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Block 34 - Metabolic > Diabetes mellitus > Flashcards

Diabetes mellitus Flashcards

1
Q

1) What percentage of people with DM have type 1?
2) What is a normal capillary blood glucose level?
3) What is DM characterised, defined and diagnosed by?
4) In DM, what do patients have difficulty in doing?

A

1) 10%
2) 3.5-8mmol/litre.
3) high CBG levels.
4) Patients have difficulty moving glucose from the blood into cells.

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2
Q

In basic terms in T1DM, what is the underlying pathophysiology?

A

The pancreas does not make enough insulin due to a type IV hypersensitivity response where a person’s T cells attack the pancreas. This is caused by a cell-mediated immune response.

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3
Q

In T1DM, there is a genetic abnormality which causes what?

A

Loss of self tolerance amongst T cells.
Causes T cells to attack Beta cell antigens.
T cells recruit other cells which also attack Beta cells.
Loss of Beta cells = less insulin produced = more glucose in the blood.

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4
Q

1) What are the 2 HLA genes which most people with T1DM have in common?
2) What do HLA genes code for?
3) If a person has T1DM predisposition genes, what can cause them to develop T1DM?

A

1) HLA-DR3 and HLA-DR4.
2) MHC proteins which are important for foreign antigen presentation and self-tolerance.
3) Environmental factors can then trigger beta cell destruction.

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5
Q

Name 5 environmental associations which may trigger beta cells destruction and T1DM development in susceptible patients.

A

1) Viruses - human enterovirus
2) Dietary factors - cow’s milk, early cereal introduction. vitamin D may be protective.
3) Coeliac disease

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6
Q

1) What percentage of beta cells need to be destroyed before symptoms appear in a patient?
2) When does destruction of beta cells usually begin?
3) What does beta cell destruction proceed subclinically as?
4) How long can the subclinical phase of T1DM last for?
5) What occurs when 80-90% beta cells have been destroyed?

A

1) 90%
2) Early in life.
3) Insulinitis.
4) Months to years.
5) Hyperglycaemia.

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7
Q

Basically, describe the pathophysiology of T2DM.

A

The pancreas produces insulin, but the tissue cells do not respond to it. This is because the tissue cells do not move glucose transporter cells to the cell membranes and so the cells cannot take up glucose.

This is known as insulin resistance.

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8
Q

Name 3 factors which can aggravate insulin resistance in patients with T2DM.

A

Ageing, physical inactivity and obesity.

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9
Q

Name 3 risk factors for the development of T2DM.

A

Obesity, lack of exercise and HTN.

** Genetics also plays a role.

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10
Q

1) What role does obesity play as a risk factor for T2DM?

2) In T2DM, when the tissues do not respond well to normal levels of insulin, what happens?

A

1) It is thought that excess adipose tissue releases free fatty acids and adipokines which can cause inflammation.
2) The body must produce more insulin in order to achieve the same effect.

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11
Q

1) How does the body produce more insulin initially in patients with T2DM and insulin resistance?
2) Eventually in patients with T2DM, why do insulin levels then decrease?
3) When do clinical symptoms tend to appear in patients with T2DM?

A

1) Beta cell hyperplasia and hypertrophy.
2) Because increased production is not sustainable, so beta cells undergo hypotrophy and hypoplasia so insulin levels decrease.
3) When the insulin levels begin to decrease.

**In T2DM, DKA does not usually develop as there is still some insulin present.

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12
Q

Name 6 main presenting factors of T1DM.

A 
Weight loss
Polyphagia
Glycosuria
Polyuria
Polydipsia
Blurred vision
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13
Q

Describe why weight loss occurs in patients with T1DM.

A

Glucose in the blood cannot enter cells.
This leaves cells starved of energy.
Adipose tissue starts breaking down fat for energy.
Muscle tissue starts breaking down muscle protein for energy.
This causes weight loss.

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14
Q

Describe why polyphagia occurs in patients with T1DM.

A

Patients experience increased hunger due to the high catabolic state and the fact that the body is not covering glucose to energy.

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15
Q

Describe why glycosuria occurs in patients with T1DM.

A

There are such high levels of glucose in the blood, not all of it is reabsorbed and so is secreted and spills over into the urine.

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16
Q

Describe why polyuria occurs in patients with T1DM.

A

Glucose is osmotically active, so increased glucose in the urine causes increased volumes of water to be secreted into the urine. So water follows glucose, and so with glycosuria there will be an increased urine volume.

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17
Q

Describe why polydipsia occurs in patients with T1DM.

A

Polyuria causes patients with diabetes to become dehydrated and therefore thirsty.

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18
Q

Describe why blurred vision occurs in patients with T1DM.

A

Blurred vision occurs with high or fluctuating glucose levels.

Increased levels of glucose damage the retina.

Increased levels of glucose can also cause damage to the blood vessels supplying the retina.

Increased levels of glucose can also cause the lens in the eye to swell.

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19
Q

1) What is a main difference in presentation between patients with T1 and T2 diabetes mellitus?
2) How is type 2 diabetes often detected?

A

1) T2DM presents more insidiously than T1DM. T1DM tends to cause symptoms over days to weeks, whereas T2DM causes symptoms over months.
2) Through screening.

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20
Q

Name 6 features of clinical presentation which are more common in patients with T2DM.

A 
Candidal infections
Skin abscesses
Fatigue
Paraesthesia
Acanthosis nigrans
Frequent UTIs
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21
Q

Aside from type 1 and type 2 DM, name two other subtypes of diabetes mellitus.

A

1) Gestational diabetes: where pregnant women have an increased CBG.
2) Drug-induced diabetes.

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22
Q

Describe gestational diabetes.

A

Usually occurs in the third trimester of pregnancy. It is thought to be caused by hormones which interfere with insulin’s action on insulin receptors.

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23
Q

Describe drug induced diabetes.

A

Medications can have side effects which tend to increase blood glucose levels. Mechanisms are thought to be related to insulin resistance.

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24
Q

State the diagnostic levels that the WHO uses for diabetes mellitus for the following investigations:

a) Random plasma glucose
b) Fasting plasma glucose
c) HbA1c\d
d) Oral glucose tolerance test

A

a) >11mmol/L
b) >6.9mmol/L
c) >/=48mmol/L
d) >11mmol/L

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25
Q

Describe how fasting C peptide can be used as a diagnostic investigation for diabetes mellitus.

A

C-peptide is produced when insulin is produced from pro-insulin.
Levels of C-peptide reflect insulin production.

So, fasting C-peptide can be helpful in differentiating between T1 and T2 DM.

**In T1DM, fasting C-peptide levels will be low or undetectable because insulin is not being produced or is only being produced at very low levels.

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26
Q

Describe results which would be indicative of pre-diabetes for the following investigations:

a) Fasting blood glucose
b) Random blood glucose
c) Oral glucose tolerance test
d) HbA1c

A

a) >6.1
b) >7.8
c) >7.8
d) 42-48

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27
Q

1) How do you reduce the risk of micro- and macrovascular complications in patients with diabetes mellitus?

A

1) Through intensive glycaemic control.

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28
Q

1) How do you reduce the risk of micro- and macrovascular complications in patients with diabetes mellitus?
2) What is a major cause of death and morbidity in patients over 30 with DM?
3) What is the main cause of death in patients under 30 with DM?

A

1) Through intensive glycaemic control.
2) CVD.
3) Acute diabetic complications.

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29
Q

Describe how often HbA1c should be monitored for patients with diabetes.

A

HbA1c should be checked twice yearly for patients with T1DM meeting their Rx goal:

  • <59 for patients <18 years with T1Dm
  • <53 for adults.

HbA1c should be checked monthly for patients with T1DM not meeting their Rx goal.

In adults with type 2 diabetes, measure HbA1c levels at:

  • 3–6-monthly intervals (tailored to individual needs), until the HbA1c is stable on unchanging therapy
  • 6-monthly intervals once the HbA1c level and blood glucose lowering therapy are stable.
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30
Q

1) How should BP be monitored in patients with DM?
2) When should lipid profiles be monitored in patients with DM?
3) Describe how diabetic retinopathy should be monitored.

A

1) Check BP at each patient visit.
2) At diagnosis and then every 5 years.
3) At diagnosis and then annually if >12 years.

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31
Q

Describe the blood pressure targets for patients with diabetes outlined by NICE.

A
  • T1DM: <135/85
  • T2DM: <140/80
  • Patient with diabetic nephropathy, diabetic retinopathy, cerebrovascular disease or 2 signs of metabolic syndrome: <130/80
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32
Q

Name 3 other areas which should be monitored annually for patients with diabetes mellitus.

A

eGFR in patients with DM for >5 years.
Distal polyneuropathy
Dental exams to control periodontal disese

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33
Q

Which 3 conditions should there be a low threshold for screening for with patients with diabetes?

A

Thyroid diseases
Coeliac disease
Depression

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34
Q

What is the first line management option for patients with T1DM?

How does this method of management work?

A

First line treatment is with basal bolus insulin. An initial basal dosing of insulin is given each day alongside insulin boluses which are given before meals.

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35
Q

1) What is the initial total daily dose of insulin that is prescribed?
2) How are meal time insulin doses given?
3) What type of insulin is used for the basal doses?
4) What type of insulin is used for bolus doses?

A

1) 0.2-0.4 units/kg/day
2) As a range of doses (i.e. certain insulin dose for a certain meal size) or through carbohydrate counting.
3) Intermediate/ long acting insulins
4) Short/ rapid acting insulins.

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36
Q

Describe when short or rapid acting insulin boluses should be administered with regards to meal times.

A

Short acting insulins should be given 30 minutes prior to a meal.

Rapid acting insulins should be given 15 minutes before a meal or very shortly after a meal.

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37
Q

Name 2 adjunct treatments which can be used for patients with type 1 diabetes mellitus.

A

1) Pre-meal correction insulin: can be added to bolus insulin based on pre-meal blood glucose measurements.
2) Amylin anaglogues: reduces post prandial glucose increases by prolonging gastric emptying time and reduces food intake through centrally mediated appetite suppression. (e.g. Pramlintide)

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38
Q

1) Which patients is use of Amylin often reserved for?
2) What combination of insulins can be used in order to provide better background blood glucose maintenance?
3) What is a main benefit of rapid acting insulins?

A

1) Mainly used for patients with post-prandial hyperglycaemia that cannot be controlled with pre-meal insulin alone.
2) Short acting can be combined with longer acting (30:70 ratio) for better background maintenance.
3) Offers patients more flexibility over when meals are eaten.

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39
Q

Name 4 short acting insulins.

A

Actrapid
Humulin S
Velosulin
Hypurin Natural

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40
Q

Name 3 rapid acting insulins.

A

Novorapid
Humalog
Insulin lispro

**Rapid acting insulins act quickly to minimise rises in blood sugar.

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41
Q

Name 2 intermediate acting insulins.

A

Hypurin Isophane

Humulin I

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42
Q

Give 3 examples of long acting insulins.

A 
Insulin glargine
Insulin determine
Insulin degludec
Hypurin Bovine Lente
Hypurin Bovine Pzi (activity can last for up to 36 hours)
  • *Long acting insulins are appropriate in those with hyperglycaemia throughout the day and night.
  • **Useful for those needing help with injections as activity can last for up to 24 hours.
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43
Q

1) What is the first stage of management for patients with T2DM?
2) What is often the second line management for patients with T2DM?
3) When do you move up a step of the T2DM management ladder?

A

1) Lifestyle modifications.
2) Monotherapy normally with metformin.
3) If the current level of therapy is not sufficient to keep HbA1c below target (<58).

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44
Q

State 6 lifestyle modifications that need to be suggested for patients with T2DM.

A
  • Increased complex carbs, less simple carbs.
  • Exercise and weight loss
  • Decreased alcohol intake
  • Substitute sugars for artificial sweeteners
  • Eat low glycaemic index foods
  • Spread nutrient load throughout the day to reduces blood glucose swings (eat 3 meals a day).
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45
Q

List the third line dual therapy options for patients with type 2 diabetes mellitus.

A
  • metformin and a DPP-4 inhibitor (sitagliptin)
  • metformin and pioglitazone
  • metformin and a sulfonylurea (gliclazide)
  • metforming and an SGLT-2 inhibitor (gliflozin)
46
Q

In which 5 situations should you not offer pioglitazone to a patient?

A
  • heart failure or history of heart failure
  • hepatic impairment
  • diabetic ketoacidosis
  • current, or a history of, bladder cancer
  • uninvestigated macroscopic haematuria.
47
Q

What are the two options for triple therapy for a patient with type 2 diabetes mellitus?

A

metformin, a DPP-4 inhibitor and a sulfonylurea OR
metformin, pioglitazone1 and a sulfonylurea.\

**If these combinations are not tolerated, try Metformin + sulphonylurea + GLP-1 agonist.

48
Q

1) What is the final level of management for a patient with type 2 diabetes?
2) What oral medications should you continue when starting a patient with type 2 diabetes mellitus on insulin?

A

1) Insulin.

2) Metformin should be continued and the necessity considered at reviews.

49
Q

What insulin regimens are more commonly used for patients with type 2 diabetes mellitus?

A

NPH insulin is usually injected as part of a once daily or twice daily regimen.

NPH insulin and a short acting insulin can be used separately or in a biphasic mix and may be considered if a patient has a very high HbA1c level (>78).

50
Q

1) In the body, what do GLP and GIP normally do?
2) What are GLP and GIP normally broken down by?
3) Why are GLP-1 agonists known as insulin mimetics?

A

1) Increase insulin secretion.
2) DPP-4 (so DPP-4 can be inhibited to increase insulin secretion).
3) Because they increase insulin secretion when used pharmaceutically.

51
Q

List the 5 main causes/ precipitants of diabetic ketoacidosis.

A

1) Infection
2) Intoxication
3) Infarction
4) Inappropriate withdrawal of insulin
5) Intercurrent illness

** Can be memorised as the 5 I’s.

52
Q

1) Pathophysiologically, what does a lack of insulin cause on the lead up to diabetic ketoacidosis.
2) What happens pathophysiologically after free fatty acids are produced in diabetic ketoacidosis?

A

1) Lack of insulin causes lipolysis (this is especially prominent when the body is not getting enough energy).
2) Free fatty acids travel to the liver and undergo ketogenesis to form ketone bodies.

53
Q

1) In diabetic ketoacidosis, increased presence of ketones causes what?
2) What is the effect of excess ketones present in the body in diabetic ketoacidosis?

A

1) Ketonaemia and Ketonuria.

2) Ketones are acidic so they reduce the pH of the blood and urine.

54
Q

1) What is the effect of acidosis on the respiratory system in diabetic ketoacidosis?
2) What is the mechanism of hyperkalaemia in diabetic ketoacidosis?

A

1) Acidosis can cause Kussmaul breathing because a patient is trying to remove and expire excess CO2 present in the body.
2) Increased H+ and decreased insulin causes more potassium to remain in the blood, causing hyperkalaemia.

**More potassium present in the blood means that more K+ is excreted and so overtime, potassium stores in the body begin to be low.

55
Q

Why is there a high anion gap in diabetic ketoacidosis?

A

Due to the build up of ketoacids because of the metabolism of ketones.

Raised levels of acid (H+) bind to bicarbonate to form carbon dioxide as in the Henderson-Hesselbalch.

This results in metabolic acidosis.

56
Q

Briefly describe how increased stress on a patient can lead to diabetic ketoacidosis.

A

Stress causes adrenaline release and adrenaline causes glucagon release.
Glucagon increases CBG so there is a loss of glucose in the urine which also causes a loss of water and then dehydration.
There is therefore the need for an alternative energy source.
Ketone bodies are then generated from lipolysis and this leads to ketoacidosis.

57
Q

What can cause a patient with DKA to have a fruity smell to their breath?

A

Ketone bodies can break down into acetone which is then released as a gas through breathing.

58
Q

What biochemical triad characterises diabetic ketoacidosis?

A

Hyperglycaemia
Ketonaemia
Acideaemia

**All three of these occurring with a rapid symptom onset is indicative of DKA.

59
Q

List 10 potential presenting features of a patient with diabetic ketoacidosis.

A
  • gradual drowsiness and potential mental state changes
  • N+V
  • Dehydration
  • Polyuria
  • Polydipsia
  • Weakness
  • Weight loss
  • Abdominal pain
  • Acetone breath
  • Hypotension
  • Kussmaul breathing
  • Tachycardia
  • Poor skin turgor
  • Dry mucous membranes
  • SHOCK
60
Q

Give 4 potential diagnostic features of diabetic ketoacidosis.

A

1) Acidaemia: pH on VBG <7.3 or HCO3- <15mmol/L.
2) Hyperglycaemia: blood glucose >11mmol/L or known DM.
3) Ketonaemia: >3mmol/L
4) Ketonuria: >2+ on a dipstick.

61
Q

State which blood tests you would do for a patient with suspected diabetic ketoacidosis.

A 
Capillary and lab glucose
Ketones
pH (VBG; ABG only if deceased GCS or hypoxia)
U&amp;E
Osmolarity
FBC
LFT
62
Q

State 5 other investigations (excluding blood tests) that you might do for a patient with suspected diabetic ketoacidosis.

A 
ECG
CXR
Urine dipstick and MSU
?ABG if needed
Cardiac biomarkers
63
Q

State 4 features upon presentation which may indicate to you that a patient with DKA would be classified as severe.

A 
Blood Ketones >6
Venous bicarb <5
Venous/ arterial pH <7
Potassium <3.5
GCS <12
O2 sats <92% on air
SBP <90
HR >100 or <60
Anion gap >16
64
Q

If a patient presents with severe features of diabetic ketoacidosis, what should you do?

A

Consider transfer to HDU/ ICU for monitoring and access.

Get senior help.

65
Q

Why is it important to measure Potassium levels when you begin treating a patient with DKA?

A

Because use of insulin can cause hypokalaemia which could trigger arrhythmias.

66
Q

1) Basically, what does the management of diabetic ketoacidosis involve?
2) What approach should be taken for a patient with diabetic ketoacidosis?

A

1) management of diabetic ketoacidosis involves the replacement of fluid and electrolytes and the administration of insulin.
2) ABCDE approach should be taken plus 2 large bore cannula inserted.

67
Q

What are the 3 treatment aims when treating a patient with diabetic ketoacidosis?

A
  1. Blood ketones to fall by at least 0.5mmol/L/hour

2. Venous bicarbonate to rise by at least 3mmol/L/hour 3. Blood glucose to fall by at least 3mmol/L/hour

68
Q

Describe how IV fluids should be prescribed initially for patients with DKA.

A 
1L 0.9% NaCl (no K+) over 1st hour
1L 0.9% NaCl (±K+) over 2 hours
1L 0.9% NaCl (±K+) over 2 hours
1L 0.9% NaCl (±K+) over 4 hours
1L 0.9% NaCl (±K+) over 4 hours

**Make sure to anticipate a fall in Potassium and replace.

69
Q

In which 5 groups of people should you take extra caution with when administering fluids and why?

A

Caution in elderly, CCF, ESRF adolescence (18-25), pregnancy (risk of cerebral and pulmonary oedema).

**In these patients, fluid administration may need to be slower.

70
Q

In a patient with diabetic ketoacidosis, when the CBG level falls to below 14mmol/L, what should you do?

A

Add 125ml/hour of 10% glucose to run alongside 0.9% Sodium Chloride
(consider reducing rate of 0.9% sodium chloride to reduce risk of fluid overload)

71
Q

1) What type fo insulin is used to treat a patient with DKA?
2) What is the standard insulin prescription to treat a patient with DKA?
3) If DKA treatment aims are not being met, what should you do?
4) With regards to a patients normal insulin regimen (if they are already diagnosed with T1DM), what should you do?

A

1) Short acting insulin such as ActRapid.
2) A fixed rate intravenous insulin infusion of 0.1 units/kg/hour.
3) Increase insulin infusion rate by 1 unit/ hours until biochemical levels are falling at target rates.
4) Continue it.

72
Q

1) How often should blood ketone and blood glucose levels be measured in a patient with DKA?
2) When should you continue fixed rate insulin until?

A

1) Hourly.

2) Ketones <0.6mmol/L, venous pH >7.3 and bicarb >15.

73
Q

1) What diabetic emergency specifically occurs in type 2 diabetics?
2) Why is it very rare for DKA to occur in patients with T2DM?

A

1) Hyperosmolar Hyperglycaemic state
2) Because there is still some circulating insulin in patients with T2DM and so the insulin glucagon balance is such that DKA doesn’t usually occur.

74
Q

What is a main difference in presentation between DKA and HHS and what is the consequence of this?

A

Whilst DKA presents within hours of onset, HHS comes on over many days, and consequently the dehydration and metabolic disturbances are more extreme.

75
Q

Give 3 characteristic features of a patient presenting with HHS.

A

1) Hypovolaemia
2) Marked hyperglycaemia (>30 mmol/L) without significant hyperketonaemia (<3.0 mmol/L) or acidosis (pH>7.3, bicarbonate >15 mmol/L
3) Osmolality >320 mosmol/kg

**There can sometimes be mild ketonaemia or acidosis/

76
Q

1) Why is there an increased plasma osmolarity in patients with HHS?
2) What events lead to polyuria and total body dehydration in patients with HHS?

A

1) Due to extreme dehydration and the concentration of blood.
2) Glucose is a polar molecule and acts as a solute. Increased glucose levels in the blood cause water to leave body cells and enter vessels leading to increased urination and total body dehydration.

77
Q

Describe the clinical presentation of patients with HHS in comparison to those with DKA.

A

HHS has a similar presentation to DKA, however the mental state changes are usually more pronounced due to the more severe level fo dehydration. This history of the onset of symptoms of HHS also tends to be longer.

**In HHS, changes in mental performance can correlate with the severity of hyperosmolarity.

78
Q

Due to the high serum osmolarity which can occur with HHS, what is a major risk to patients and how should this be prevented?

A

The high osmolarity means that occlusive events are a dangerous and so LMWH should be given to all these patients unless otherwise contraindicated.

79
Q

Give the 3 treatment goals of HHS.

A

Normalise the osmolality
Replace fluid and electrolyte losses
Normalise blood glucose

80
Q

1) What is the goal of initial therapy for patients with HHS?
2) How is fluid therapy alone effective in those patients with HHS?

A

1) The goal of the initial therapy is expansion of the intravascular and extravascular volume and to restore peripheral perfusion.
2) Fluid replacement alone (without insulin) will lower blood glucose which will reduce osmolality causing a shift of water into the intracellular space.

81
Q

Why should insulin treatment not be given prior to fluid therapy in patients with HHS?

A

Insulin treatment prior to adequate fluid replacement may result in cardiovascular collapse as water moves out of the intravascular space, with a resulting decline in intravascular volume (a consequence of insulin-mediated glucose uptake and a diuresis from urinary glucose excretion).

82
Q

What is the standard fluid algorithm used for patients with HHS?

A 
1L 0.9% NaCl (no K+) over 1st hour
1L 0.9% NaCl (±K+) over 2 hours
1L 0.9% NaCl (±K+) over 2 hours
1L 0.9% NaCl (±K+) over 4 hours
1L 0.9% NaCl (±K+) over 4 hours

**Make sure to anticipate a fall in Potassium and replace.

83
Q

1) When should you prescribe insulin for patients with HHS?

2) What is the standard treatment prescription of insulin for patients with HHS?

A

1) If CBG not falling by 5mmol/L/hour or if there is significant ketonaemia.
2) Short acting insulin (ActRapid). 0.05units/kg/hour as a fixed rate intravenous insulin infusion.

**Shoudl keep CBG at 10-15 for the first 24 hours to avoid the risk of cerebral oedema.

84
Q

1) Describe hypoglycaemia.
2) In true cases of hypoglycaemia, which symptomatic triad may be present?
3) What is the main cause of hypoglycaemia in diagnosed diabetics?
4) In what instances might post-prandial hypoglycaemia occur?

A

1) The commonest endocrine emergency where plasma glucose levels will be <3mmol/L.
2) In true cases, Whipple’s triad may be present (hypoglycaemic symptoms, low CBG and symptom resolution after restoring CBG to normal).
3) The main cause of hypoglycaemia in diabetics is insulin/ sulphonylureas.
4) After gastric/ bariatric surgery and in T2DM.

85
Q

State 5 features which may be involved in the clinical presentation of a patient with hypoglycaemia.

A 
Rapid onset of symptoms
Odd behaviour and personality abnormalities (aggression, sweating, anxiety)
Tachycardia
Seizures/ focal symptoms/ coma
Hunger
Tremor, palpitations and dizziness.
Confusion and drowsiness
Visual disturbances
Incoherence
Mutism
Restlessness
86
Q

List 6 causes of hypoglycaemia which can also occur in non-diabetics.

A

1) Exogenous drugs
2) Pituitary insufficiency
3) Liver failure
4) Addison’s disease
5) Insulinomas/ immune hypoglycaemia
6) Non-pancreatic neoplasms

**Mnemonic ‘EXPLAIN’.

87
Q

How should you treat a hypoglycaemic patient who is:

a) conscious, orientated and able to swallow?
b) conscious but uncooperative?
c) unconscious or not responding to initial measures?

A

a) 15-20g of a quick acting carbohydrate up to 3 times (3-4 heaped teaspoons of sugar dissolved in water/ 150-200mL OJ/ 4-7 glucose tablets).
b) Squirt glucose gel between teeth and gums.
c) IVI glucose (10% at 200ml/ hour if conscious. 10% at 200ml/ 15 mins if unconscious) OR glucagon 1mg IM/ IV.

**Glucagon will not work in malnourished patients.

88
Q

1) In a patient with hypoglycaemia, once glucose is >4mmol/L and patient has recovered, what should you do?
2) What should you advise for patients who suffer frequent episodes of hypoglycaemia?\
3) How long should blood glucose monitoring be done for after an episode of hypoglycaemia?
4) What is lactic acidosis normally caused by in patients with diabetes?

A

1) Give a long acting carbohydrate.
2) Advise them to eat frequent high-starch meals.
3) 24-48 hours.
4) Metformin or septicaemia.

89
Q

What can long term diabetic complications be classified as?

Name 3 complications in each category.

A

Microvascular or macrovascular.

Microvascular: retinopathy, neuropaty, nephropathy.
Microvascular: CVD, cerebrovascular disease and peripheral vascular disease.

**It is vascular changes which often lead to micro- and microvascular complications in diabetes.

90
Q

1) When do the eyes of a diabetic patient need to be screened for retinopathy?
2) State 4 abnormalities which can occur in the eye in diabetic retinopathy.
3) What 2 conditions might result due to diabetic retinopathy?

A

1) at the time of diabetes diagnosis and then annually if the patient is >12.
2) Cotton wool spots, flame haemorrhages, micro aneurysms, macular thickening.
3) Glaucoma and cataracts.

91
Q

Describe how high blood glucose levels can damage the eyes.

A

High glucose levels weaken and damage small blood vessels in the retina, causing haemorrhages, exudates and swelling.
The retina is then starved of O2 and this can cause abnormal blood vessels to grow.

92
Q

How can macular oedema occur within the eye?

A

When abnormal blood vessels in the retina swell up this is known as macular oedema. Macular oedema can cause fluid to leak into the rear of the eye.

93
Q

Name 3 types of diabetic retinopathy.

A

Background retinopathy
Diabetic maculopathy
Proliferative retinopathy

94
Q

Describe background retinopathy.

A

Occurs when micro aneurysms have developed on the retina.
There is swelling of the capillaries supplying the retina.
The presence of small numbers of micro aneurysms will not normally affect vision.

95
Q

Describe Diabetic maculopathy.

A

The macula sustains some damage, for example, from macula oedema where fluid or protein is leaked onto the macula.

96
Q

Describe proliferative retinopathy.

A

Where new but weak blood vessels form on the retina to help to restore blood flow. This can cause scarring, vitreous haemorrhages or a detached retina.

97
Q

1) What might peripheral neuropathy involve?
2) What also may occur alongside peripheral neuropathy in patients with DM?
3) In diabetic patients, what causes damage to the nerves?

A

1) Can involve an increase or decrease in pain sensation, painless injuries and decreased reflexes peripherally.
2) Autonomic neuropathy with resting tachycardia, increased urinary frequency and ED in men.
3) Hyperglycaemia.

98
Q

1) What type of distribution is seen in peripheral neuropathy?
2) High levels of what compound are also associated with the development of nerve damage in patients with DM?

A

1) Peripherally, there is often a glove and stocking distribution.
2) High levels of triglycerides.

99
Q

1) What 2 conditions can be involved in diabetic nephropathy?
2) In diabetic nephropathy, what major histological changes happen?
3) In advanced cases of diabetic nephropathy, what can occur?

A

1) Glomerulosclerosis and pyelonephritis.
2) Interstitial fibrosis with tubular atrophy develops.
3) Infiltration of macrophages and T lymphocytes into renal tissues.

100
Q

Name 3 changes that can occur in diabetic nephropathy.

A

Mesangial expansion
Thickening of the basement membrane
Nodular glomerulosclerosis

101
Q

What 3 changes occur to the basement membrane in diabetic nephropathy?

A

Basement membrane thickening
Podocyte loss
Reduced endothelial cell fenestrations

102
Q

What occurs functionally with the kidneys in diabetic nephropathy?

A

Early glomerular hyperfiltration
Increased albumin excretion
Increasing proteinuria
Decreased GFR eventually

**Follows the same pattern of pathophysiology of CKD.

103
Q

1) What effect can diabetes have on blood vessels?
2) What does hypertriglyceridaemia cause?
3) How does the atherosclerotic process differ in patients with diabetes to patients without diabetes?

A

1) Glycated Hb causes damage to blood vessel endothelium, accelerating the atherosclerotic process. More glucose can also stick to glycated Hb in the bloodstream.
2) Increased cholesterol levels.
3) In DM, the atherosclerotic process is rapid and produces clinical disease at a younger age.

104
Q

Briefly describe how diabetes can lead to cerebrovascular disease.

A

Glucose in the blood can damage blood vessels in a similar way to cardiovascular disease.

A build up of glycated Hb can block and damage blood vessels.

These mechanisms can cause ischaemic and haemorrhages strokes and memory problems.

105
Q

1) What 3 conditions are included in the term Peripheral vascular disease?
2) What does the combination of loss of sensation and a compromised vascular supply cause in PVD?
3) Where are common ulceration sites for patients with PVD?

A

1) Atherosclerosis, gangrene and ulcerations.
2) Poor healing and poor detection of wounds which an lead to infections, gangrene and amputation.
3) On the sole of the foot where most of the pressure is exerted.

106
Q

1) Describe the main features of diabetic vascular malfunction.
2) In states of hyperglycaemia, what do endothelial cells do?
3) What do the endothelial cells then release as a biproduct?

A

1) The alteration of vascular homeostasis due to endothelial and smooth muscle cell dysfunction.
2) Take up a lot more glucose in order to produce energy.
3) They release reactive oxygen species as a byproduct.

107
Q

What do reactive oxygen species cause in the process of vascular changes in diabetic patients?

A 
Formation of glycated products
Stimulation of PKC activity leading to:
-increased VEGF production
-increased endothelin production
-increased nuclear factor kappa B production
108
Q

1) To cause vascular changes in diabetics, what does endothelin do?
2) To cause vascular changes in diabetics, what does nuclear factor kappa B do?
3) During the process of vascular change in diabetics, what do inflammation and vascular permeability cause?

A

1) Promotes platelet aggregation.
2) Promotes the inflammatory process.
3) Monocytes and LDLs to enter the tunica intima.

109
Q

1) What causes foam cell formation?
2) What do macrophages and foam cells do?
3) What do foam cells cause smooth muscle cells to do?
4) Eventually, what happens to foam cells?

A

1) Monocytes become macrophages and engulf LDLs, causing foam cell formation.
2) Release TNF-alpha and IL-1 which cause inflammation.
3) Migrate into the tunica intima.
4) They rupture, releasing lipids, inflammatory cytokines and growth factors which create a plaque.

110
Q

What 3 processes lead to microvascular and macrovascular complications in patients with diabetes mellitus?

A

Atherothrombosis, endothelial dysfunction and inflammation.

Block 34 - Metabolic (18 decks)

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