
  3. Hepatic insufficiency
49
Q

Give 2 side effects of taking metformin for T2DM treatment.

A
  1. GI upset
  2. Lactic acidosis
50
Q

How does sulfonylurea work?

A

Stimulates insulin release
- By binding to channels (SUR K+ channels) on beta cells to increase fusion of insulin with cell membrane.

51
Q

Give 2 potential consequences of taking Sulfonylurea for the treatment of T2DM.

A
  1. Hypoglycaemia
  2. Weight gain
52
Q

Give an example of a sulfonylurea.

A

Tolazamide
Gliclazide
Glimiperide

53
Q

What class do DPP-4 inhibitors + GLP-1R agonists?

A

Incretin-based agents

54
Q

How do GLP-1R agonists work in T2DM treatment?

A

Incretin mimetic which inhibits glucagon secretion.

  1. Activates GLP-1 receptors
  2. Increases GLP-1 levels
  3. Inhibit glucagon release + Increase insulin release
  4. Delays gastric emptying
  5. Increases satiety
55
Q

Give an example of GLP-1R agonist.

A

-tides.

Exenatide.
Liraglutide.
Lixisenatide.
Dulaglutide.
Semaglutide.

56
Q

Give 2 possible side effects of GLP-1R agonists.

A
  1. Weight loss
  2. Increase risk of Pancreatitis when used with DPP-4 inhibitors
  3. GI upset/irritation
  4. Renal impairment
57
Q

How do DPP-4 inhibitors (-gliptins) work in T2DM treatment?

A

Increases incretin levels which inhibit glucagon secretion.

  1. Block the enzyme dipeptidyl peptidase-4 (DPP-4)
  2. Increases incretin levels (GLP-1 and GIP)
  3. Incretins inhibit glucagon release, which in turn increase insulin secretion, decreases gastric emptying, and decreases blood glucose levels
58
Q

Give an example of DPP4-inhibitors.

A

-gliptins.

Sitagliptin.
Linagliptin.
Saxagliptin.
Algoliptin.

59
Q

Give 2 side effects of DPP4-inhibitors.

A
  1. Hypoglycaemia
  2. GI upset
60
Q

How do TZDs / glitazones work in T2DM treatment?

A

Interact with PPAR-gamma, which regulates lipid metabolism and insulin action.
Fatty tissue is redistributed and lower free fatty acid levels.
Promotes glucose consumption by muscles.

61
Q

Give an example of a TZD / glitazone.

A

Pioglitazone

62
Q

Give 2 side effects of TZDs/glitazones.

A
  1. Weight gain
  2. Fluid retention
63
Q

How do SGLT-2 inhibitors work?

A

Inhibit sodium-glucose transport protein 2 (SGLT2).
Inhibit reabsorption of glucose in the kidney.
Lower blood sugar.

64
Q

Give a side effect of SGLT-2 inhibitors.

A
  1. Weight loss
  2. UTIs
65
Q

Which 2 oral medications for T2DM cause weight gain?

A
  1. Sulfonylureas
  2. TZDs / glitazones
66
Q

Which 2 oral medications for T2DM cause weight loss?

A
  1. GLP-1R agonists
  2. SGLT-2 inhibitors
67
Q

Which 2 oral medications for T2DM cause hypoglycaemia?

A
  1. Sulfonyureas
  2. DPP-4 inhibitors
68
Q

Give 3 general measures that should be undertaken in DM.

A

Inform DVLA.
Foot care.
Exercise.
Diet - low in sat fats and sugar, high in starchy carbs.
Avoid binge-drinking - delayed hypo.
Educate on managing hypoglycaemia - sugary drinks, dextrose tablets.

69
Q

Give 3 possible complications of DM.

A

Infection/lipohypertrophy at injection sites.
MI, stroke.
Nephropathy - microalbuminuria.
Retinopathy.
Cataracts.
Diabetic foot.
Neuropathy.
Hypoglycaemia - due to insulin spikes, skipped meals, incorrect dose adjustment for exercise etc.

70
Q

Name 3 ketone bodies.

A
  • Acetoacetate
  • Acetone
  • Beta hydroxybutyrate
71
Q

Where does ketogenesis occur?

A

In the liver.

72
Q

Explain the pathophysiology of DKA.

A
  1. Excess glucose
  2. Complete absence of insulin
  3. Unrestrained increased hepatic gluconeogenesis
  4. Decreased peripheral glucose uptake
  5. Hyperglycaemia
  6. Osmotic diuresis
  7. Dehydration
  8. Peripheral lipolysis
  9. Increase FFA
  10. Oxidised to Acetyl CoA
  11. Ketone production

= SEVERE ACIDOSIS

73
Q

Give 3 risk factors for DKA.

A
  1. Unknown.
  2. Infections / Illness
    - e.g. UTI, surgery, MI, pancreatitis, chemotherapy, antipsychotics
  3. Untreated T1DM
  4. Treatment errors - wrong insulin dose
  5. Non-compliance with medication
  6. Having undiagnosed T1DM.
74
Q

Describe the triad of DKA.

A
  1. Acidaemia – blood pH < 7.3
  2. Hyperglycaemia – blood glucose > 11mmol/L.
  3. Ketonaemia.
75
Q

Give 4 signs of DKA.

A
  1. Hypotension.
  2. Tachycardia.
  3. Kussmaul’s respiration (deep and laboured).
  4. Breath smells of ketones (~ pear drops).
  5. Dehydration.
  6. Reduced consciousness.
76
Q

Give 5 symptoms of DKA.

A
  1. Polyuria.
  2. Polydipsia.
  3. Weight loss/Anorexia.
  4. Nausea/vomiting.
  5. Confusion.
  6. Weakness/Lethargy.
77
Q

Does DKA generally occur in T1DM or T2DM?

A

Type 1 - rare in Type 2.

78
Q

Why do you rarely see DKA in T2DM?

A

Insulin secretion is impaired but there are still low levels of plasma insulin.

Even low levels of insulin can prevent muscle catabolism and ketogenesis.

79
Q

Investigations to diagnose DKA.

A

Hyperglycaemia: Random Plasma Glucose >11 mmol/l

Ketonaemia: Plasma ketones > 3 mmol/l

Acidosis: Blood pH < 7.35 or Bicarbonate <15 mmol/l

Urine dipstick: glycosuria / ketonuria

80
Q

Give 4 potential complications of untreated DKA.

A
  1. Cerebral oedema.
  2. Hypokalaemia.
  3. Aspiration pneumonia.
  4. Thromboembolism.
  5. Adult respiratory distress syndrome.
  6. Coma.
  7. Death.
81
Q

Mangement of DKA.

A
  1. ABCDE + catheterise
  2. Rehydration - replace fluid loss with 0.9% saline IV
  3. IV insulin infusion
  4. Restore electrolytes e.g. K+ replacement
  • FIG-PICK
    • Fluids → 1 l stat then 4 over 12 hours
    • Insulin → add infusion (0.1/kg/hour)
    • Glucose → add dextrose if below 14 mmol/l
    • Potassium → correction
    • Infection → treat underlying causes
    • Ketones → monitor
82
Q

Define Hyperglycaemic Hyperosmolar State (HHS) /
Hyperglycaemia Hyperosmolar non-ketotic coma (HONK).

A

A syndrome characterised by extreme elevations in serum glucose concentrations, hyperosmolality and dehydration without significant ketoacidosis.

83
Q

Explain the pathophysiology of HHS / HONK

A

Hyperglycaemia -> osmotic diuresis -> hyperosmolarity leading to fluid shift of water into intravascular compartment -> severe dehydration.

No ketoacidosis as enough insulin to suppress ketogenesis.

84
Q

List the 3 characteristics of HHS / HONK.

A
  1. Marked hyperglycaemia
  2. Hyperosmolality
  3. Mild/no ketoacidosis
85
Q

Presentation of HHS / HONK.

A
  1. Extreme dehydration
    -> Result of osmotic diuresis
  2. Decreased levels of consciousness
    -> altered mental state ± seizures ± delirium
    -> result of elevated plasma osmolality
  3. Polyuria
86
Q

Is HHS / HONK more likely to affect T1DM or T2DM?

A

T2DM

87
Q

Management of HHS / HONK

A
  1. Fluid replacement - 0.9% IV saline (NaCl)
    - 1L in 30 mins 🡪 1L in 1 hour 🡪 1L in 2 hours 🡪 1L in 4 hours 🡪 1L in 6 hours
  2. Restore electrolyte loss (K+)
  3. Low-Molecular-Weight-Heparin (LMWH)
    - Hyperosmolality causes blood viscosity to increase = more likely to clot = MI, stroke, arterial thrombosis
    - e.g. Subcutaneous enoxaparin to decrease risk of thromboembolism
  4. Insulin
    – Only if severe, 3 units/hour instead
88
Q

Name 3 complications of HHS / HONK.

A

Cardiac arrest.
Cardiovascular collapse.
Myocardial infarction.
Pulmonary oedema.
Stroke.
Cerebral oedema and brain injury.
Venous thrombosis (DVT, PE)
Aspiration.

89
Q

Give a potential consequence of acute hyperglycaemia?

A

Diabetic ketoacidosis and hyperosmolar coma.

90
Q

Give a potential consequence of chronic hyperglycaemia?

A

Micro/macrovascular tissue complications e.g. diabetic retinopathy, nephropathy, neuropathy, CV disease etc.

91
Q

What is the main risk factor for diabetic complications?

A

Poor glycaemic control!

92
Q

Give 3 microvascular complications of diabetes mellitus.

A
  1. Diabetic peipheral neuropathy
  2. Diabetic retinopathy
  3. Diabetic nephropathy
93
Q

Give a macrovascular complication of diabetes mellitus.

A

CV disease and stroke.

94
Q

How might diabetic neuropathy present?

A

Stocking and glove distribution of loss of sensation
Absent ankle jerks
Deformities
May develop ulcers and ischaemia if there’s accompanying peripheral vascular disease.

95
Q

What is the commonest form of diabetic neuropathy?

A

Distal symmetrical polyneuropathy.

96
Q

Give 3 major clinical consequences of diabetic neuropathy.

A
  1. Pain.
  2. Autonomic neuropathy.
  3. Insensitivity.
97
Q

Describe the pain associated with diabetic neuropathy.

A
  • Burning.
  • Paraesthesia.
  • Nocturnal exacerbation.
98
Q

Diabetic neuropathy clinical consequences: what is autonomic neuropathy?

A

Autonomic neuropathy - damage to the nerves that supply body structures that regulate functions such as BP, HR, bowel/bladder emptying.

99
Q

Diabetic neuropathy: give 5 signs of autonomic neuropathy.

A
  1. Hypotension.
  2. HR affected.
  3. Diarrhoea/constipation.
  4. Incontinence.
  5. Erectile dysfunction.
  6. Dry skin.
100
Q

What are the consequences of insensitivity as a result of diabetic neuropathy?

A

Insensitivity -> foot ulceration -> infection -> amputation.

101
Q

Describe the distribution of insensitivity as a result of diabetic neuropathy?

A

Insensitivity starts in the toes and moves proximally. Glove and stocking distribution.

102
Q

Give 5 risk factors for diabetic neuropathy.

A
  1. POOR GLYCAEMIC CONTROL.
  2. Hypertension.
  3. Smoking.
  4. HbA1c.
  5. Overweight.
  6. Long duration of DM.
103
Q

Management of diabetic peripheral neuropathy.

A

Special foot care and diabetic shoes needed.

Control pain with:
paracetamol => amitriptyline => gabapentin => baclofen.

Improve glycaemic control.
Antidepressants.

104
Q

PVD - peripheral vascular disease - is a potential complication of Diabetes. Give 6 signs of acute ischaemia.

A
  1. Pulseless.
  2. Pale.
  3. Perishing cold.
  4. Pain.
  5. Paralysis.
  6. Paraesthesia.
105
Q

Give 5 ways in which amputation can be prevented in someone with diabetic neuropathy.

A
  1. Screening for insensitivity.
  2. Education.
  3. MDT foot clinics.
  4. Pressure relieving footwear.
  5. Podiatry.
  6. Revascularisation and antibiotics.
106
Q

Would there be increased or decreased pulses in a diabetic neuropathic foot?

A

There would be increased foot pulses.

107
Q

Describe the pathophysiology of diabetic retinopathy.

A

Micro-aneurysms -> pericyte loss and protein leakage -> occlusion -> ischaemia.

108
Q

Give 5 risk factors for diabetic retinopathy.

A
  1. Long duration DM.
  2. Poor glycaemic control.
  3. Hypertension.
  4. Insulin treatment.
  5. Pregnancy.
  6. High HbA1c.
109
Q

How can diabetic retinopathy be sub-divided?

A

Diabetic retinopathy is divided into:

  • Proliferative - evidence of neovascularisation in retina.
  • Non-proliferative.
110
Q

What would you see in someone with an R1 retinopathy grade?

A

R1 - non-proliferative/background.

  • Micro-aneurysms.
  • Intraretinal haemorrhages.
  • Exudates.
111
Q

What would you see in someone with an R2 retinopathy grade?

A

R2 - pre-proliferative.

  • Venous beading.
  • Growth of new vessels.
112
Q

What would you see in someone with an R3 retinopathy grade?

A

R3 - proliferative.

  • New blood vessel on disc.
113
Q

What is the treatment for diabetic retinopathy?

A

People with diabetes are offered regular screening to assess visual acuity.

  • Laser therapy treats neovascularisation.
114
Q

What is the hallmark of diabetic nephropathy?

A

Development of proteinuria and progressive decline in renal function.

115
Q

What happens to the glomerular basement membrane in someone with diabetic nephropathy?

A

On microscopy there is thickening of the glomerular basement membrane.

116
Q

Give one way in which the presentation of diabetic nephropathy differs between T1 and T2DM.

A

T1 DM: microalbuminuria develops 5-10 years after diagnosis.

T2 DM: microalbuminuria is often present at diagnosis.

117
Q

Describe the treatment for diabetic nephropathy.

A
  1. Glycaemic and BP control.
  2. ARB/ACEi.
  3. Proteinuria and cholesterol control.
118
Q

Other than T1DM + T2DM, name 4 other types of diabetes.

A
  1. Mature Onset Diabetes of the Young (MODY)
    – Rare autosomal dominant form of T2DM affecting young people
  2. Latent Autoimmune Diabetes of Adults (LADA)
    – Form of T1DM with slower progression to insulin dependence later on in life
  3. Primary Neonatal Diabetes
  4. Gestational Diabetes
    – Diabetes during pregnancy, usually in third trimester

5. Endocrinology (20 decks)

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