Week 2 Flashcards

(140 cards)

1
Q

Characteristics of Diabetes

A

An ineffective response to insulin at the target cells → known as insulin resistance
OR
Insufficient (hyposecretion) or no release of insulin, by the Islets of Langerhans cells in the pancreas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Type 1 Diabetes (T1DM)

A
  • A life-long chronic pancreatic disorder, similar in ways to T1DM.
  • The cause of T1DM is unknown. It is widely accepted as an autoimmune disease, where the islet cells in the pancreas are destroyed. Other possible considerations are genetics and exposure to viruses and other environmental factors.
  • T1DM can occur at any age but there are two main peaks for diagnosis. these are between 4-7 years old and 10-14 years old.
  • There is no known way to prevent T1DM
  • In the past, T1DM was known as juvenile diabetes or Insulin Dependent Diabetes Mellitus (IDDM). These terms are no longer used as was used in the past to refer to T2DM however people with T2DM can become insulin dependent as their disease progresses.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

T1DM - Pathophysiology

A
  • An autoimmune condition which triggers the immune system to destroy all the beta cells found in the Islet of Langerhans
  • This leads to absolute insulin deficiency (zero production)
  • The exact cause is unknown, however there is a strong link to genetic susceptibility (non-modifiable risk factor)
  • Some environmental factors, such as viral exposure to mumps, rubella, coxsackievirus (Hand-Foot-Mouth), or chronic illnesses such as pancreatitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

T1DM FACTS

A

T1DM can be characterised by:
1. Absence or extremely ↓ insulin in bloodstream
2. ↑ Blood Glucose Levels (BGLs)
3. Insulin-sensitivity is normal (which means, if we administered insulin to this patient, their body would know what to do with it - in fact, it might even be overly sensitive since the body has been starved of insulin for some time)
4. ↓ Amylin secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is Amylin?

A

Co-released with insulin from the beta cells in the cluster of pancreatic cells to suppress the release of glucagon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is Glucagon?

A

Glucagon is released from alpha cells, a hormone that is needed to raised the blood glucose levels by breaking down glycogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What happens when a T1DM eats food?

A

Oral intake (regardless of sugar content)
→ Glucose absorbed by the digestive tract and into the bloodstream
→ BGL rises which signals the pancreas to release insulin & amylin
→ T1DM Pancreas cannot produce any insulin because there are no/insufficient beta cells in the Islet of Langerhans
→ No insulin, no amylin is released which leads to excessive glucagon build-up in the bloodstream
→ BGL continues to rise to critically high levels which causes an imbalance in homeostasis
→ The metabolic alterations result in serum ↑ BGL and even ↑ Ketonaemia (ketones present in the blood)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

T1DM - Clinical Manifestations

A

The 3 main presentations that bring our patients to their initial diagnosis of T1DM:
1. Polyphagia (increased hunger)
2. Polyuria (increased volume of urine)
3. Polydipsia (increased thirst)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

NURSING MANAGEMENT-T1DM

A
  1. Maintain normoglycaemia as much as possible
  2. Initiate Food Chart
  3. Monitor conscious state
  4. Initiate Wound Chart, Skin Integrity Assessments and Referral to Wound Care/Stoma Nurses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Type II Diabetes (T2DM)

A
  • Type 2 Diabetes Mellitus (T2DM) is a life-long chronic pancreatic disorder, similar in ways to T1DM.
  • The main difference is that T2DM is considered a ‘silent but progressive disorder that develops over many years’ rather than being viewed as an autoimmune disorder
  • T2DM represents 85-90% of all diabetic cases globally
  • Although this term is no longer used, Non-Insulin Dependent Diabetes Mellitus (NIDDM) was used in the past to refer to T2DM however people with T2DM can become insulin dependent as their disease progresses.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

PATHOPHYSIOLOGY- T2DM

A
  • The exact cause is unknown, however this type of diabetes is strongly linked to non-modifiable factors like:
    ○ Certain Ethnicities
    ○ Genetic risk factors
  • The cause of many T2DM diabetics can be attributed to modifiable risk factors, such as:
    ○ Having hypertension
    ○ Dyslipidaemia
    ○ Obesity
    ○ Sedentary lifestyle
    ○ Poor diet
    ○ Smoking
  • There are two possible pathophysiological explanations which lead to the pancreas losing the capacity to secrete sufficient insulin in T2DM:
    1. Insulin deficiency → relative shortage of insulin supply → persistent hyperglycaemia
    2. Insulin resistance → ineffective response to insulin from target cells OR loss of insulin-sensitivity → persistent hyperglycaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What happens when insulin-deficient T2DM eats food?

A

Oral intake (regardless of sugar content)
→ Glucose absorbed by the digestive tract and into the bloodstream
→ BGL rises which signals the pancreas to release insulin & amylin
→ Insufficient insulin produced by T2DM pancreas which leads to excessive glucagon build-up in the bloodstream
→ BGL continues to rise to critically high levels which causes an imbalance in homeostasis
→ The metabolic alterations result in serum ↑ BGL and even ↑ Ketonaemia (ketones present in the blood)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What happens when insulin-resistant T2DM eats food?

A

Oral intake (regardless of sugar content)
→ Glucose absorbed by the digestive tract and into the bloodstream
→ BGL rises which signals the pancreas to release insulin & amylin
→ Pancreatic beta cells secrete insulin BUT target cells respond ineffectively and trigger the pancreas for more insulin
→ Excessive insulin in bloodstream → Hyperinsulinaemia
→ Overtime, chronic hyperglycaemia causes pancreatic beta cells to fatigue and ↓ their responsiveness to ↑ BGL
→ Gradually, pancreatic beta cells die from fatigue and result in a severe lack of insulin which further contributes to hyperglycaemia
→ Since the body still requires energy and the insulin and target cells no longer function, the body turns to lipids and ketosis for fuel → Ketonaemia
* The final point illustrates the pathophysiology behind ketones appearing in chronic T2DM *

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

T11DM-CLINICAL MANIFESTATIONS

A
  • Chronic hyperglycaemia which is ↑ blood glucose levels (BGLs)
  • There can also be alterations in the way their bodies metabolise proteins, carbohydrates, and fats
  • People are often asymptomatic and do not realise they have T2DM until they experience some more extreme like a diabetic foot ulcer or even a myocardial infarction!
  • This is because the actual clinical manifestations of T2DM can be mild, vague, and non-specific:
    ○ Fatigue
    ○ Recurrent infections
    ○ Recurrent Candida infections
    (fungal yeast infections)
    ○ Poor wound healing
    ○ Vision changes like blurred
    vision, cataracts, retinopathy
    ○ Paraesthesia (neuropathies
    from nerve degeneration and
    delayed conduction)
    ○ Peripheral neuropathy (altered
    nerve sensation of the hands
    and feet)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

NURSING ASSESSMENTS FOR T1DM AND T2DM

A
  1. Fasting Blood Glucose Level (BGL)
    ○ Normal physiological range is 5.5 - 6.9 mmol/L
    ○ Diabetic (abnormal) range is ≥ 7.0 mmol/L
    ○ Blood test must be done on empty stomach and fasting state (8-12 hours)
  2. Random BGL
    ○ Normal physiological range is 7.8 - 11.0 mmol/L
    ○ Diabetic (abnormal) range is ≥ 11.1 mmol/L
    ○ This blood test can be done at anytime
  3. Oral glucose tolerance test
    ○ Normal physiological range is 7.8 - 11.0 mmol/L
    ○ Diabetic (abnormal) range is ≥ 11.1 mmol/L
    ○ The patient must drink a highly concentrated glucose drink, and their BGL is taken within the timeframe
  4. Presence of serum HbA1c
    ○ Normal physiological range is 4.0 - 5.5% HbA1c
    ○ Diabetic (abnormal) range is ≥ 7.0% HbA1c
    ○ A relatively standard blood test to diagnose diabetes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is HbA1c?

A

As glucose circulates in the blood, some of it binds to haemoglobin → resulting in HbA1c.
- The amount of HbA1c formed is directly related to the amount of glucose in the blood
- Because Red Blood Cells (RBCs) can survive for 3 - 4 months, HbA1c levels do not change rapidly
- Therefore the HbA1c level reflects the average amount of blood glucose during the last 2 - 3 months
- If patients’ average BGL ↑ → ↑ HbA1c levels meaning this patient has had uncontrolled diabetes for months!
- Another purpose to undergo HbA1c testing for patients is that it can aid treatment decisions
□ If treatment plans have been changed OR if their diabetes is considered unstable, HbA1c will be tested more frequently (3 - 4 monthly according to the RBC lifespan)
□ Otherwise, when diabetes is considered stable, HbA1c is only tested twice a year to monitor progress
□ It can be used to diagnose both T1DM and T2DM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Nursing Considerations for diabetes

A
  • When to take BGL
  • Care of wounds
  • National Standard documents
  • Falls risk assessment
  • Skin integrity assessments
  • Fluid balance chart
  • Follow Medical advice regarding medication
  • Documentation
  • Escalate care promptly if there are any concerns or patient deterioration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Promotion and Prevention for diabetes

A
  • Pre - post operative stages
  • Critically unwell
  • With infections
  • Who are stressed
  • Have poor understanding of their condition
  • That can not self manage appropriately
  • With chronic complications of DM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

HYPOGLYCAEMIA causes

A
  • Imbalance between blood glucose and insulin. For example - mismatched food intake with diabetic medications
  • Reduced or poor timing intake of food
  • Increased exercise
  • Dehydration
  • Illness
  • Stress
  • Medications / Drugs
  • Surgery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

HYPOGLYCAEMIA-Clinical Manifestations

A

Confusion, altered conscious state, combative and agitated state, difficulty speaking, visual disturbances, seizures, coma, death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Management of Hypoglycaemia

A

It is important to escalate care for hypoglycaemic patients, such as a Medical Emergency Team call or notifying the nurse. Effective treatment is crucial for reversing hypoglycemia. Adherence to hospital protocols is crucial for managing hypoglycemia, as values may differ between hospitals.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Hypoglycaemia- Conscious patient

A
  • Administration of 15–20 grams of quick-acting carbohydrate (e.g. 150 mL of soft drink, 8–10 jelly beans, 1 tablespoon of syrup or honey, 4 teaspoons of jam, 120 mL juice, commercial glucose [per label instructions])
  • Check blood glucose levels after 15 minutes
  • Repetition of quick-acting carbohydrate administration after 15 minutes if no improvement in blood glucose
  • Administration of additional food of longer-acting carbohydrate (e.g. slice of bread, dry biscuits) after symptoms subside
  • Immediate notification of healthcare provider or emergency service (if patient outside hospital) if symptoms do not subside after two to three administrations of quick-acting carbohydrat
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Hypoglycaemia- Worsening symptoms or unconscious patient

A
  • Subcutaneous or intramuscular injection of 1 mg glucagon
  • Intravenous administration of 50 mL 50% glucose
  • Determine cause of hypoglycaemia (after correction of condition)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

HYPERGLYCAEMIA

A
  • Hyperglycaemia refers to high blood glucose levels.
  • Results from increased hepatic glucose production and impaired glucose utilisation, reduced insulin and excess counter-regulatory hormones. Blood glucose levels are greater than 15mmol/L.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
HYPOGLYCAEMIA
* Hypoglycaemia refers to low blood glucose levels. * Occurs when there is too much insulin in proportion to available blood glucose and blood glucose levels drop to less than 4 mmols/L
26
HYPERGLYCAEMIA- causes
* Imbalance between blood glucose and insulin. For example - mismatched food intake with diabetic medications or not taking medication * Being less active than usual * Eating too much high carbohydrate or high sugar foods * Medicines / Drugs / alcohol * Stress * Infection, illness * Critical illness or injury * Surgery
27
Management of Hyperglycaemia
* If indicated, administer insulin and/or diabetic medication as prescribed. * Escalate the care of a hyperglycaemic patient to the nurse in charge and doctor to prevent further complications. * Check for ketones * If able, encourage water and avoid high sugar food and drinks
28
Hyperglycaemia- Clinical Manifestations
Thirst, tired or lethargic, increased urination. blurred vision, hard to concentrate and irritable.
29
Long term complications of hyperglycaemia
heart disease, stroke, renal disease, retinopathy and neuropathy
30
DIABETIC KETOACIDOSIS (DKA)
Most typically will occur in people with T1DM and is characterised by severe hyperglycaemia and ketoanaemia, acidosis and severe dehydration. * ↑ metabolism of fat and protein because the body cannot metabolise the glucose for energy → fat releases chemical by-product called ketones into the blood → pH drops → ketoacidosis → buffering systems triggered to compensate for imbalanced homeostasis → respiratory compensation * Symptoms include deep rapid respiratory rate (Kussmaul breathing), fruity breath (acetone blown out), ketonuria, diabetic coma, death
31
HYPEROSMOLAR HYPERGLYCAEMIC STATE (HHS)
Patients with T2DM can become severely hyperglycaemic with high osmolarity as a direct result of a physiological stress such as an acute infection or, for example, an episode of dehydration. With HHS, there are no blood ketones present, so the patient will not exhibit signs of acidosis. * Associated symptoms are usually subtle and occur over a period of many weeks which contributes to ongoing osmotic dehydration. This results in extreme dehydration, lethargy and confusion eventually leading to seizures, altered conscious state, coma and death.
32
DIABETIC FOOT DISEASE
Peripheral neuropathy, a severe complication of diabetes, leads to paraesthesia in the hands and feet, causing foot ulcers. Around 15% of diabetics develop ulcers, with 85% requiring amputation. These ulcers significantly impact quality of life and healthcare costs.
33
NURSING MANAGEMENT- DIABETIC FOOT DISEASE
There are six key elements for the prevention of diabetic foot problems: 1. Assess all people with diabetes and determine their risk of developing foot complications 2. Perform regular focused assessments on the feet of high-risk people 3. Education of the patient and their support persons 4. Routine wearing of appropriate footwear, including well fitting shoes and socks 5. Treatment of pre-ulcerative signs 6. Early referrals to the interprofessional team
34
Dressing/s Considerations-DIABETIC FOOT DISEASE
Factors to consider when choosing a dressing for a diabetic foot ulcer include the following: 1. Type of dressing required to promote wound healing 2. Dressing should be comfortable - to prevent increased pain or discomfort 3. Infection management as required 4. Frequency of dressing change 5. If the person is managing their wound at home - access to dressings may influence choice of dressing PATIENT EDUCATION FOR PREVENTION OF DIABETIC FOOT ULCERS
35
PHARMACOLOGY- DIABETIC FOOT DISEASE
The key things to know are: * the different types of agents * how they affect glucose * mechanism of action * onset and peak of therapeutic indices * potential adverse reactions. There are three main types of medications used in the treatment of DM * Insulin * Oral hypoglycaemic agents * Glucose-elevating agents *TIP - Relate each of the classifications back to the physiology of the endocrine system to make it easier to understand Insulin
36
Mode of Action- DIABETIC FOOT DISEASE
* Facilitates the metabolism and storage of glucose through cellular transport and uptake by enhancing cellular glucose uptake * Inhibits endogenous glucose output and the breakdown of fats (endogenous means that this has been made within the person's body) * The onset, time to peak, and duration of action of insulin depends on the type of insulin and dosage administered
37
Indications- DIABETIC FOOT DISEASE
* Exogenous insulin is used when an individual has no insulin of their own and cannot regulate their blood glucose levels.
38
Short-Acting insulin
*Neutral Insulin (Actrapid, Humulin R) To be administered as Subcutaneous Injection, 15-30 minutes before meals. Can be administered by IV infusion in an emergency.
39
Intermediate-Acting insulin
Intermediate-acting insulin is often combined with short-acting or long-acting insulin. It is administered as a subcutaneous injection before meals or bedtime, serving as a 'background insulin' to maintain stable blood glucose levels.
40
Long-Acting insulin
* Insulin Glargine (Optisulin) * Insulin Detemir (Levemir) To be administered as Subcutaneous Injection, before evening meals or bedtime, considered a 'background insulin' to maintain stable blood glucose levels between meals / overnight.
41
ORAL HYPOGLYCAEMIC AGENTS (OHA)
* Classified as 'insulin sensitizers' * OHAs stimulate insulin release from the beta cells in the pancreas * Lowers insulin resistance by increasing glucose uptake and utilisation in skeletal muscle * Improves binding to insulin receptors * Rapidly absorbed from the GI tract to undergo hepatic metabolism * Reduces glucose production in the liver * Sensitises cells to the actions of insulin * Alters absorption of carbohydrates * Excreted in the urine * Peak and duration, mechanisms of action each differ with different OHA
42
Indications- OHA
* Adjunct to diet and exercise to lower blood glucose levels in T2DM. * Can not be used for T1DM as OHAs depend on residual insulin secretion or functioning insulin receptors in order to work effectively (which type 1 diabetics do not have). * May have combination of treatment of OHAs and an intermediate or long-acting insulin at bedtime
42
Biguanide
Generic name = Metformin Reduces hepatic glucose production, increases peripheral utilisation of glucose
43
Sodium-glucose cotransporter-2 Inhibitors
Generic name = Dapagliflozin, Empagliflozin, Ertugliflozin *TIP: suffix -flozin drugs are all SGLT2 inhibitors Inhibits sodium-glucose co-transporter 2, reducing glucose reabsorption in the kidney
44
DPP-4 inhibitors or Gliptins
Generic name = Alogliptin, Linagliptin, Saxagliptin, Sitagliptin, Vildagliptin *TIP: all DPP-4 inhibitors end with suffix -gliptin Increases the concentration of the incretin hormones; glucose-dependent insulin secretion is increased and glucagon production reduced.
45
Sulfonylureas
Generic name = Glibenclamide, Gliclazide, Glimepiride, Glipizide *TIP: all sulfonylureas start with prefix gli- Increases pancreatic insulin secretion; may decrease insulin resistance
46
Thiazolidinedione
Generic name = Pioglitazone Increases the sensitivity of peripheral tissues to insulin; decreases hepatic glucose output
47
Dose OHA
OHA effectiveness may decrease over time due to secondary failure → increased severity of disease or decreased responsiveness to the drug → dosages may need to be adjusted Dosage requirements change with stability of patient condition
48
Adverse Effects OHA
* Hypoglycaemia * Gastrointestinal upset = nausea, vomiting, anorexia, diarrhoea * Allergic (skin) reactions
49
Contraindications OHA
* Allergies * Diabetic Complications * T1DM
50
Nursing Considerations- OHA
* Use with caution with individuals with renal or gastrointestinal problems * Should be avoided with severe liver or kidney disease, severe burns, dehydration, or severe infections
51
Drug-to-drug Interactions- OHA
OHAs are not to be administered / review administration with other substances and drugs that: * Acidify the urine * Impair glucose tolerance * Reduce the clearance of Metformin (eg. Warfarin, Trimethoprim, Cimetidine) * Beta blockers * Alcohol - increases lactic acidosis
52
GLUCOSE ELEVATING AGENTS
used to treat hypoglycaemic events
53
GLUCOSE ELEVATING AGENTS- Mode of Action
* Increases the blood glucose levels by decreasing insulin release and accelerating the breakdown of glycogen in the liver to release glucose * Rapidly absorbed and distributed throughout the body * Excreted in the urine
54
GLUCOSE ELEVATING AGENTS-Indications
* Rapid treatment for hypoglycaemic events, especially in hospital
55
GLUCOSE ELEVATING AGENTS- Types / Route / Dosage
Glucose ○ 10 - 20 grams orally in adults, repeated in 10 minutes if BGL still hypoglcaemic ○ 50 mLs of 50% glucose solution can be given as an IV infusion ○ 50 mLs of 10% glucose solution, IV infusion, used for children ○ Supplied as a liquid, a vial (IV), or an IV ready-to-hang infusion bag Glucagon ○ Used if the patient is unconscious and cannot take medication orally = severe hypoglycaemic event ○ Must be parenterally administered = SC, IM, IV ○ Has a half-life of 5 - 10 mins ○ Onset of action depends on the route chosen § IV fastest onset 5 - 20 mins § IM onset 15 mins § SC onset up to 45 mins ○ Supplied as an emergency kit as 1mg in pre-made syringe (with sterile water) ○ Patients with severe hypoglycaemia should respond within 5 - 10 mins if treatment has been effective
56
GLUCOSE ELEVATING AGENTS-Adverse Effects
* Gastrointestinal upset * Vascular effects
57
GLUCOSE ELEVATING AGENTS-Nursing Care Considerations
* Used with caution in people with hepatic dysfunction or cardiovascular disease * Contraindicated in pregnancy and breastfeeding * To be avoided if there is a known allergy to glucose elevating agents
58
GLUCOSE ELEVATING AGENTS- Drug-to-drug interactions
* Thiazide diuretics interfere with glucose elevating agents * Anticoagulants
59
Diabetes Nurse Educators (DNEs) 👩‍⚕️
* Any person with diabetes that require hospitalisation likely already has a relationship with a diabetes nurse educator or team, particularly for people newly diagnosed with diabetes, it is important for nurses to refer every new patient to the DNEs as they tend to have a holistic, diabetes-focused view on this patient's admission * DNEs assist with referring our patient's to other interprofessional team members like dieticians, occupational therapists and beyond so they are necessary for all patients with diabetes today.
60
Pharmacists 💊
* Insulin will be the main pharmacological intervention required for diabetics but there are many other oral medications that require referral to pharmacists when adding or removing medication that impacts the delicate balance of insulin-glucose * Pharmacists are crucial in the admission and discharge process of diabetic patients' to ensure everything required for the patient is smoothly transitioned from the start of their inpatient journey so they can get back into community and into their homes while the interprofessional team prioritises maintaining normoglycaemia * There are often pharmacists that work specifically for the Diabetes Education Team and will preferred to be contacted first prior to other pharmacists that might be floating on your ward
61
Dieticians 🍎
* Some patients' will be making changes to their diet for the first time since diagnosis during their admission with you, a referral to the dietician can be a handy way for the patient to discuss any necessary changes to their diet, especially when they are preparing to return to their homes * Specifically in diabetes, management of diabetic-friendly foods that meet their body's energy needs is crucial in recovery and ongoing nutritional support for our patients but dieticians also provide important education so that patients' can maintain their new dietary changes at home * The glucose requirements change when a person gets sick so the dietician can account for some of these change by slightly altering the patients' caloric intake while they are acutely unwell
62
Wound Care Nurses or Stoma Nurse 💢
* When patient's exhibit poor wound healing, it is always a good idea to refer them to Wound Care Nurse Specialists who can assist with choosing the right bandages, source anti-bacterial bandages, re-dress old wounds, help to support your patients' wound healing while they recover from other symptoms related to their adrenal disorder.
63
Social Workers 🤝
* When learning of a new diabetes diagnosis, it can be a lifelong disorder and almost seen as a 'life sentence' for some patients. Social workers can converse with patients to ease their concerns, establish any relationships that may outlive their inpatient stay and possibly community supports our patients' might need on discharge: such as meal services, at-home physiotherapy, and more * Social workers are important to the whole family when a patient has been admitted to hospital, holistically they can gauge where support systems already exist for the patient and support other members of their family in providing the best care possible
64
Physiotherapists 👟
* In conjunction with regular nurse-initiated pressure area care and encouraging our patients' to sit out of bed, physiotherapists can assist in their recovery by strengthening their muscles during the acute phase * Exercise has been proven to assist with maintaining a normal blood glucose level and often lifts the spirits of our patients encouraging them to get better to return home sooner ultimately assisting in the smooth transition and preparation for their discharge * Additionally, by ensuring that blood is pumping through the body during exercise, this can promote perfusion to the skin especially in the extremities which can help reduce the burden of impaired wound healing in some patients
65
Occupational Therapists 🚽
* Due to the physiological changes, for example from a wound that failed to heal, our diabetic patients experience weakness and occupational therapists work together with physiotherapists to gather equipment for the home, in preparation for their transition back into community post-discharge from the hospital * This equipment might be bathroom assist devices, handles for the steps at the front of their house, even handles for their bed frames to assist with turning while they maintain good pressure area care techniques at home
66
Type 3c Diabetes Mellitus
Over recent years, scientists have described another classification of diabetes that is directly related to damage, trauma or surgery to the exocrine pancreas. This is known as pancreatogenic diabetes.
67
Causes of Type 3c diabetes
* Pancreatitis (acute or chronic) * Pancreatectomy * Trauma * Pancreatic carcinoma * Cystic fibrosis * Haemochromatosis
68
Clinical manifestations- Type 3c diabetes
differ slightly from those of Type 1 or Type 2 diabetes as they are generally associated with additional symptoms related to dysfunction from the exocrine function of the pancreas including: * nausea * diarrhoea * malabsorption * weight loss The normal signs of diabetes will usually also be present including increased appetite, thirst and urinary frequency.
69
Diagnosis of Type 3c diabetes
linked to the presenting history and generally includes some form of damage/injury to the pancreas as identified above.
70
Management of Type 3c diabetes
invariably include insulin therapy due to the pancreatic trauma/injury.
71
Gestational Diabetes Mellitus [GDM]
This form of diabetes mellitus develops during pregnancy. It is characterised by high or fluctuating blood sugar levels that occur for the first time during pregnancy and typically resolves after childbirth. There are increased risks of complications for both the mother and baby when GDM has been diagnosed. The main thing to note is that if the baby grows 'too big' as a result of the mother's GDM there are consequences during birth and in the immediate period of time post-birth.
72
risk factors GDM
obesity, family history of diabetes, being over the age of 25, having previously given birth to a baby weighing > 4 kgs (>9 pounds), and certain ethnicities are at a greater risk. If you are found to have GDM, there is a 30-50% increased risk that you will develop Type 2 diabetes later in life.
73
Pregnant women have to undergo a screening for GDM
between the 24 - 28 weeks gestation period of their pregnancy; this test is called the Oral Glucose Tolerance Test (OGTT). They check your fasting glucose, 1hr post blood glucose and 2hr post blood glucose after you have ingested the entire contents of a small bottle
74
Management- GDM
can be as simple as diet controlling: eating lower GI foods, increasing your protein intake and not snacking as much. Or treatment may include insulin at night, to ensure your fasting glucose levels are stable for the next day.
75
What are the Adrenals?
Small glands found at the top of each kidney, the adrenals have a vital role in metabolism, the stress response, sexual function, immune responses, and blood pressure regulation. Many disorders of the adrenal gland can have life threatening imbalances of homeostasis. Particular focus will be placed on Cushing's Syndrome and adrenocortical insufficiency in this unit.
76
77
PATHOPHYSIOLOGY- Cushing Syndrome
* A group of manifestations caused by the chronic exposure of excessive circulating levels of the hormone cortisol (technically known as hypercortisolism) * Some known causes of Cushing Syndrome include: ○ Tumours on the adrenal glands ○ Pituitary adenomas ○ Lung Cancer ○ Pancreatic Cancer ○ Long-term use of exogenous steroids, like prednisolone → this results in a 'cushingoid appearance' § This type of 'cushingoid appearance' is usually reversible once steroid treatment ceases § But all steroid use must be weaned slowly or it can result in acute adrenal insufficiency (the opposite of Cushing Syndrome)
78
Why do Steroids require 'weaning off'?
Gradual withdrawal from high-dose steroid therapy is necessary as it allows the anterior pituitary gland the opportunity to secrete increasing amounts of adrenocorticotropic hormone (ACTH), which stimulates the adrenal glands to secrete cortisol naturally again.
79
Diagnosis of Cushing Syndrome
is achieved through taking patients' history and performing a physical exam. Grouping of subjective and objective data obtained from key clinical manifestations and physical assessment is key to a clear diagnosis. We already know that each of the different body systems could be effected to some extent, thus a thorough head-to-toe assessment followed by necessary focused-assessments would benefit the patient.
80
Pathology & Diagnostic Testing of crushing syndrome
1. Cortisol Blood Levels and/or saliva swab for cortisol levels ○ if the patient has ↑ cortisol levels, they are likely to have adrenal abnormalities leading to hypersecretion of cortisol 2. 24-hour urine collection testing ○ if the patient has ↑ cortisol levels where normal is 80-120mcg/24hours, with other subjective and objective data, likely Cushing Syndrome 3. Dexamethasone Suppression Test (Click for more information) * please note: patients' can be prone to false positive results when they have high levels of daily alcohol consumption, and certain medications (such as phenytoin or rifampicin) can interfere with the above tests so we normally have a questionnaire prior to diagnostic testing *
81
NURSING MANAGEMENT of crushing syndrome
The primary treatment goal is to normalise hormone secretion. If the hypersecretion is caused by a tumour: * Excision of tumour via surgical removal * Radiotherapy to shrink tumour If the cause of hypersecretion is not tumour-related * Gradual tapering of dose and discontinuation of exogenous steroids 1. Review Steroid Regime with Pharmacists 2. Fluid Balance Chart (FBC) 3. Blood Glucose Levels (BGLs) 4. Skin Integrity Chart & Wound Assessments & Regular Pressure Area Care 5. Psychological & Emotional Support 6. Targeted Education
82
PHARMACOLOGY of crushing syndrome
While there are medications that treat cortisol hypersecretion (Cushing Syndrome), for this unit we ask that you focus on the nursing management and other diagnostic testing of this disease. The reason for this is because medication and treatment plans are highly dependent on the cause and patient's comorbidities.
83
Adrenocortical Insufficiency of crushing syndrome
Adrenocortical Insufficiency is essentially the 'opposite' to Cushing Syndrome where the body has a hyposecretion of the hormones normally secreted by the adrenal glands OR pituitary glands. Any Adrenal Insufficiencies can be from: * Either a primary cause, which is known as Addison's Disease * Or a secondary cause, which occurs as a result of hyposecretion of adrenocorticotropic hormone (ACTH) from the pituitary gland to communicate with the adrenals in the first place * Adrenal insufficiencies are more common in women (non-modifiable risk factor) than men ○ And of these women, their age (non-modifiable risk factor) is most commonly between 30-50 years
84
Pathophysiology of crushing syndrome
A step-by-step explanation of pathophysiology from dysfunction to clinical manifestations (what we see in our patients in hospital). For ease, a diagram of the normal functions and hormones of the Hypothalamic-Pituitary-Adrenal Axis and how they normally communicate has been included from your textbook.
85
Primary Adrenocortical Insufficiency (Addison's Disease)
* Although considerably rare, the most common cause of Addison's Disease is autoimmune adrenalitis ○ 80% of Addison's Disease patients have this pathophysiology ○ The immune system mistakenly attacks and damages the adrenal glands ○ Inflammation and destruction of the adrenal cortex (the outer layer of the adrenal glands) occurs ○ Where the adrenal cortex is normally responsible for the production of cortisol and aldosterone ○ Therefore a ↓ in production and functionality of these hormones is seen in our patients * The other 20% of patients' with primary adrenocortical insufficiency have the following causes: ○ Any infection that causes destruction of the adrenal glands, like Tuberculosis ○ Surgery or Cancer of the Adrenal glands ○ Genetic factors, very rare to have genetic factors that contribute to Addison's Disease ○ Haemorrhaging or infarction as blood flow changes can heavily impact the adrenal glands ○ Long-term use of medications, like corticosteroids, can suppress the normal functioning of adrenal glands * please note: regardless of the cause of disorder, the pathophysiology of the adrenal glands occurs in a similar way. *
86
Secondary Adrenocortical Insufficiency (Addison's Disease)
* This cause and pathophysiology is more common than primary adrenocortical insufficiency * If the cause of secondary adrenocortical insufficiency originates from the hypothalamus, the pathophysiology is: ○ Diseases or Dysfunction of the Hypothalamus, like tumours or lesions ○ Normally, the hypothalamus secretes corticotropin-releasing hormone (CRH) which stimulates the pituitary gland to produce ACTH (See Figure 3.4 above) ○ ACTH acts on the adrenal cortex to release its own hormones: cortisol in particular ○ When there is a disruption to any of the pathways mentioned above, this will result in ↓ cortisol production/secretion * If the cause of secondary adrenocortical insufficiency originates from the pituitary gland, the pathophysiology is: ○ Diseases or Dysfunction of the Pituitary Gland, like tumours or lesions ○ As ACTH pathways have been disrupted, the adrenal glands do not get signalled to release cortisol → the result is ↓ cortisol production/secretion * Other causes can be due to suppression of pituitary function due to exogenous corticosteroid administration ○ Where the 'synthetic' corticosteroid hampers the secretion of the body's own ACTH → thus ↓ cortisol production/secretion
87
Addison's Crisis
* Life-threatening complication that can arise from critically low blood cortisol levels i.e. if Addison's Disease went untreated * Can result when the patient's existing glucocorticoid medications are suddenly withheld * Can also occur as a result of acute physiological changes such as: ○ vomiting and diarrhoea ○ infection ○ trauma ○ ↑ stress ○ surgery * Early intervention is essential in preventing critical deterioration
88
Clinical Manifestations of Addison's Crisis
The following symptoms are considered critical and include: * Loss of consciousness * Alterations in mental status - confusion, fear, restlessness, agitation, delirium * Visual and auditory hallucinations * High fever >39°C * Sudden onset pain in lower back, abdomen, or legs * Death
89
CLINICAL MANIFESTATIONS of Addison's Crisis
* Extreme fatigue, irritability, depression, mental imbalances and other behavioural symptoms * Weight loss and ↓ appetite * Hyperpigmentation (darkening of skin) * ↓ Blood pressure, particularly postural hypotension, some experience fainting * Cravings for salt * ↓ BGL * Nausea, vomiting, diarrhoea, abdominal pain * Muscle or joint pain * Hyperkalaemia (↑ K+) and Hyponatraemia (↓ Na+) * notice the head-to-toe format of these symptoms allowing for easy recall
90
Diagnosis of adrenocortical insufficiency
is achieved through taking patients' history and performing a physical exam. Grouping of subjective and objective data obtained from key clinical manifestations and physical assessment is key to a clear diagnosis. We already know that each of the different body systems could be effected to some extent, thus a thorough head-to-toe assessment followed by necessary focused-assessments would benefit the patient.
91
Pathology- adrenocortical insufficiency
1. ACTH Stimulation Test ○ to begin this test, the patient is given a dose of synthetic ACTH ○ then a blood test and/or urine sample is taken to check their cortisol levels ○ if ↓ cortisol levels post-test, likely adrenal insufficiency 2. Serum Cortisol and ACTH Levels ○ If ↓ cortisol or ACTH levels in bloodstream, likely adrenal insufficiency 3. Electrolytes: potassium and sodium ○ particularly testing for any presence of hyperkalaemia or hyponatremia 4. Glucose Levels ○ if the patient is considered hypoglycaemic, with other subjective and objective data, likely adrenal insufficiency 5. 24-hour urine collection testing ○ if the patient has ↓ cortisol levels where normal is 80-120mcg/24hours with other subjective and objective data, likely adrenal insufficiency
92
NURSING MANAGEMENT- adrenocortical insufficiency
The primary treatment goal for this patient cohort is to normalise hormone secretion by: * Focusing on managing the underlying cause of their adrenal insufficiency 1. Medication: Hormone Replacement 2. Fluid Balance Chart (FBC) particularly Electrolyte Balance 3. Psychological & Emotional Support 4. Skin Integrity Chart & Wound Assessments 5. Targeted Education
93
Pharmacology- Glucocorticoids
Glucocorticoids are used widely to suppress immune responses but applications of this type of medication vary from suppression of graft rejections to treatment of asthma, even used in the therapy of autoimmune disorders like Multiple Sclerosis (MS). There are multiple effects on elements of the immune system, for this reason, extra caution must be taken when Medical staff prescribe and Nurses’ administer this medication.
94
GLUCOCORTICOIDS
Glucocorticoids are used widely to suppress immune responses but applications of this type of medication vary from suppression of graft rejections to treatment of asthma, even used in the therapy of autoimmune disorders like Multiple Sclerosis (MS). There are multiple effects on elements of the immune system, for this reason, extra caution must be taken when Medical staff prescribe and Nurses’ administer this medication.
95
HYDROCORTISONE
* Brand name examples: Hysone, Hydrocortisone Viatris Available form Tablets → 5 mg, 10mg, 20mg
96
Mode of Action- Hydrocortisone
* Hydrocortisone is a glucocorticoid used to treat corticosteroid-responsive dermatoses, endocrine disorders, immune conditions, and allergic disorders * Hydrocortisone binds to glucocorticoid receptors leading to downstream effects, such as: ○ Decreased vasodilation ○ Changes permeability of capillaries ○ Decreased leukocyte migration to sites of inflammation Lower doses of corticosteroids, like hydrocortisone provide an anti-inflammatory effect, while higher doses are immunosuppressive.
97
Indications- Hydrocortisone
* Hydrocortisone tablets are indicated for certain: ○ Endocrine ○ Rheumatic ○ Collagen ○ Allergic ○ Ophthalmic ○ Respiratory ○ Haematological ○ Gastrointestinal conditions
98
Adverse Effects- Hydrocortisone
* Higher doses of glucocorticoids for an extended period bind to the mineralocorticoid receptors, raising sodium levels and decreasing potassium levels * Dizziness * Headaches * Oedema * Fatigue * Affects on immune system mean increase risk of infection over longer periods of administration
99
Nursing Care Considerations- Hydrocortisone
* To be administered with food or milk (not to be taken on empty stomach) * Titrate dose up gradually if long term use * Concurrent use with NSAIDs increases risk of ulceration and GI bleeding, use both with caution * Glucocorticoids promote hyperglycaemia, patients with diabetes may require increased doses of a glucose-lowering drug/insulin or other hypoglycaemic agents. Patients without a diagnosis of diabetes will usually require a minimum of daily BGLs whilst having hydrocortisone. * Because of their immunosuppressant actions, glucocorticoids can decrease antibody responses to some vaccines ○ eg) If the patient has just had a 'live vaccine', the immunosuppressive action of glucocorticoids increases the risk of them acquiring the viral disease * Not able to be ceased abruptly
100
PREDNISOLONE
* Brand name examples: Predsone, Solone, Presolone, Panafcortelone Available form Tablets → (1mg, 2.5mg) 5mg, 10mg, 20mg
101
PREDNISOLONE mode of action
* PREDNISOLONE is a glucocorticoid used to treat corticosteroid-responsive dermatoses, endocrine disorders, immune conditions, and allergic disorders * PREDNISOLONE binds to glucocorticoid receptors leading to downstream effects, such as: ○ Decreased vasodilation ○ Changes permeability of capillaries ○ Decreased leukocyte migration to sites of inflammation Lower doses of corticosteroids, like PREDNISOLONE provide an anti-inflammatory effect, while higher doses are immunosuppressive.
102
indications - PREDNISOLONE
* PREDNISOLONE tablets are indicated for certain: ○ Endocrine ○ Rheumatic ○ Collagen ○ Allergic ○ Ophthalmic ○ Respiratory ○ Haematological ○ Gastrointestinal conditions
103
Dosage prednisolone
* 15 - 25mg/day
104
Adverse Effects- PREDNISOLONE
* Fluid retention * Weight gain * Irregular periods * Muscle cramps * Osteoporosis * Hypertension * High blood glucose levels
105
Nursing Care Considerations- PREDNISOLONE
* Prednisolone is only available as a tablet and if other routes are required, Medical Staff and Pharmacy may look to other types of Glucocorticoid replacement * Not able to be ceased abruptly
106
FLUDROCORTISONE
* Brand name examples: Florinef Available form Tablets → 0.1 mg
107
Mode of Action- Fludrocortisone
* Fludrocortisone is a potent mineralcorticoid that also possesses significant glucocorticoid activity. Fludrocortisone is the only mineralocorticoid available and is the drug of choice for chronic mineralocorticoid replacement (such as in Adrenal Insufficiency)
108
Indications- Fludrocortisone
* Fludrocortisone is a preferred drug for treating primary adrenal insufficiency, primary hypoaldosteronism and in most cases is used in combination with a glucocorticoid (eg. Hydrocortisone)
109
Dosage- Fludrocortisone
* 0.05 - 0.1mg/day
110
Adverse Effects- Fludrocortisone
* As a direct consequence of mineralocorticoid actions, when dosage is too high, sodium and water are retained in excess whereas potassium is lost in excess * Weight gain, bloating * Expansion of blood volume * Hypertension * Oedema * Cardiac enlargement * Hypokalaemia * Darkened urine * Black, tarry stool * Unusual bruising
111
Nursing Care Considerations- Fludrocortisone
* If any adverse reactions above are noticed, patients’ should temporarily cease medication on medical advice and fluid and electrolyte imbalances should resolve spontaneously in a few days * Please note, never withhold medications without escalating to appropriate staff members i.e. Nurse in Charge, Pharmacy and/or Medical Staff
112
What is the Thyroid?
A butterfly-shaped gland that sits anterior of the oesophagus, below the 'Adam's Apple' (which is thyroid cartilage). It uses dietary iodine to make 2 main hormones: thyroxine (T4) and tri-iodthyronine (T3). T3 & T4 work to regulate vital bodily functions such as metabolism, energy usage, growth and development
113
Hypothyroidism
Hypothyroidism is the under-secretion of thyroid hormones. * Sustained insufficient levels of circulating thyroid hormones resulting in changes to metabolism and use of energy * All organ in the body are impacted by elevated thyroid hormone levels, results in a progressive and general slowing of the metabolic rate * Thyroid deficiency from either ○ Primary or secondary cause ○ Transient causes like subacute thyroiditis, discontinuance of thyroid hormone replacement therapy * Hypothyroidism is more common in women than men * Generally, the most common causes of hypothyroidism ○ Hashimoto's Thyroiditis ○ Iodine Deficiency ○ Treatment for hyperthyroidism, such as thyroidectomy, radio- iodine therapy ○ Medication for other diseases, like lithium, amiodarone * 3% of the population has an underperforming thyroid gland
114
Primary Hypothyroidism
* Occurs from the destruction of thyroid tissue OR defective hormone synthesis * Considered an autoimmune disorder if no prior surgery on the thyroid has been established * Essentially, the thyroid gland does not secrete enough of its usual hormones (T3 and T4) * Hypothyroidism is commonly seen as the end result of the following diseases: Hashimoto's Thyroiditis or chronic Graves' Disease
115
Secondary Hypothyroidism
* Occurs due to either decreased Thyroid Releasing Hormone (TRH) from the hypothalamus OR decreased secretion of Thyroid Stimulating Hormone (TSH) from the pituitary gland
116
Hashimoto's Thyroiditis
* Most common cause of hypothyroidism * An autoimmune disorder when antibodies attack the thyroid gland so that it can no longer secrete enough hormone to ensure stability * A slow, progressive disease with no symptoms initially
117
Clinical Manifestations of Hashimoto's Thyroiditis
* Hypercholesterolaemia and heart disease/s * Myxoedema Coma (a change in physical appearance with puffiness to skin, periorbital oedema, and a mask-like appearance) * When patients' with myxoedema coma deteriorate, it leads to drowsiness, lethargy, loss of consciousness, hyponatraemia, hypoglycaemia, hypoventilation, lactic acidosis, cardiovascular collapse, and death (hence the term myxoedema coma) ○ Precipitated by infection, medications such as opioids, exposure to cold, and trauma ○ Treated with IV thyroid hormone replacement therapy
118
Hypothyroidism- CLINICAL MANIFESTATIONS
Symptoms for hypothyroidism have a systemic effect characterised by slowing the body's processes: * Loss of consciousness, apathy, lethargy and extreme fatigue, blank facial expressions, * Weight gain, despite anorexic-tendencies * Brittle nails & hair * Intolerance of cold * Receding hairline * Facial & periorbital (around the eyes) oedema * Dry skin * Menstrual disturbances * Constipation * Muscle aches & weakness * notice the head-to-toe format of these symptoms allowing for easy recall *
119
Diagnosis of Hypothyroidism
is achieved through taking patients' history and performing a physical exam. Grouping of subjective and objective data obtained from key clinical manifestations and physical assessment is key to a clear diagnosis. We already know that each of the different body systems could be effected to some extent, thus a thorough head-to-toe assessment followed by necessary focused-assessments would benefit the patient.
120
Pathology of Hypothyroidism
1. Serum thyroid hormone levels ○ if the patient has ↑ TSH levels, likely a primary cause (from the thyroid gland itself) of hypothyroidism ○ but if the patient has ↓ TSH levels, likely a secondary cause of hypothyroidism ○ ↓ free thyroxine/T4 levels may also indicate hypothyroidism 2. Thyroid Antibodies ○ the presence of thyroid antibodies could indicate a level of autoimmune involvement with this patients' hypothyroidism 3. Cholesterol and Triglycerides ○ both usually ↑ in hypothyroidism 4. Full Blood Count (FBC) ○ ↓ Red Blood Cells (RBC) indicative of anaemia is often present in hypothyroidism 5. Urea, Electrolytes, Creatinine (UEC) ○ creatinine ↑ in hypothyroidism
121
Imaging
* CT scan OR MRI of thyroid gland
122
NURSING MANAGEMENT of Hypothyroidism
The primary treatment goal for this patient cohort is to normalise hormone secretion by * Focusing on managing the underlying cause of their Hypothyroidism. * Symptom management: Block any uncomfortable clinical manifestations * Prevent any long-term complications 1. Medication to regulate hormone levels 2. Stool Chart 3. Fluid Balance Chart (FBC) 4. Blood Glucose Levels (BGLs) 5. Skin Integrity Chart & Wound Assessments 6. Targeted Education
123
PHARMACOLOGY of Hypothyroidism
Regardless of the cause of hypothyroidism, people who do not produce enough thyroid hormone will need to have replacement therapy for the rest of the life. Thyroxine Sodium (synthetic T4) * Drug Classification: Synthetic thyroxine/T4, also known as L-thyroxine sodium * Brand names: Eltoxin, Orxine, Eutroxsig * Available forms and Dosage: 25mcg ¦ 50mcg ¦ 75mcg ¦ 100mcg ¦ 125mcg ¦ 200 mcg tablets ♦ Initially 1.6mcg/kg ideal body weight, orally, once daily * Mechanism of Action: ○ Converted to T3 which is a more active form of thyroxine ○ T3 will work as it physiologically would, at the end-organs that require T3 to function * Nursing Considerations: ○ Slow onset of action, can take up to 8 weeks for hormone levels to stabilise ○ Peak action usually found in 1-3 weeks from initial dose ○ Long duration that this drug stays within the bloodstream, 7-21 days even if the drug has been ceased ○ Treatment is lifelong ○ Should be taken on an empty stomach preferably before breakfast, often before medication rounds (i.e. 0700) ○ Natural fluctuations in hormone levels mean dosages will need to be adjusted from time to time § Perhaps the patient has comorbidities, generally aged, increased stressors, acute viral infections etc § This is when the pharmacists become a wealth of knowledge and referrals can be made to them regarding this
124
Hyperthyroidism
Hyperactivity of the thyroid gland puts the body in a state of hyperthyroidism. * Sustained elevated levels of circulating thyroid hormones resulting in changes to metabolism and use of energy * All organ in the body are impacted by elevated thyroid hormone levels, so the body is constantly working harder and faster * Some risk factors to developing hyperthyroidism across the lifespan are: ○ Being born female ○ Aged between 20 - 40 years of age ○ Family history of thyroid disease ○ Comorbidities such as pernicious anaemia, T1DM, primary adrenal insufficiency ○ Low dietary intake of iodine ○ Pregnancy in the last 6 months
125
Primary Hyperthyroidism
is also known as Graves' Disease (an autoimmune disease) * Any type of thyroid pathology, such as an autoimmune disorder, a tumour (cancerous or otherwise), enlarged thyroid, nodules on your thyroid * Causes the thyroid glands to secrete too much T3 and T4 * Graves' Disease is an autoimmune disease where antibodies mimic the actions of a hormone called Thyroid Stimulating Hormone (TSH) * These antibodies attack the thyroid resulting in hypersecretion of T3 and T4, the hormones usually secreted by the thyroid gland * Unfortunately, there is an unknown aetiology but some precipitating factors have been found: ○ Insufficient dietary iodine ○ Infections ○ Increased stress ○ Genetic factors ○ Cigarette smoking
126
Secondary Hyperthyroidism
* Occurs due to elevated release of TSH from either the hypothalamus or the pituitary gland resulting in the thyroid gland excessively secreting T3 and T4
127
CLINICAL MANIFESTATIONS In Graves' Disease or Primary Hyperthyroidism
Because all the end-organs are needed in metabolism, they are each effected to some extent: * Headaches, nervousness, emotional instability * Weight loss * Tremors * Exophthalmos (bulging eyeballs) * Goiter (physical enlargement of thyroid glands) * Increased perspiring (excessive sweating) * Cardiac arrhythmias and tachycardia * Increased respiratory drive and ultimately respiratory rate * Nausea and diarrhoea * Muscle weakness * notice the head-to-toe format of these symptoms allowing for easy recall *
128
Diagnosis of Hyperthyroidism
A clear diagnosis is achieved through a thorough history and physical examination, combining subjective and objective data to benefit the patient.
129
Pathology of Hyperthyroidism
1. Serum thyroid hormone levels ○ if the patient has ↓ TSH levels with ↑ free thyroxine/T4 levels ○ always used in conjunction with objective data from your patient assessment 2. Radioactive iodine uptake test ○ used to differentiate between Graves' disease and other forms of thyroid disorders
130
Imaging of Hyperthyroidism
* CT scan OR MRI of thyroid gland
131
NURSING MANAGEMENT of Hyperthyroidism
The primary treatment involves managing the underlying cause, managing symptoms, and preventing long-term complications. Treatment plans are individualized due to autoimmune origins, severity, causes, ages, adverse effects, and comorbidities. Common options include medication, radio-iodine therapy, and thyroid surgery.
132
Anti-thyroid Agents
* Drug Classification: Thioamides * Brand names: Carbimazol, Aristo, Neo-Mercazole * Available forms and Dosage: 5mg tablets ♦ Initially 15-20mg/day, orally (doses divided throughout waking hours), ↑ dosage according to severity and response to drug
133
Mechanism of Action: Anti-thyroid Agents
○ Depresses thyroid hormone synthesis by inhibiting the binding of iodine to tyrosine ○ Has no effect on iodine uptake by the thyroid gland
134
* Nursing Considerations: Anti-thyroid Agents
Clinical response occurs after thyroid hormone levels stabilize, and abrupt discontinuation can lead to hyperthyroidism. Doses require collaboration with nursing, pharmacy, and medical teams. Patients are monitored monthly for the first year, and adverse reactions usually occur 8 weeks post-treatment.
135
* Adverse Effects: Anti-thyroid Agents
○ Rash, itchy skin ○ ↓ White Blood Cell (WBC) count (which means ↑ susceptibility to infections) ○ Liver failure with prolonged use ○ Weakness, fatigue, fever, sore throat ○ Nausea, mild gastric disturbances such as abdominal pain, loss of taste and appetite
136
Iodine (synthetic)
* Drug Classification: * Brand names: * Available forms and Dosage: mg tablets ♦ Initially 15-20mg/day, orally (doses divided throughout waking hours), ↑ dosage according to severity and response to drug
137
Mechanism of Action: Iodine (synthetic)
○ Inhibits T3 and T4 synthesis ○ Blocks these hormones from being released into circulation ○ Also decreases vascularity of the thyroid gland, thus often used in combination with antithyroid agents to prepare the patient for thyroidectomy (removal of the thyroid surgery)
138
* Nursing Considerations: Iodine (synthetic)
○ Can be used in the treatment of thyroidtoxiocosis
139
Beta Blockers (see Cardiac Drugs)
* In the context of symptom management, Hyperthyroidism patients sometimes require prompt treatment in the form of beta blockers for their cardiac symptoms: arrhythmias, tachycardia, some tremors and nervousness too. ○ It will not prevent thyroid hormone production as this is not the mechanism of action of Beta Blockers