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Flashcards in Diabetes - Presenting problems Deck (48):
1

In a patient with newly discovered hyperglycaemia, what is the key goal?

The key goals are to establish whether the patient has diabetes, what type of diabetes it is, and how it should be treated.

2

How is the diagnosis of diabetes established in a patient with newly discovered hyperglycaemia?

If the patient is symptomatic (i.e. polyuria, polydipsia, fatigue, dehydration etc), then the diagnosis can be confirmed by a random plasma glucose concentration of >11.1 mmol/l or a fasting plasma glucose concentration of >7 mmol/l. In an asymptomatic patient two samples are required.

An oral glucose tolerance test (OGTT) is indicated when plasma glucose levels are elevated but not diagnostic of diabetes: fasting range 6.1-7 mmol/l, or random plasma glucose range 7.8-11.0 mmol/l. These values come from the WHO diagnostic criteria for diabetes and are based on the risk of developing microvascular disease.

Patients who do not meet the criteria for diabetes may have "impaired glucose tolerance" (IGT) or "impaired fasting glucose". These patients have an increased risk of progression to frank diabetes and of macrovascular disease.

3

What is stress hyperglycaemia?

Stress hyperglycaemia occurs when conditions impose a burden on the pancreatic beta cells - e.g. during pregnancy, infection or treatment with corticosteroids. It usually disappears after the acute illness has resolved, but blood glucose should be measured.

4

When diabetes is confirmed what other investigations should be considered?

U&Es
Creatinine
LFTs and TFTs
Lipids
Urine testing for protein or microalbuminaemia

5

How should a patient with newly discovered hyperglycaemia be assessed clinically?

Hyperglycaemia causes: thirst, polyuria, fatigue, bluured vision, pruritis vulvae/ balanitis, nasuea, hyperphagia, irritability, poor concentration, headache

Uncontrolled diabetes is associated with an increased susceptibility to infection and patients may present with skin infections. A history of pancreatic disease (particularly with alcohol excess) makes insulin deficiency more likely.

The clinical features of the 2 main types of diabetes can overlap. This occurs particularly at age of onset, duration of symptoms and family history. Typical type 2 diabetes increasingly occurs in obese young people. Older adults may have evidence of autoimmune activity against B cells, a slowly evolving variant of type 1 diabetes (LADA). More than 70% of patients with type 2 diabetes are overweight, 50% have hypertension and hyperlipidaemia are common.

6

Summarise the typical features of type 1 diabetes

Typical age at onset: <40 years
Duration of symptoms: weeks
Body weight: normal or low
Ketonuria: Yes
Rapid death without insulin treatment: Yes
Autoantibodies: Yes
Diabetic complications at diagnosis: No
Family history of diabetes: Uncommon
Other autoimmune diseases: Common

7

How should a patient with newly discovered hyperglycaemia be managed?

- Dietary/ lifestyle modification
- Oral anti-diabetic agents
- Insulin by injection
- Suspected type 1 diabetes: urgent therapy with insulin and prompt referral to a specialist
- Suspected type 2 diabetes: advice about dietary and lifestyle modification, followed by initiation of oral anti-diabetic drugs if needed
- Hypertension, dyslipidaemia and smoking cessation need to be addressed

8

What are the key aspects of educating patients with newly diagnosed diabetes?

This can be achieved by a multidisciplinary team (doctor, dietition, specialist nurse and podiatrist) in the outpatient setting. However, patients requiring insulin initially need daily advice and possibly admission to hospital. They need to learn how to measure insulin doses, give their own injections and adjust the dose depending on glucose monitoring, excecise, illness and hypoglycaemia. They must understand the principles of diabetes, recognise the symptoms of hypoglycaemia, and receive advice about risks of driving with diabetes.

9

How should patients with newly diagnosed diabetes self monitor?

Urine testing has limitations, as persistent hyperglycaemia may be masked and hypoglycaemia not detected. However, it is inexpensive and may suffice for those with well controlled type 2 diabetes or those treated with diet alone. Those treated with insulin should be taught to perform capillary blood glucose measurements at home. This allows patients to make appropriate adjustments in treatment on a day-to-day basis. Thus, changes in routine can be accommodated, ketoacidosis avoided and dietary compliance encouraged while avoiding hypoglycaemia.

10

What advice should be given to patients with impaired glucose tolerance?

The same lifestyle advice recommended for type 2 patients may reduce the risk of progression ofIGT to diabetes.
Treat other cardiovascular risk factors reduces the risk of macrovascular disease.
Patients with IGT should be monitored - e.g. with annual fasting blood glucose

11

Outline a checklist for follow up of patients with diabetes

1) Body weight (BMI)
2) Urinalysis (fasting) - glucose, ketones, macro and microalbuminaemia
3) Glycaemic control - HbA1c, inspection of home blood glucose monitoring record
4) Hypoglycaemic episodes - number and time of day, severe and mild episodes, nature of symptoms, awareness
5) BP
6) Eye examination - visual acuity, ophthalmoscopy, digital photography
7) Lower limbs - peripheral pulses, tendon reflexes, sensory: proprioception, vibration, light touch
8) Feet - callus skin indicating pressure areas, nails, podiatry, ulceration, deformity

12

What are the therapeutic goals for long term diabetic patients?

The aim of treatment is as near normal metabolism as is practical. Recommended target HbA1c is <7% to minimise vascular complications. However, type 2 diabetes progresses in severity with time, making this target difficult to achieve. In addition, strict control in type 1 diabetes increases the risk of hypoglycaemia. Glycaemic targets should therefore be appropriate: strict control may be inappropriate in the very young, the elderly and people with cancer.

Blood glucose targets are:
- fasting <6 mmol/l in type 2
- pre prandial 5-8 mmol/l in type 1

Treatment of hypertension and dyslipidaemia is often required following assessment of cardiovascular risk. Targets are:
- BP < 140/80 mmHg
- Total cholesterol <5.0 mmol/l
- LDL cholesterol <3.0 mmol/l

13

What is diabetic ketoacidosis (DKA)?

Ketoacidosis is a major medical emergency, principally occuring in patients with type 1 diabetes. A significant number of newly diagnosed diabetic patients present with ketoacidosis. In established disease, any form of stress, particularly infection, can precipitate DKA. Patients lose their appetite, and stop or reduce their dose of insulin in the mistaken belief that less insulin is required. No obvious precipitating cause can be found in many cases. The average mortality in developed countries is 5-10%.

Ketoacidosis occurs because insufficient insulin prevents glucose uptake into cells. This produces a catabolic state, where fats and proteins are broken down to provide substrates for gluconeogenesis. Ketone bodies are produced as a biproduct of lipid breakdown and when supply outweighs demand hyperketonaemia occurs. This produces an acidosis.

14

What are the cardinal biochemical abnormalities in DKA? What are the consequences of this?

Hyperglycaemia
Hyperketonaemia
Metabolic acidosis

Hyperglycaemia causes an osmotic diuresis leading to dehydration and electrolyte loss. Ketosis is caused by insulin deficiency, exacerbated by stress hormones resulting in unrestrained lipolysis supply FFAs for hepatic ketogenesis. When this exceeds the capacity to metabolise acidic ketones, these accumulate in the blood. The resulting acidosis forces hydrogen ions into cells, displacing potassium ions, which are lost in urine or through vomiting.

Patients with DKA have a total body potassium deficit but this is not reflected by plasma potassium levels, which may initially be raised due to disproportionate water loss. However, once insulin is started, plasma potassium levels can fall precipitously, due to dilution by iv fluids, potassium movement into cells and continuing renal loss of potassium.

15

What are the symptoms of DKA?

Polyuria, thirst
Weight loss
Weakness
Nausea, vomiting
Blurred vision
Abdominal pain (especially in children)

16

Signs of DKA

Dehydration
Tachycardia, hypotension (supine/ erect)
Cold extremities/ peripheral cyanosis
Air hunger (Kussmaul breathing)
Smell of acetone
Hypothermia
Apathy, confusion, drowsiness, coma (10%)

17

What is the average fluid and electrolyte loss in adult DKA of moderate severity?

Water: 6 litres
Sodium: 500 mmol
Potassium: 350 mmol
Chloride: 400 mmol

These need to be replenished differently. Water and sodium are principally extracellular so should be replaced with normal saline. Potassium and chloride and intracellular, so need to be replaced with dextrose (dextrose is metabolised by the liver to give free water which is distributed evenly across all compartments). But beware! Do not give dextrose to a patient with DKA straight away as this will feed the ketogenesis. Give insulin first (see management questions).

18

What investigations are required in DKA?

The following investigations are important, but should NOT delay iv fluid and insulin replacement:

- U&Es, blood glucose, plasma bicarbonate (at admission and at 1, 2, 3, 6, 12, 24 hours)
- ABG to assess severity of acidosis (rapid assessment by plasma bicarbonate: <12 mmol/l is severe)
- Urine and plasma for ketones
- ECG
- Infection screen: FBC, blood/ urine culture, CRP, CXR (leucocytosis invariably occurs, representing a stress response rather than an infection)
- Serum amylase may be elevated, but rarely indicates pancreatitis

19

How should DKA be managed? How much insulin should be administered?

DKA should be treated in hospital, preferably in a high-dependency unit. Regular clinical and biochemical monitoring is essential, particularly during the first 24 hours. The principles of management are insulin, fluid and potassium.

If iv insulin is not possible, 10-20 U can be given i.m. followed by 5 U i.m. hourly thereafter. A rapid fall in blood glucose can cause cerebral oedema, particularly in children. The half life of i.v. insulin is short so the infusion should not be interrupted. Restoration of the usual subcutaneous insulin regimen should be delayed until the patient is eating and drinking normally.

Infusions are normally set up for 50 U soluble insulin in 50ml 0.9% saline and given i.v. via infusion pump. The rate is 6 U/hr initially, followed by 3 U/hr when blood glucose is <15 mmol/l, and 2 U/hr if blood glucose <10 mmol/l.

Blood glucose should be checked hourly initially, and if no reduction in first hr increase the infusion rate. Aim for a fall in blood glucose of 3-6 mmol/l per hour.

20

How is plasma potassium managed in DKA?

The plasma potassium is often high at initial presentation; treatment should be started cautiously and carefully monitored. Large amounts may be required (100-300 mmol in the first 24 hours). Cardiac rhythm should be monitored in severe cases because of the risk of arrhythmia.

If the K+ is <3.0 mmol/l then none should be supplemented in the first litre of fluid. After insulin the K+ may drop precipitously because of movement into cells, dilution by i.v. fluids and continued renal loss. If it is <3.5 mmol/l then give 40 mmol added potassium in 1 litre fluid

A potassium of >5.0 mmol/l, or if the patient is anuric, also requires no additional supplementation.

21

What fluid should be used initially to treat DKA?

0.9% salive i.v.: 1 litre over 30 mins, 1 litre over 1 hour, 1 litre over 2 hours, 1 litre over 2-4 hours.

When blood glucose is <15 mmol/l switch to 5% dextrose, 1 litre 8 hourly.

A typical treatment requirement is 6L over 24 hours (avoid overload in the elderly).

Dextrose should not be administered initially as it can fuel ketogenesis. Blood glucose should be brought down with insulin first (with potassium) then dextrose to replace fluids.

22

If a patient is severely acidotic what else can be administered?

A pH of <7.0 suggests severe acidaemia and the infusion of sodium bicarbonate (with potassium) could be considered. Its use is controversial however, and should only be considered in exceptional circumstances.

23

What are the complications of DKA?

Cerebral oedema
ARDS
Thromboembolism
DIC
Acute coronary failure

24

What is HONK?

HONK (or hyper-osmotic non ketotic coma) is a condition characterised by severe hyperglycaemia (>50 mmol/l) without significant ketoacidosis. Severe dehydration and pre-renal uraemia are common. It usually affects elderly patients who often have undiagnosed diabetes. Mortality is high (40%). Patients are sensitive to insulin and half the dose of insulin recommended for the treatment of ketoacidosis is used (i.e. 3 U/hr).

25

How is plasma osmolarity calculated and what is the normal range?

Plasma osmolarity = 2[Na+] + 2[K+] + [glucose] + [urea] (all mmol/l).

The normal value is 280-300 mmol/kg and the conscious level is depressed when it is >340 mmol/kg.

26

How is HONK treated?

The patient should be given 0.45% saline until osmolarity reaches normal, when 0.9% saline is substituted. Replaced fluid guided by central venous pressure, check plasma sodium frequently and give prophylactic heparin (due to VTE risk).

27

What diabetic patients does lactic acidosis occur? How does the patient present and how is it treated?

In a coma due to lactic acidosis the patient is likely to be taking metformin for type 2 diabetes and is very ill and overbreathing, but not as dehydrated as in come due to ketoacidosis. The patients breath does not smeel of acetone and ketonuria is mild/ absent, yet pH is markedly reduced pH < 7.2) and the anion gap is increased. The diagnosis is confirmed by a high blood lactate (usually > 5.0mmol/l). treatment is with i.v. sodium bicarbonate sufficient to raise the arterial pH to > 7.2 along with insulin and glucose. Despite treatment mortality mremains > 50%. Sodium dichloroacetate may lower blood lactate.

28

What plasma glucose level defines hypoglycaemia?

A blood glucose of <3.5 mmol/l defines hypoglycaemia. It occurs in a person with diabetes as a result of treatment with insulin and occassionally sulphonylureas. Hypoglycaemia in a non diabetic person is called "spontaneous" hypoglycaemia. The risk of hypoglycaemia limits the attainment of a near normal glycaemia, fear of hypoglycaemia is common among patients and their families.

29

What are the symptoms of hypoglycaemia?

Symptoms can be divided into:

i) Symptoms of autonomic nervous system activation: sweating, trembling, palpitation, hunger, anxiety

ii) Symptoms of glucose deprivation of the brain (neuroglycopenia): confusion, drowsiness, poor coordination and speech difficult

Symptoms recognition is an important aspect of patient education. Mood changes such as irritability or anger can occur, and behavioural changes are common in children. Elderly patients are more likely to experience neurological symptoms.

30

How does a patients awareness of symptoms change over time following a diagnosis of diabetes?

Patients usually recognise the symptoms of hypoglycaemia and take appropriate remedial action. In certain circumstances (e.g. deep sleep) warning symptoms of neuroglycopenia may not be perceived by the patient. In those who are chronically hyperglycaemic, awareness may develop at a higher blood glucose level; conversely patients who have strict glycaemic control or frequent hypoglycaemic episodes may only be symptomatic if the blood glucose is <2.5 mmol/l.

The prevalence of impaired hypoglycaemia awareness increases with the duration of insulin treatment; after 20 years 50% of patients with type 1 diabetes are affected. In patients with chronically impaired awareness, the frequency of severe hypoglycaemic is increased sixfold; intensive insulin therapy should be avoided and frequent blood glucose self monitoring is mandatory.

31

How do counter regulatory hormonal responses change over time in patients with diabetes?

In response to a falling blood glucose, there is normally suppression of endogenous insulin secretion (absent in type 1 diabetics) and a brisk secretion of counter regulatory hormones (glucagon and adrenaline) which antagonise the blood glucose lowering effect of insulin. Hypoglycaemic induced secretion of glucagon becomes impaired within 5 years of developing type 1 diabetes. After several years many also develop defective adrenaline response, which autonomic neuropathy may exacerbate.

32

List some causes of hypoglycaemia

Missed/ delayed meal
Unexpected or unusual exercise
Alcohol
Error in insulin dose
Lipohypertrophy causing variable insulin absorption
Gastroparesis due to autonomic neuropathy
Malabsorption - e.g. ceoliac disease
Unrecognised other endocrine disorder - e.g. Addison's disease

Insulinoma is a rare cause of hypoglycaemia

33

What are some risk factors for developing hypoglycaemia?

Strict glycaemic control
Impaired awareness of hypoglycaemia
Extremes of age
Increasing duration of diabetes
History of previous hypoglycaemia
Renal impairment

34

What are the complications of hypoglycaemia?

Coma
Convulsions
Strokes
Cardiac arrhythmias
Myocardial ischaemia
Hypothermia
Accidents (e.g. RTA)

35

How can hypoglycaemia be prevented?

The frequency of hypoglycaemia can be reduced by patient education. People treated with insulin should carry glucose drinks or tablets at all times. Nocturnal hypoglycaemia in type 1 diabetes is common. It is a sensible precaution for patients to measure blood glucose before bed and to eat a carbohydrate snack if the reading is <6.0 mmol/l.

36

Outline the management of hypoglycaemia?

Treatment of acute hypoglycaemia depends on severity and on whether the patient is conscious:
- if recognised early, oral carbohydrate is sufficient
- in those unable to swallow, i.v. glucose (30-50 ml of 20-50% dextrose) or glucagon (1 mg i.m.) should be administered
- viscous glucose gel solution or jam can be applied into the buccal cavity but should not be used if the person is unconscious

It is important to note that full recovery may not occur immediately and reversal of cognitive impairment may take 60 mins. The possibility of recurrence should be anticipated in those on long acting insulins or sulphonylureas; a 10% dextrose infusion, titrated to the patient's blood glucose may be necessary.

Cerebral oedema may have developed in patients who fail t regain consciousness after blood glucose is restored to normal. This has a high mortality rate and requires urgent treatment with mannitol and high dose-oxygen.

37

What is gestational diabetes?

Glucose metabolism changes during normal pregnancy. Marked insulin resistance develops, particularly in the second half of pregnancy. Fasting glucose decreases slightly, while blood glucose may be increased post-prandially.

Gestational diabetes is defined as diabetes with first onset or recognition during pregnancy. While this includes women with clinically undetected diabetes, the majority can expect to be restored to normal glucose tolerance immediately after pregnancy.

WHO definition: those meeting the criteria for IGT or diabetes after a 75g OGTT.

38

What are risk factors for gestational diabetes?

Obesity
Ethnicity (black, Hispanic or South Asian)
Family history of type 2 diabetes
Previous macrosomia or gestational diabetes

39

What are the implications of gestational diabetes for the mother?

Gestational diabetes is managed by dietary modification, blood glucose monitoring and introduction of insulin if glycaemic control is unsatisfactory. Gestational diabetes is associated with an increased risk of later development of type 2 diabetes.

Glucose tolerance is re-assessed at 6 wks post partum. If this is normal, advice on lifestyle changes should be given to minimise the risk of developing type 2 diabetes.

40

What are the implications of gestational diabetes for the foetus?

Maternal glucose crosses the placenta, promoting foetal insulin production which stimulates growth. Maternal hyperglycaemia is therefore associated with increased foetal size (macrosomia) which may complicate labour and delivery, resulting in higher caesarean section rate. Reduction of maternal blood glucose by insulin therapy can reduce foetal growth.

41

What are the problems of pregnancy in women with established type 1 diabetes?

Maternal hyperglycaemia early in pregnancy has teratogenic effects. Foetal abnormalities include cardiac, renal and skeletal malformations, of which caudal regression syndrome is the most characteristic. Diabetic women should receive pre-pregnancy counselling and be encouraged to achieve excellent glycaemic control before conceiving. Later in pregnancy maternal hyperglycaemia is associated with macrosomia. Faetal macrosomia increases the risk of birth injury during delivery, and of subsequent neonatal hypoglycaemia. Babes are also at increased risk of polycythaemia, hyperbilirubinaemia and hypocalcaemia.

42

How should pregnancy in a woman with established type 1 diabetes be managed?

Plan the pregnancy!
Give folic acid supplementation
Achieve strict glycaemic control (insulin requirements increase during pregnancy)
Avoid hypoglycaemia
Avoid ketosis: ketoacidosis during pregnancy is associated with a high rate of foetal mortality (10-35%)
Arrange eye screening: retinopathy worsens during pregnancy

Despite improvements, perinatal mortality rate remain 3-4 times that of the non-diabetic population and the rate of congenital malformation is increased 5-6 fold.

43

How is diabetes affected by surgery?

Surgery causes catabolic stress and secretion of counter-regulatory hormones. This results in increased glycogenolysis, gluconeogenesis, lipolysis, proteolysis and insulin resistance. This normally leads to increased secretion of insulin, which exerts a restraining and controlling influence. In diabetic patients, insulin deficiency leads to increased catabolism and ultimately metabolic decompensation. In addition, hyperglycaemia increases infection risk and impairs wound healing. Hypoglycaemia risk, particularly dangerous in the semiconscious patient should be minimised.

44

How should a diabetic patient be assessed pre-operatively?

This include assessment of:
- cardiovascular and renal function
- neuropathy
- glycaemic control (HbA1c and pre-prandial glucose)
- review of diabetic treatments

If significant alterations need to be made, patients may need admission prior to surgery. For emergency patients with significant hyperglycaemia or ketoacidosis, this should be corrected first with an i.v. infusion of saline and/or dextrose plus insulin 6 U/hr and potassium as required.

45

Outline the management of patients with type 1 diabetes undergoing surgery

For ALL patients (regardless of diabetic status):
- establish diabetic control 2-3 days pre-operatively
- stop metformin 24-48 hours before surgery
- inform anaesthetist well in advance
- perform operation in the morning
- on morning of surgery omit usual insulin or oral anti-diabetic drug and check blood glucose and creatinine

Then, for type 1 diabetics (and type 2 diabetics undergoing major surgery):
- at 0800-0900 hrs establish i.v. infusion of 500 ml 10% dextrose + 10-20 U short acting (soluble) insulin + 20 mmol K+ given at 100ml/hr
- check blood glucose using meter or strop 2-4 hourly and adjust insulin content of infusion to maintain between 5-10 mmol/l

46

How should diabetic patients be managed post operatively?

A glucose/ insulin/ potassium infusion should be continued until the patient's intake of food is adequate, when the normal regimen can be resumed. If the infusion is prolonged, urea, electrolytes and urinary ketones should be checked daily. If fluids need to be restricted, e.g. in cardiovascular or renal disease, the rate of infusion can be halved by using a 20% dextrose solution and doubling the concentration of insulin and potassium.

47

In what age group should a diagnosis of MODY be considered?

Children and teenagers are generally prone to insulin deficient type 1 diabetes with ketosis, but cases of type 2 diabetes in obese children are now occurring and a diagnsis of MODY (mature onset diabetes of the young) should be considered, especially when there is a strong family history of diabetes. Insulin therapy requires modification to accommodate physiological changes associated with growth and puberty. Deterioration in glycaemic control is common during adolescence as adherence to treatment may be erratic.

48

Its 10.30 at night and a staff nurse rings you to inform you that a patients BMs are 25? How do you manage the patient?

This is a fairly common problem and the temptation to jump straight to insulin should be resisted!

First establish whether the patient has any metabolic disturbances caused by the hyperglycaemia (i.e. DKA or HOS/ HONK). For DKA you need to check their BM, ketones and do a VBG to confirm acidosis (and check the potassium). In HONK you must calculate the plasma osmolarity which requires [Na+], [glucose] and [urea]. HONK develops over days (not hours) so the days U&E values should be fine to rule it out.

Once these are ruled out, think DDDISH - Diet (any supplementary sugar), drugs for insulin (have they been changed, or stopped?), drugs that could cause hyperglycaemia (e.g. steroids, immunosuppressants (especially tacrolimus and micofenolate), anti-retrovirals and anti-psychotics), infection screen, stress hyperglycaemia, and check their most recent HbA1c (preferably in the last 3 months). A consistently high HbA1c should relieve you because the patient has had high BMs for a while.

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