Week 5 Endocrine 1 Flashcards
This module provides an overview of the foundations of providing person-centered nursing care to a patient experiencing a disorder of the endocrine system, with a particular focus on diabetes. Diabetes encompasses several distinct types and understanding each variation is essential for providing effective and safe person-centred nursing care.
Diabetes
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.
Diabetes complications
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.
Classification of Type 1 Diabetes
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.
Aetiology of Type 1 Diabetes
→ 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.
Classification of Type 2 Diabetes
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
Aetiology of Type 2 Diabetes
→ 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)
Prediabetes
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.
Gestational Diabetes (GDM)
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.
Clinical Manifestations
Type 1 Diabetes
Rapid onset
Signs & symptoms evident within weeks
Can be extreme in nature until treatment commenced
Clinical Manifestations
Type 2 Diabetes
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
Common Clinical Manifestations Experienced with Both Type 1 and Type 2
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
Polyuria
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
Polydipsia
Excessive fluid drinking → also caused by the osmotic effects of increased glucose
Polyphagia
Excessive appetite or eating → from cellular malnourishment when glucose cannot be used for energy
Glucosuria
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
Variable Clinical Manifestations
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
Diabetes Diagnosis
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.
Random blood glucose
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
Fasting or random blood glucose
<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
Oral Glucose Tolerance Test (OGTT)
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.
HbA1c
The main biomaker used to assess long-term glycaemic control:
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
Treatment and Management Goals
Type 1
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.
Treatment and Management Goals
Type 2
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
Inpatient Nursing Management of Diabetes
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.
Target Levels for BGL from a finger prick test outside of these ranges is considered abnormal and interventions need to be implemented
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
General Goals for nursing management:
Diabetes
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
When to Test Ketones
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
Blood Glucose Testing with Diabetic Patients
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
Managing Blood Glucose Levels During Perioperative Period
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
As nurses on the ward, we must consider providing education to patients living with diabetes. Education involves:
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
Hypoglycaemia
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.
Classification of hypoglycaemia
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.
Causes of Hypoglycaemia
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
Hypoglycaemia
Clinical Manifestations that occur due to the release of adrenaline:
pallor, hunger, anxiety / nervousness, sweating (diaphoresis), tremor, fatigue, tachycardia, palpitations, restlessness, altered sensation to peripheries
Hypoglycaemia
Clinical Manifestations that occur due to the interrupted supply of glucose to cells, particularly in the the brain
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.
Untreated hypoglycaemia
loss of consciousness, seizures, coma, and death
Clinical Manifestations of Hypoglycaemia
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.
Treatment
Hypoglycaemia can be reversed quickly with the right treatment
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
15 - 15 RULE → immediate action
→ 15g fast-acting carbohydrate using one of the following options:
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
15g of slow acting carbohydrate using one of the following options:
250ml milk
1 tub of yoghurt
1 slice of bread
2 sweet biscuits
1 piece of fruit
Hyperglycaemia
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.
Diabetic ketoacidosis (DKA)
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.
Diabetic ketoacidosis (DKA)
Characterised by:
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
Diabetic ketoacidosis (DKA)
Individuals at risk include those with:
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
Diabetic ketoacidosis (DKA)
Clinical Manifestations
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
Diabetic ketoacidosis (DKA)
Treatment
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.
Hyperosmolar Hyperglycaemic State (HHS)
Less common complication than DKA but one of the most serious acute metabolic complications of type 2 diabetes with a high mortality rate.
Hyperosmolar Hyperglycaemic State (HHS)
Characterised by:
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.
Hyperosmolar Hyperglycaemic State (HHS)
Individuals at risk include:
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
Hyperosmolar Hyperglycaemic State (HHS)
Clinical Manifestations
Diuresis with polyuria
Hypotension
Hypovolaemia
Severe dehydration
Tachycardia
Hypoperfusion
Nausea / vomiting
Abdominal pain
Hypothermia
Acute weight loss
Drowsiness
Stupor, coma, seizures and death
Hyperosmolar Hyperglycaemic State (HHS)
Treatment
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.
Stress Hyperglycaemia
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
Steroid-Induced Hyperglycaemia
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.
Chronic Complications of Diabetes
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
Angiopathy
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.
Diabetic Retinopathy
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.
Diabetic Dermopathy
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
Diabetic Nephropathy
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
Diabetic Neuropathy
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
Infection
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)
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.
Increased susceptibility to infection is the result of an impaired ability of granulocytes to respond to infectious agents.
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
Hypoglycaemia
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.
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.
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.
Pancreas doesn’t produce insulin.
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.
Corticosteroids can result in hyperglycaemia. Vera should use this medication in consultation with advice from her GP.
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
Hyperglycemia, hyperketonemia and metabolic acidosis
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.
Hyperglycemia, neurologic impairment, profound dehydration and absence of ketosis.
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.
The amount of HbA1c formed is directly related to the amount of glucose in the blood over the last 3 months.
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.
Immediately administer 120mls of juice and escalate to the Nurse in Charge.
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.
Four times a day; before meals and immediately before bed.
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.
Ketones are acidic, soluble forms of fatty acids.
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.
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.
