Week 5 Endocrine 1

Question 1

Diabetes

Answer 1

A chronic multisystem disease, diabetes is classified as a group of disorders that have one common sign - an elevation in blood glucose levels caused by defects in insulin secretion, insulin action, or both. Almost ⅓ of cases are undiagnosed and it’s prevalence is increasing globally.

Question 2

Diabetes complications

Answer 2

The long-term complications of diabetes make this chronic disease devastating, both economically and personally, often resulting in end-limb amputations, vision impairment, end-stage kidney failure, stroke, and heart disease.

Question 3

Classification of Type 1 Diabetes

Answer 3

A chronic and life-threatening, autoimmune condition.
The immune system develops antibodies to destroy insulin and/or the beta cells in the pancreas, which produce insulin → absolute loss of insulin → in the absence of insulin → the body is unable to utilise plasma glucose → hyperglycaemia.
80-90% of the normal function of the Islet of Langerhans cells will reduce before clinical manifestations are evident.
10-15% of all cases.
Most often diagnosed around puberty but can occur at any age.
Onset
Children → rapid onset.
Adults → slower onset.

Question 4

Aetiology of Type 1 Diabetes

Answer 4

→ the exact cause of the autoimmune processes that lead to type 1 diabetes is not completely understood with environmental, toxic, nutritional, viral, infective, and genetic factors all being implicated.
Not linked to lifestyle.
No cure → can only be managed.

Question 5

Classification of Type 2 Diabetes

Answer 5

A progressive combination of insulin resistance (reduced sensitivity to insulin) and reduced insulin secretion from impaired beta cell function
The pancreas can produce endogenous insulin which is either not an adequate supply or this supply is not used effectively, or both
Endogenous insulin is a major difference between type 1 and type 2 diabetes → there is no endogenous insulin in type 1 diabetes.
85-90% of all cases.
Most often diagnosed in people over the age of 45 years but is becoming more common in adolescents.
Onset
Insidious → slow and progressive glucose intolerance

Question 6

Aetiology of Type 2 Diabetes

Answer 6

→ genetic links and strong association with modifiable risk factors → obesity, poor diet, smoking, and inactivity.
Can be treated, and in some cases reversed, by modifying these lifestyle risk factors (increase exercise, cease smoking, reduce body mass index, low calorie diet with limited processed foods)

Question 7

Prediabetes

Answer 7

1:4 adults >25years of age has impaired glucose metabolism. This condition is referred to as prediabetes.

Defined as impaired glucose tolerance (IGT), impaired fasting glucose (IFG), or both, and is the intermediate stage between normal glucose homeostasis and diabetes, in which the blood glucose levels are elevated but not enough to meet the criteria for diabetes diagnosis.
Individuals with prediabetes:
Are at an increased risk for development of type 2 diabetes.
Are usually asymptomatic.
Microvascular and macrovascular changes associated with long-term complications, such as those affecting the cardiovascular system, are already occurring.
Require ongoing monitoring and education on lifestyle modification to prevent or delay the development of type 2 diabetes.

Question 8

Gestational Diabetes (GDM)

Answer 8

A further type of diabetes occurs when there is derangement in plasma blood glucose levels indicative of diabetes in a woman who is pregnant and has no history of diabetes. This type of diabetes usually resolves when the pregnancy is over with most women who developed GDM having normal blood glucose levels within 6 weeks postpartum.

Can affect 3-9% of pregnant women globally.
Can result when a hormone made by the placenta prevents the body from using insulin effectively.
Increased risk correlates with obesity, advanced maternal age and with family history.
If there is a previous history of GDM, the risk of developing GDM with subsequent pregnancies increases 30%.
Diagnosis of GDM can be made with an oral glucose tolerance test (please see section on diagnosis for further information).
Screening occurs between 26-28 weeks gestation.
If risk factors present, a 2nd screening will be ordered between 26-28 weeks gestation if the initial screening was negative.
GDM increases the risk of caesarean deliveries, perinatal death, birth injury and neonatal complications.

Question 9

Clinical Manifestations
Type 1 Diabetes

Answer 9

Rapid onset
Signs & symptoms evident within weeks
Can be extreme in nature until treatment commenced

Question 10

Clinical Manifestations
Type 2 Diabetes

Answer 10

Slow, insidious onset → a person can go many years without clinical manifestations, such as hyperglycaemia, being detected
Some cases of type 2 diabetes remain asymptomatic → symptoms usually occur when 50-80% of beta cells are no longer secreting insulin
Signs are often dismissed as due to ‘getting older’ thereby delaying diagnosis

Question 11

Common Clinical Manifestations Experienced with Both Type 1 and Type 2

Answer 11

The 3 P’s
Polyuria
Polydipsia
Polyphagia

Extreme variations in blood glucose levels (BGLs) → hyperglycaemia & hypoglycaemia

Glucosuria

Fatigue and weakness → body cells lack energy they require from glucose metabolism

Unintentional weight loss
→ Body cannot access glucose for energy → other energy sources, such as fat and protein, are then utilised
→ Fluid loss in osmotic diuresis

Blurred vision → water balance in eyes fluctuates with elevated blood glucose levels

Delayed wound healing and recurrent wound infections → growth of microorganisms stimulated by elevated blood glucose levels combines with impaired blood supply

Genital pruritus elevated levels of blood glucose, combined with glycosuria → fungal growth → candidal infections → pruritus

Question 12

Polyuria

Answer 12

Excessive urination → caused by the osmotic effects of increased glucose → increased glucose in urine results in extra water in the tubular fluid and increases urine volume

Question 13

Polydipsia

Answer 13

Excessive fluid drinking → also caused by the osmotic effects of increased glucose

Question 14

Polyphagia

Answer 14

Excessive appetite or eating → from cellular malnourishment when glucose cannot be used for energy

Question 15

Glucosuria

Answer 15

Glucose from blood is filtered through the kidneys, to be reabsorbed back into the blood stream
With hyperglycaemia, excess glucose is filtered through the kidneys but the concentration of glucose being passed into the tubular fluid exceeds the capacity of transporters → glucose appears in urine

Question 16

Variable Clinical Manifestations

Answer 16

Ketoacidosis (discussed further in complications)
→Most common with type 1
→Can also occur with type 2 but rare and usually only with extreme circumstances such as being acutely unwell with an infection

Nausea & vomiting
→Most common with type 1

Hyperinsulinaemia
→Results from insulin resistance
→Common with type 2

Weight gain
→Excess energy from glucose is stored as fat but hyperinsulinaemia impairs the body’s ability to use this fat for energy → weight gain → obesity
→More common with type 2

Question 17

Diabetes Diagnosis

Answer 17

Formal diagnosis of diabetes can be made using a combination of:

Health history
Clinical presentation → subjective and objective data, clinical manifestations
Results of diagnostic tests obtained using venepuncture
→There are a number of tests available.
→Two abnormal test findings that demonstrate hyperglycaemia are required to diagnose diabetes as one method used in isolation is not considered conclusive.

Question 18

Random blood glucose

Answer 18

5.5 - 11.0mmols/L → considered normal range → diabetes uncertain → if diabetes is suspected based on the presence of clinical manifestations, an alternative test would be required for diagnosis

≥11.1mmols/L → diabetes likely

Question 19

Fasting or random blood glucose

Answer 19

<5.5mmols/L → normal → diabetes unlikely

5.5 - 6.9mmols/L → impaired fasting glucose → diabetes uncertain → likely to be prediabetes → oral glucose tolerance test required

≥ 7.0mmols/L → diabetes likely

Question 20

Oral Glucose Tolerance Test (OGTT)

Answer 20

After fasting overnight:

Bloods are collected on arrival to determine fasting blood glucose level
75g of glucose is given orally (as a drink)
The patient waits 2 hours post consumption and a second plasma blood glucose level is obtained
If a person does not have diabetes, the BGL levels will rise with absorption of the glucose into the bloodstream and then decrease to <7.8mmol/L within 2 hours.

Results interpreted as:

Blood glucose <7.8mmols/L → normal
Blood glucose 7.8 - 10.9mmols/L → impaired glucose tolerance → prediabetic
Blood glucose >11mmols/L → diabetes confirmed
This test is unreliable for the diagnosis of type 2 diabetes and is more commonly used when diagnosing gestational diabetes.

Question 21

HbA1c
The main biomaker used to assess long-term glycaemic control:

Answer 21

Used mostly to diagnose type 2 diabetes as the OGTT is not as reliable with this condition.
Also used to determine effectiveness of treatment by monitoring how well BGLs are being controlled in those people that are already diagnosed with diabetes
Hb = haemoglobin → the iron-containing, oxygen-transport protein in erythrocytes, or, red blood cells (RBC)
HbA = normal adult haemoglobin
HbA1c → develops when haemoglobin attaches to glucose in the blood → becoming glycated → dependent on the interaction between the concentration of blood glucose and the lifespan of the erythrocyte
A1c = the name of the test which determines the percentage level of glycated haemoglobin

Question 22

Treatment and Management Goals
Type 1

Answer 22

Because there is no cure for type 1 diabetes, close management with daily care is key to preventing complications.

How is type 1 diabetes managed?

Insulin replacement
→In healthcare settings → subcutaneous insulin injections or an intravenous insulin infusion.
→This is a medical intervention. Nurses are responsible for ensuring insulin is administered appropriately and on time, as prescribed and reassessing as required.
→Self-management → subcutaneous insulin injections can be administered with a prefilled cartridge or pen, or a person can manage their diabetes with a continuous subcutaneous insulin infusion

Monitoring BGLs
→Finger-prick test (up to 6 times daily or as directed by treating clinician) (see further details below)
→Continuous glucose monitor → a small wearable device that continuously shows a person’s current BGL and alarms when an abnormal level is detected.

Adhering to a diabetic diet

Participating in regular exercise

For people living with type 1 diabetes, keeping BGLs within the optimum range is a careful balance between what food is consumed, physical activity, medication and preventing illness such as vomiting and infections. BGLs which are too high, could result in hyperglycaemia or ketoacidosis. BGLs which are too low, could result in hypoglycaemia, seizures, and death. It is important to learn about each reaction and respond promptly and appropriately.

Question 23

Treatment and Management Goals
Type 2

Answer 23

Providing optimal nutrition → all essential food constituents → must include education and ongoing monitoring taking into consideration a person’s behaviour, cultural and religious aspects, cognitive and socioeconomic factors.
Meet energy needs
Achieving and maintaining a reasonable weight
Increasing exercise tolerance
Preventing wide fluctuations in BGLs → to reduce the risk of complications
Reducing serum lipids and maintaining a normotensive state, if elevated → to reduce the risk of heart disease
Preventing or slowing the rate of development of chronic complications → can be achieved by modifying nutrient intake and increasing exercise
Optimising enjoyment in life

Question 24

Inpatient Nursing Management of Diabetes

Answer 24

Given the prevalence of diabetes among inpatients (25%) and the risks associated with hypo / hyperglycaemia, nurses must be vigilant in assessing and referring appropriate patients requiring interprofessional team input.

Hospitalisations are a key danger time for glycaemic derangements. A person with diabetes can be admitted to hospital for unrelated reasons but may experience unstable BGLs whilst in hospital.

Question 25

Target Levels for BGL from a finger prick test outside of these ranges is considered abnormal and interventions need to be implemented

Answer 25

Type 1 Diabetes Targets

Before meals → 4.0 - 6.0 mmol/L
2 hours after starting a meal → 4.0 - 8.0mmol/L
Type 2 Diabetes Targets

Before meals → 4.0 - 7.0mmol/L
2 hours after starting a meal → 5.0 - 10.0mmol/L

Question 26

General Goals for nursing management:
Diabetes

Answer 26

Monitor BGL before meals and before bed i.e., QID

Maintain BGL between 5 - 10mmols/L
→BGLs >12mmols/L → leads to dehydration, white cell dysfunction, impaired healing and increase infection risk

Know the diagnosis
→type 2 diabetic patients requiring insulin are not considered type 1 diabetics

Have a good understanding of diabetes medications – oral and/ or injectables

Check pathology (HbA1c) results

Early and appropriate referrals → all type 1 diabetic patients must have a review with the interprofessional team, e.g., CDE

Consider risk assessments → e.g., daily skin integrity checks for pressure areas including feet, daily falls risk assessment (consider peripheral neuropathy)

Discharge planning → start early

NEVER withhold insulin in people with type 1 diabetes → even when fasting → they are insulin deficient so if hypoglycaemic, this is due to carbohydrate deficiency → skipping insulin can lead to DKA

Question 27

When to Test Ketones

Answer 27

When type 1 diabetes is suspected, and the patient is experiencing clinical manifestations

Diabetic Ketoacidosis (DKA) is suspected

Hyperglycaemia (>14mmol/L) is persistent

If the patient looks unwell

Question 28

Blood Glucose Testing with Diabetic Patients

Answer 28

QID → immediately pre meals and before bed unless otherwise specified by the Medical Officer

If patient is receiving continuous feeds → 4-6 hourly

Fasting patients until able to recommence food and fluids → 2-hourly

Patients on a continuous insulin infusion → HOURLY → until 3 consecutive stable readings are obtained → then 2 hourly

During hypoglycaemia → every 15 minutes → until BGL has normalised

During hyperglycaemia → repeat BGL 1 hour after administering supplemental insulin

Long-term stable patients → at the discretion of the Medical Officer

Question 29

Managing Blood Glucose Levels During Perioperative Period

Answer 29

Monitor BGLs 1-2 hourly

Have a source of fast acting carbohydrate readily available due to potential erratic glycaemic control

For people taking insulin
→Administer insulin as per medical orders
→Perioperative fasting → usually require long-acting insulin or insulin infusion with 5% dextrose → depends on expected fasting time
→BGLs are controlled intraoperatively with intravenous insulin via infusion, which is balanced with a glucose infusion
→Postoperatively, the insulin infusion and glucose infusion will continue until the patient can resume eating and drinking → follow organisational guidelines for insulin infusion management

For people taking OHG
→Take as usual the night before surgery
→On the day of surgery, take OHGs as directed by medical orders → some will be withheld and others, such as metformin, will need to be administered

Question 30

As nurses on the ward, we must consider providing education to patients living with diabetes. Education involves:

Answer 30

How to use a blood glucose monitor

When to take a BGL

How to interpret and record BGL

Medication compliance

How/when to administer insulin correctly

Clinical manifestations of hypo / hyperglycaemia

What to do in the case of hypo / hyperglycaemia

Importance of follow-up reviews with
multidisciplinary team

Keep unused insulin in the fridge

Current pen will last a month at room temperature

Rotate injection sites

Hold injection for several seconds before withdrawing needle

No skipping meals

Dispose of needle tips after every use in my sharps bin

Phone number for support at home

See the Diabetes Support Service (DSS) 4-6 weeks after discharge to review progress

Visit your GP

Question 31

Hypoglycaemia

Answer 31

Occurs when there is an excess insulin in proportion to available glucose in the blood.

This leads to:

BGLs dropping to levels <4 mmol/L
In response
→ Counter-regulatory hormones are released → suppresses further insulin secretion and production of glucagon
→ Autonomic nervous system is simultaneously activated → release of adrenaline → results in clinical manifestations listed below

Onset is usually rapid

Individuals at risk include those with:
→ type 1 diabetes
→ rapidly fluctuating BGLs
→ type 2 diabetes using insulin or sulfonylureas

Predisposing factors
→ Can occur at any time but usually when insulin is at its peak of action or when an individual’s routine is disrupted and diet, medications and activity are not adjusted in response to these disruptions.
→Disruptions can be caused by, for example, acute illness such as gastroenteritis or infections, periods of planned fasting, excessive exercise, drinking excessive amounts of alcohol and excessive sweating from hot and humid conditions.

Question 32

Classification of hypoglycaemia

Answer 32

Mild: patients experience symptoms and self-treat their low BGL

Moderate: patients need help to treat their low BGL

Severe: patients are unconscious or unable to treat their low BGL and require a third party to do this for them.

Question 33

Causes of Hypoglycaemia

Answer 33

Mismatch between timing of food intake and peak action of insulin or oral hyperglycaemic agents which increases endogenous insulin secretion

Administration of too much insulin

Not eating enough carbohydrates

Severe illness such as infection, gastroenteritis

Malnourishment or period of fasting

Question 34

Hypoglycaemia
Clinical Manifestations that occur due to the release of adrenaline:

Answer 34

pallor, hunger, anxiety / nervousness, sweating (diaphoresis), tremor, fatigue, tachycardia, palpitations, restlessness, altered sensation to peripheries

Question 35

Hypoglycaemia
Clinical Manifestations that occur due to the interrupted supply of glucose to cells, particularly in the the brain

Answer 35

Impaired mental functioning → fatigue, confusion, difficulty speaking (slurring words, incoherent), visual disturbances, irritability, combative, stupor → these symptoms can mimic alcohol intoxication

Headache, loss of concentration, visual disturbances, dizziness, hunger, transient sensory and motor defects.

Question 36

Untreated hypoglycaemia

Answer 36

loss of consciousness, seizures, coma, and death

Question 37

Clinical Manifestations of Hypoglycaemia

Answer 37

pallor, hunger, anxiety / nervousness, sweating (diaphoresis), tremor, fatigue, tachycardia, palpitations, restlessness, altered sensation to peripheries

Impaired mental functioning → fatigue, confusion, difficulty speaking (slurring words, incoherent), visual disturbances, irritability, combative, stupor → these symptoms can mimic alcohol intoxication

Headache, loss of concentration, visual disturbances, dizziness, hunger, transient sensory and motor defects.

loss of consciousness, seizures, coma, and death

An individual can experience clinical manifestations of hypoglycaemia within the normal range of BGLs if their BGL is below what they usually experience → always ask a patient what their usual BGL range is.

Question 38

Treatment
Hypoglycaemia can be reversed quickly with the right treatment

Answer 38

Check BGL to confirm hypoglycaemia → if BGL <3.9mmol/L → commence treatment immediately by using the 15-15 rule
→ obtain history if appropriate → should not delay immediate interventions
→ DO NOT administer insulin → this will worsen the hypoglycaemia → the patient will experience severe clinical manifestations and even death

15 - 15 RULE → immediate action
→ 15g fast-acting carbohydrate
→ Wait 15 minutes for the glucose to be absorbed into the bloodstream and re-check BGL

If after 15 minutes blood glucose is:
→<4mmol/L → give another 15g fast-acting carbohydrate
→>4mmol/L → provide 15g of slow acting carbohydrate

Escalate event to MO and/or nurse in charge

Repeat BGL after 1 hour

Document event

Be aware of recurrent (rebound effect) hypoglycaemia as there is an increased risk after oral carbohydrates
→ Ensure BGL monitoring is continued for 24-48 hours

Question 39

15 - 15 RULE → immediate action
→ 15g fast-acting carbohydrate using one of the following options:

Answer 39

100ml of Lucozade
150ml of any non-diet drink
150ml of pure fruit juice
3 - 5 glucose tablets
3 - 4 regular sweets e.g., jellybeans

Question 40

15g of slow acting carbohydrate using one of the following options:

Answer 40

250ml milk
1 tub of yoghurt
1 slice of bread
2 sweet biscuits
1 piece of fruit

Question 41

Hyperglycaemia

Answer 41

Occurs when there is insufficient insulin (endogenous or exogenous) in proportion to available glucose in the blood, thereby preventing glucose from entering cells for energy.
This leads to:

BGLs increasing to levels above >7.0mmol/L
In response
→ Lipid and muscle is metabolised to meet cellular energy requirements.
→ For an individual with diabetes, increasing BGLs if left untreated can lead to acute neurological changes.

Treatment
→ Administration of insulin or oral hypoglycaemic agents.

Question 42

Diabetic ketoacidosis (DKA)

Answer 42

An acute, serious complication of diabetes → considered a medical emergency and carries a significant risk of mortality for the patient as their condition may change rapidly.

Question 43

Diabetic ketoacidosis (DKA)
Characterised by:

Answer 43

Extreme hyperglycaemia → BGL >14.0mmol/L

Insufficient insulin to meet the body’s basal metabolic requirements

Increase in insulin counter-regulatory hormones such as adrenaline, cortisol and glucagon → ↑ hepatic glucose production → ↓ peripheral glucose usage

Ketosis
Glucose cannot be properly used for energy → the body will compensate by breaking down other sources of fat as a secondary fuel → results in increased ketones (acidic byproduct of fat breakdown) → pH <7.3 → ketoacidosis

Onset is slow to rapid

Question 44

Diabetic ketoacidosis (DKA)
Individuals at risk include those with:

Answer 44

Type 1
Type 2 diabetes → 10% of cases
Severe illness or stress
Non-adherence to medical regimen
Undiagnosed diabetes

Predisposing factors
Usually occurs following stress
Infection
Trauma
Emotional
Insulin deficiency, i.e., inadequate insulin dosage
Factors that antagonise insulin, including use of steroids, glucagon and growth hormones
Poor self-management and neglect

Question 45

Diabetic ketoacidosis (DKA)
Clinical Manifestations

Answer 45

Ketones present in urine → ketonuria
Malaise
Polyuria
Dry mouth
Nausea and vomiting
Dehydration
Diaphoresis
Fruity smell on the breath (acetonic breath)
Deep laboured breathing (Kussmaul breathing) or hyperventilation
Abdominal pain
Dyspnoea
Tachycardia
Confusion and disorientation
Coma

Question 46

Diabetic ketoacidosis (DKA)
Treatment

Answer 46

Treatment goals of DKA → replacement of insulin, replacement of electrolytes and correction of dehydration:

Initially

Clinical presentation suggests DKA → hyperventilating, fruity breath, dehydrated, oliguric, abdominal pain +/- vomiting, impaired consciousness
finger prick to test BGL and ketones
BGL >14mmol/L
Ketones >0.6 → indicative of DKA risk
Escalate to medical team → MET call
Follow DKA protocol

On arrival of medical team

Venous/arterial blood gases to assess pH and HCO3

If patient is acidotic (pH <7.3)
→ Insertion 2 x large-bore PIVCs → doctor will order fluid and electrolyte (potassium) replacement therapy.
→ Administer 0.9% sodium chloride at a rate (determined by the doctor) to restore urine output to 30-60ml/hr.
→ Administer intravenous insulin infusion as per policy or as ordered → titrated to BGL.
Unit specific protocols must be followed.
Standard management
50 units actrapid is diluted in 49.5ml 0.9% sodium chloride (concentration of 1 unit/ml).
Initial infusion rate → 0.1 unit/kg/hr.
Maximum infusion rate → 10 units/hr.
→ When BGL reaches a pre-determined level (as per protocol) an infusion of 5% glucose is usually commenced → must be as per medical order
→ Monitor BGL 1/24
→ Re-assess vital signs 1/24 → determines cardiovascular and respiratory status
→ Re-assess blood gases 1/24 → determines status of acidosis
→ Assess precipitating factors, i.e., missed insulin dose, infection, myocardial infarction.

Question 47

Hyperosmolar Hyperglycaemic State (HHS)

Answer 47

Less common complication than DKA but one of the most serious acute metabolic complications of type 2 diabetes with a high mortality rate.

Question 48

Hyperosmolar Hyperglycaemic State (HHS)
Characterised by:

Answer 48

BGL >30mmol/L
Normal pH
Absence of ketosis → presence of small amounts of endogenous insulin inhibits the breakdown of fats.
Severe fluid loss → poor glucose control → high BGL → high plasma osmotic pressures → severe dehydration. Many patients experience a fluid deficit of up to 9 litres.
Elevated creatinine.

Question 49

Hyperosmolar Hyperglycaemic State (HHS)
Individuals at risk include:

Answer 49

Type 2
Elderly or very young, especially those with acute or chronic comorbidities
Those with renal impairment
Undiagnosed diabetes

Predisposing factors
Newly diagnosed type 2
Dialysis
Severe infection → UTIs, pneumonia, sepsis, and any acute illness
High-carbohydrate diets
Medications that antagonise insulin including steroids, glucagon and growth hormones

Question 50

Hyperosmolar Hyperglycaemic State (HHS)
Clinical Manifestations

Answer 50

Diuresis with polyuria
Hypotension
Hypovolaemia
Severe dehydration
Tachycardia
Hypoperfusion
Nausea / vomiting
Abdominal pain
Hypothermia
Acute weight loss
Drowsiness
Stupor, coma, seizures and death

Question 51

Hyperosmolar Hyperglycaemic State (HHS)
Treatment

Answer 51

Treatment
Goal of treatment is agressive fluid and electrolyte replacement and normalisation of BGL.

Similar to DKA
When insulin treatment is commenced → serum potassium levels (K+) can decrease rapidly → rapid extracellular shift of potassium once insulin becomes available→ influences cardiac functioning.
Cardiac monitoring is useful in detecting hyperkalaemia and hypokalaemia because characteristic changes are observable on ECG tracings.
Monitoring for hypovolaemia and hypovolaemic shock is also extremely important.

Question 52

Stress Hyperglycaemia

Answer 52

Acute illness, such as infections or severe inflammation, can de-stabilise previously well managed diabetes by causing stress hyperglycaemia in those with normal pre-admission glucose tolerance. Additionally, it is well recognised that undiagnosed diabetes is common in hospital inpatients. Those with undiagnosed diabetes, or impaired glucose tolerance, are more likely to experience stress hyperglycaemia.

Stress hyperglycaemia is thought to be triggered by sympathetic nervous system activation, increased circulating cortisol and cytokine levels. It is unknown if stress hyperglycaemia predicts future development of diabetes, but it does increase morbidity

Question 53

Steroid-Induced Hyperglycaemia

Answer 53

Hyperglycaemia caused by glucocorticoids (GCs) typically has a rise and fall pattern, with the peak glucose reading in the afternoon following a morning GC dose. The glucose readings usually fall back to normal following the overnight fast.

→ Only measuring BGLs once a day before breakfast may miss the hyperglycaemia triggered by high-dose GCs
→ Treatment should be the simplest regimen that avoids nocturnal hypoglycaemia and can flexibly change with weaning GC doses.

Overall, hospitalisations provide an opportunity to assess and improve glycaemic control and, if needed, to refer to allied health services if their HbA1c is above target.

Question 54

Chronic Complications of Diabetes

Answer 54

Primarily end-organ from damage to large and small blood vessels secondary to chronic hyperglycaemia
Exact mechanisms unknown, but theories are:
Accumulation of damaging by-products that glucose metabolism is associated with, damage nerve cells
Formation of abnormal glucose molecules in basement membrane of small blood vessels
Derangement in red blood cell function that leads to decreased oxygenation to the tissues

Question 55

Angiopathy

Answer 55

Long-term exposure to high blood sugar causes inflammation of the blood vessels and contributes to the build-up of fatty plaques within them.

Blood vessel disease that accounts for majority of deaths among patients with diabetes.

Macrovascular complications: disease of the large and medium-sized blood vessels
Accelerated atherosclerotic changes
Cerebrovascular, cardiovascular, and peripheral vascular diseases
Insulin resistance syndrome

Microvascular complications: thickening of vessel membranes in capillaries and arterioles
Specific to diabetes → manifestations typically occur 10-20 years after onset of diabetes
Diabetic retinopathy, dermopathy, nephropathy
Neuropathic changes
Peripheral neuropath, autonomic neuropathies, hypoglycaemic unawareness, sexual dysfunction.

Question 56

Diabetic Retinopathy

Answer 56

A complication that affects the blood vessels in the retina causing the retinal capillaries to become blocked, resulting in an inhibition of sight.

Microvascular damage to the retina
→ Non-proliferative: most common form
→ Proliferative: most severe form
Without treatment, more than half will become blind

Management:
→ Early photocoagulation of retina, cryotherapy, and vitrectomy
→ Maintain good glucose control
→ Regular eye examinations to prevent vision loss.

Question 57

Diabetic Dermopathy

Answer 57

Skin disorder characterised by brown shin spots located on anterior surfaces of lower extremities:
→ Develop from leakage of small blood vessels into skin
→ Harmless and painless

Necrobiosis lipoidica diabeticorum: another disorder of integumentary system
→ Result of breakdown of collagen in skin
→ Appears as reddish-yellow lesions with atrophic skin that becomes shiny and transparent

Question 58

Diabetic Nephropathy

Answer 58

A microvascular complication that mainly affects the glomerulus of the kidney, leading to basement membrane thickening and expansion of the mesangium → declining glomerular filtration rate → renal failure.

Damage to small blood vessels that supply the glomeruli
Hypertension significantly accelerates progression
Management:
→ Aggressive BP management: ACEI’s and ARB’s
→ Also have a protective effect on kidneys
→ Yearly screening for prevention and detection
→ Presence of microalbuminuria in the urine
→ Maintain good glucose control

Question 59

Diabetic Neuropathy

Answer 59

The most common complication of diabetes with approximately 50% of indiviuals with diabetes affected. Caused by decreased blood flow to the peripheral nerves leading to neuron degeneration

Nerve damage that occurs because of metabolic derangements

Two types:

Sensory neuropathy: most common
→ Can lead to loss of protective sensation in lower extremities
→ Distal & symmetrical which affects hands and/or feet bilaterally
→“stocking-glove neuropathy”

Autonomic neuropathy:
→ Can affect nearly all body systems

Clinical manifestations can depend on which nerves are affected and include altered sensation or pain.

Sensory loss → loss of reflexes, numbness, tingling → particularly of the feet → increasing risk of falls and pressure injuries
Sexual/erectile dysfunction
Damage to limbs
Diabetic neuropathic foot ulcers
Nerve palsy
Altered bladder function

Question 60

Infection

Answer 60

Increased susceptibility to infections

Causes
→ Impaired sensation
→ Hypoxia → impaired skin integrity
→ Proliferation of pathogen due to increased glucose in the body
→ Impaired blood supply due to vascular changes and decreased white blood cells

Defect in mobilisation of inflammatory cells → impaired ability of granulocytes to respond to infectious agents.

Impairment of phagocytosis by neutrophils and monocytes

Coupled with neuropathy (sensory) may delay detection and persistent glycosuria may predispose to bladder infections especially in diabetics with neurogenic bladder (autonomic)

Question 61

Vera Ko is a 59-year-old female that lives alone. She presented to her GP because she has been feeling unwell for the last 7 days with intermittent fevers, chills, myalgia, headache, productive cough and a sore throat. The GP diagnoses Vera with community acquired pneumonia and arranges her admission to hospital for IV antibiotic treatment including gentamycin. Vera has a history of type 1 diabetes, hypercholesterolaemia, COPD and hypertension.

Vera’s history of type 1 diabetes puts her at an increased risk of infections. What is the explanation for this?

Increased susceptibility to infection is the result of the body’s inability to fight infection without adequate levels of insulin.

Increased susceptibility to infection is the result of an impaired ability of granulocytes to respond to infectious agents.

Increased susceptibility to infection is the result of bacteria thriving in an environment with elevated levels of glucose.

Increased susceptibility to infections results from the elevated levels of blood glucose destroying the white blood cells which are vital in the fight against infection.

Answer 61

Increased susceptibility to infection is the result of an impaired ability of granulocytes to respond to infectious agents.

Question 62

You return from your afternoon tea break and walk into Vera’s room to administer her medication. You notice she is pale and diaphoretic. Vera has an altered level of consciousness, is drowsy, having difficulty speaking and her hands are trembling. These are clinical manifestations of which of the following complication of diabetes?

Hyperglycaemia

Diabetes ketoacidosis

Hyperosmolar hyperglycaemic state

Hypoglycaemia

Answer 62

Hypoglycaemia

Question 63

Which of the following is a key pathophysiological feature of type 1 diabetes mellitus (T1DM)?

Increased blood glucose levels trigger a signal to be sent to the pancreas to release insulin but no insulin is released because the beta cells in the pancreas have been destroyed.

Ineffective response to insulin from target cells resulting in insulin resistance and chronic hyperglycemia.

Gradual destruction of the Islet of Langerhans cells results in the pancreas secreting lower levels of insulin.

Chronic high blood glucose levels cause beta cells to become fatigued. They gradually adapt their response to the high levels of blood glucose increasing the release of insulin.

Answer 63

Increased blood glucose levels trigger a signal to be sent to the pancreas to release insulin but no insulin is released because the beta cells in the pancreas have been destroyed.

Question 64

The endocrine system consists of glands that produce chemical messages called hormones. Which hormone and organ are responsible for type 1 diabetes?

Adrenals do not release insulin.

Liver does not convert glucagon.

Pancreas does not release glucose.

Pancreas doesn’t produce insulin.

Answer 64

Pancreas doesn’t produce insulin.

Question 65

Vera explains she often has respiratory infections throughout the year requiring prednisolone. What education should you provide regarding the use of this medication, considering Vera’s past medical history?

Corticosteroids can result in hypoglycaemia. Vera should use this medication in consultation with advice from her GP.

Aminoglycosides can result in hyperglycemia. Vera should use this medication in consultation with advice from her GP.

Corticosteroids can result in hyperglycaemia. Vera should use this medication in consultation with advice from her GP.

Antibiotics can result in hypoglycemia. Vera should use this medication in consultation with advice from her GP.

Answer 65

Corticosteroids can result in hyperglycaemia. Vera should use this medication in consultation with advice from her GP.

Question 66

Diabetic ketoacidosis is a disorder most commonly diagnosed in people with type 1 diabetes. The three main clinical manifestation of this include:

Hyperglycemia, hyperketonemia and metabolic acidosis

Hyperglycemia, lactic acidosis and hyperkalemia

Diabetes, diuresis and cerebral oedema

High glucose levels, hypovolemia and hyperkalemia

Answer 66

Hyperglycemia, hyperketonemia and metabolic acidosis

Question 67

Hyperosmolar hyperglycemic state (HHS) can be a life-threatening endocrine condition. It is often precipitated by infections, medications and undiagnosed diabetes. The key clinical manifestations of this disorder include the following:

Hypoglycemia, metabolic acidosis and elevated ketones.

Hyperglycaemia, oedema, ketosis and hypokalemia.

Hyperglycemia, neurologic impairment, profound dehydration and absence of ketosis.

Hypoglycemia, hyperkalemia and dehydration.

Answer 67

Hyperglycemia, neurologic impairment, profound dehydration and absence of ketosis.

Question 68

HbA1c is a measurement tool used to diagnose and to determine effectiveness of management. Which of the following statements is true?

HbA1c measures levels of blood glucose attached to each blood oxygen molecule over the last 3 weeks.

HbA1c can only be used to measure blood glucose levels for type 2 diabetes and not type 1 diabetes mellitus.

The lower the level of HbA1c, the higher the level of glucose in the blood.

The amount of HbA1c formed is directly related to the amount of glucose in the blood over the last 3 months.

Answer 68

The amount of HbA1c formed is directly related to the amount of glucose in the blood over the last 3 months.

Question 69

At 2am Vera presses the call bell and explains that she is not feeling well, the room is spinning and her heart feels like it is racing. You notice she is diaphoretic and trembling. You assess her vital signs and complete a random BGL and the result reads 2.6mmols/L. Which of the following nursing interventions should you immediately implement?

Call for help and commence CPR.

Check the medication administration chart and administer the 4 units of actrapid that has been written on the sliding scale.

Give Vera a cup of tea and a sandwich that she didn’t eat for dinner.

Immediately administer 120mls of juice and escalate to the Nurse in Charge.

Answer 69

Immediately administer 120mls of juice and escalate to the Nurse in Charge.

Question 70

The overall goal of diabetes management is to restore normal blood glucose levels. Considering this, when caring for Vera as an inpatient, when should you plan to test her BGLs?

Three times a day; before meals.

Four times a day; before meals and immediately before bed.

Five times a day; at meals, immediately before bed and at 02:00.

Two times a day; before breakfast and immediately after dinner.

Answer 70

Four times a day; before meals and immediately before bed.

Question 71

Your clinical facilitator asks you to explain what ketones are. You reply:

Ketones are a byproduct of muscle breakdown.

Ketones are acidic, soluble forms of fatty acids.

Ketones are secreted by the liver to breakdown insulin.

Ketones assist with metabolism of acetylcholine.

Answer 71

Ketones are acidic, soluble forms of fatty acids.

Question 72

Vera has been prescribed Optisulin, 16 units, nocte. This medication is best described as:

An endogenous insulin that has an onset of action of 30 mins and lasts 12-24 hours, and is used to maintain blood glucose levels overnight.

An endogenous insulin with an onset of action of 2 hours and lasts 24 hours making it ideal to manage blood glucose levels over the weekend when there is limited medical support.

An exogenous insulin that has an onset of action of 30 mins and lasts 12-24 hours, and is used to maintain blood glucose levels overnight.

An exogenous insulin that is short acting and used to treat variations in blood glucose levels in the event of infections.

Answer 72

An exogenous insulin that has an onset of action of 30 mins and lasts 12-24 hours, and is used to maintain blood glucose levels overnight.