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NUR2226 > WK 7: Endocrine Disorders > Flashcards

WK 7: Endocrine Disorders Flashcards

1
Q

Identify the 3 body parts included within the endocrine system

A

Pancreas
Adrenal Glands
Thyroid

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2
Q

What is DM?

A

Group of metabolic disorders where there are abnormally high levels of blood glucose over a prolonged period of time

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3
Q

Identify the 2 characterisations of DM

A

Ineffective response to insulin at the target cells (insulin resistance)
Insufficient or no release of insulin by the islet of Langerhans in the pancreas

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4
Q

Describe the function of insulin

A

To shift glucose into cells where it can be used for energy. Insulin enhances glucose absorption and is the body’s main fuel storage hormone

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5
Q

What is insulin secreted from?

A

Beta cells

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6
Q

What is T1DM?

A

An autoimmune condition where the immune system is triggered to destroy all beta cells in the Islet of Langerhans

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7
Q

Identify the cause of T1DM

A

Strong link between genetic susceptibility and environmental factors e.g. virus exposure

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8
Q

Identify the typical onset of T1DM

A

Usually <30 most commonly around puberty

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9
Q

Identify the cure for T1DM

A

No cure, lifelong disorder

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10
Q

Identify the characteristics of T1DM

A

Decreased/Absent blood insulin levels

Decreased secretion of amylin

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11
Q

What is amylin?

A

Co released with insulin from beta cells to suppress the release of glucagon from alpha cells

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12
Q

Describe the pathphyisology of T1DM

A

Glucose absorbed by digestive tract and enters blood stream, BGL increases, signal sent to pancreas to release insulin, pancreas cannot release insulin due to no Islet of langerhans so BGL continues to increase

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13
Q

Identify 3 clinical manifestations associated with T1DM

A 
Polyphagia (Increased hunger)
Polydipsia (Increased thirst)
Poly uria (Incraesed urine production)
Weight loss 
Lethargy
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14
Q

Identify the typical treatment for T1DM

A

Insulin management plans individualised according to age, weight, exercise levels etc.
Diet and exercise plans
Combination of insulin types and doses

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15
Q

What is T2DM

A

Life long chronic condition, considered “silent” as it is a progressive disorder developing over many years

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16
Q

Identify the cause of T2DM

A

Strong link to modifiable factors e.g. smoking, obesity, poor diet

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17
Q

Identify the typical onset of T2DM

A

Usually in adults >45 years, more frequently these days in younger age groups

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18
Q

Identify the cure for T2DM

A

No cure, lifelong disorder

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19
Q

Identify the characteristics of T2DM

A

Normal to increased blood insulin levels (Gradually deteriorates)

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20
Q

Describe the pathophysiology of T2DM

A

Glucose absorbed from digestive tract and enters blood stream, BGL increases, trigger sent to pancreas to release insulin, insulin released, target cells develop an ineffective response to insulin and so tell the pancreas to release more and more, but slowly the beta cells get destructed and end up not being able to release any insulin

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21
Q

Identify the 2 pathological reasons for T2DM

A
  1. Insulin deficiency: Relative shortage of insulin

2. Insulin resistance: Ineffective response to insulin from target cells = Loss of insulin sensitivity

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22
Q

Identify 3 clinical manifestations associated with T2DM

A

People often asymptomatic and undiagnosed until an AMI or DFU develops

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23
Q

Identify the typical treatment for T2DM

A

Lifestyle changes especially modifiable risk factors, oral DM management by glucose lowering medications

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24
Q

Identify the 5 characteristics which contribute to a diagnosis of DM

A
  1. Symptoms
  2. Fasting BGL 7mmol/l>
  3. Random BGL 11mmol/l>
  4. Oral glucose tolerance test 11.1mmol/l>
  5. HbA1c 7.0%>
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25
Q

Identify the normal range for Hb1Ac

A

4-5.5%

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26
Q

Describe the concept of Hb1Ac

A

As glucose circulates in the blood, some of it binds to haemoglobin which becomes Hb1Ac, the amount of Hb1Ac formed is directly related to the amount of glucose in the blood

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27
Q

Identify the range for severe hypoglycaemia

A

<2.5mmol/L

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28
Q

Identify the range for moderate hypoglycaemia

A

> 2.5-3.9mmol/L

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29
Q

Identify the range for hypoglycaemia

A

<3.9mmol/L

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30
Q

Identify the normal range pre meals for T1DM

A

6-8mmol/L

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31
Q

Identify the normal range pre meals for T2DM

A

6-10mmol/L

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32
Q

Identify the range for hyperglycaemia

A

> 14mmol/L

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33
Q

How often should BGL be tested

A

QID unless specificed by medical officer, immediately pre meals and before bed

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34
Q

What are the 3 reasons when ketones should be tested?

A
  1. T1DM is suspected
  2. DKA suspected
  3. Hyperglycaemia is persistent
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35
Q

How often should BGL be tested for patients recieiving continuous feeds

A

4-6 hourly

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36
Q

How often should BGL be tested in fasting patients unable to recommence food and fluids

A

2 hourly

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37
Q

How often should BGL be tested if on continuous infusion

A

Hourly until 3 consecutive stable readings are obtained

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38
Q

How often should BGL be tested during a hypo

A

Every 10-15 mins until stablised

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39
Q

What is glycemic index?

A

Ranks carbohydrates according to their effect on BGL, the lower the GI, the slower the rise in BGL when food is consumed

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40
Q

What types of foods are reccomned for DM patients in terms of GI?

A

Moderate amounts of carbohydrates and high fibre foods with a low GI

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41
Q

Identify the two overall management goals for Dm

A
  1. Restore normal BGl (euglycaemia)

2. Correct related metabolic disorders

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42
Q

Identify the 3 acute complications of DM

A

Hypoglycaemia
Hyperglycaemia
Hypersmolar hyperglycaemic state (HHS)

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43
Q

Describe hypoglycaemia (Complication)

A

Occurs when there is too much insulin relative to glucose levels (<4mmol/L)

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44
Q

Identify 2 causes of hypoglycaemia

A

Reduced or poor timing intake of food
Increased exercise
Dehydration

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45
Q

Identify 2 clinical manifestations associated with hypoglycaemia

A

Confusion
ACS
Visual disturbances

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46
Q

Identify the management of hypoglycaemia in a conscious state

A

Administration of 15-20g of quick acting carbs
Check BGL after 15 mins
Repetition of carbs after 15 mins and administration of additional food

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47
Q

Describe Diabetic Ketoacidosis (DKA)

A

Occurs in T1DM Severe hyperglycaemia or ketoanaemia, acidosis or severe dehydration

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48
Q

Identify 2 clinical manifestations associated with DKA

A 
Deep RR (Kussmali breathing)
Fruity breath (acetone blowout)
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49
Q

Describe the pathophysiology of DKA

A

Increased metabolism of fat and protein as glucose cannot be used, fat releases ketones into blood, pH drops, respiratory compensation

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50
Q

Describe Hyperosmolar Hyperglycaemic State (HHS)

A

Occurs in T2DM, when patients become severely hyperglycaemic with high osmolarity as a direct result of stress or dehydration, no ketones present so no signs of acidosis

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51
Q

Identify 2 complications of HHS

A

Extreme dehydration, lethargy, cofusion leading to seizures

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52
Q

Identify a chronic complication of DM

A

Diabetic foot disease

53
Q

Describe diabetic foot disease

A

Peripheral neuropathy results in paraesthesia of hans and feet and can lead to the development of diabetic foot ulcers

54
Q

What are diabetic foot ulcers

A

Ulceration, infection or ischeamia of the foot in people with diabetes and who have developed peripheral neuropathy

55
Q

Identify the classification of DFU

A

Graded as present (0), or absent (1)

56
Q

Identify 2 nursing considerations in the care of DFU

A

Education in routine wearing of appropriate footwear

Treatment of pre ulcerative signs

57
Q

What role do the adrenal glands play in the body

A

Metabolism, stress response, sex function, immune response and blood pressure regulation

58
Q

Identify the 2 disorders of the adrenal glands function

A

Cushing’s syndrome

Adrenal Cortisol Insufficiency

59
Q

What is cushing’s syndrome

A

Group of clinical manifestations caused by the chronic exposure to excessive circulating levels of cortisol

60
Q

What is the main characteristic of cushion’s syndrome

A

Hypercortisolism

61
Q

Identify 3 clinical manifestations associated with cushion’s syndrome

A

Hypertension
Osteoporosis
Poor wound healing
Brusing

62
Q

Identify 2 forms of diagnostics for cushion’s syndrome

A

Measure cortisol levels

24hr urine collection

63
Q

Identify the primary goal for treatment of cushings syndrome

A

To normalise hormone secretion

64
Q

Identify 2 nursing considerations in the management of cushing syndrome

A

Patient/Physcial assessment

Discharge planning and education

65
Q

Identify a cause of cushings syndrome

A

Long term administration of exogenous steroids, reversible once steroids are ceased but must be done slowly so the pituitary has a chance to secrete ATCH in the secretion of cortisol

66
Q

What is adrenocortisol insufficiency

A

Hyposecretion of hormones from the adrenal/pituatry gland

67
Q

Identify the 2 types of adrenocortisol insufficiency

A 
Primary insufficiency (Addisons disease)
Secondary insufficiency
68
Q

Describe primary insufficiency adrenocortisol insufficiency

A

Occurs from disorder of adrenal gland that no longer secretes adrenal hormones.

69
Q

What is the cause of primary insufficiency adrenocortisol insufficiency

A

80% autoimmune 20% physical stress or trauma

70
Q

Describe secondary insufficiency adrenocortisol insufficiency

A

Occurs as the pituitary gland does not make enough ACTH resulting in deficiency of corticosteroids

71
Q

What is the cause of secondary insufficiency adrenocortisol insufficiency

A

Pituitary disease/Supression due to exogenous corticosteroid administration

72
Q

Which type of adrenocortisol insufficiency is more common

A

Secondary adrenocortisol insufficiency

73
Q

Identify a complication of adrenocortisol insufficiency

A

Addisions crisis

74
Q

Describe Addison’s crisis

A

Life threatening complication secondary to low blood cortisol levels resulting when normal glucocorticoid medications are withheld or during an acute psychological change e.g. vomiting

75
Q

Identify 2 clinical manifestations of Addison’s crisis

A

Mental state changes
Fever
LOC

76
Q

Identify 3 clinical manifestations of adrenocortisol insufficiency

A

Hyperpigmentation
Decraesed BP
Nausea/vomiting/diarrhoea

77
Q

Identify 2 forms of diagnosis in adrenocortisol insufficiency

A

24 hr urine collection

Serum cortisol levels/ACTH levels

78
Q

Identify the primary goal in the management of adrenocortisol insufficiency

A

Normalise hormone secretion with treatment focused on underlying cause

79
Q

Identify a treatment option in the management of adrenocortisol insufficiency

A

Hormone replacement therapy:
Daily glucocorticoid replacement e.g. hydrocortisone
Daily mineralocorticoid in morning e.g. fludrocortisone

80
Q

Identify 2 nursing considerations in adrenocortisol insufficiency

A

Early discharge planning

Psychological and emotional support to decrease stress levels

81
Q

Identify the function of the thyroid gland

A

Uses iodine from the diet to make two main hormones that regulate vital bodily functions (metabolism, energy, growth)

82
Q

What are the 2 hormones involved in the thyroid gland

A

Triodthyronine (T3)

Thyroxine (T4)

83
Q

How are T3/T4 levels maintained

A

Hypothalamus produces thyroid releasing hormone (TRH) signalling pituitary to tell the thyroid gland to produce more/less T3/T4

84
Q

What happens when T3/T4 are low?

A

Pituitary gland releases more TSH to tell the thyroid gland to release more hormones

85
Q

What happens when T3/T4 are high?

A

Pituitary glands releases less TSH to the thyroid gland to slow production of hormones

86
Q

Describe hyperthyroidism

A

Hyperactivity of the thyroid gland resulting in sustained elevated levels of thyroid hormones resulting in changes to metabolism/use of energy

87
Q

Identify 2 risk factors of hyperthyroidism

A

Females 20-40
Family history
Pregnancy in last 6 months

88
Q

Identify the 2 types of hyperthyroidism

A 
Primary hyperthyroidism (Graves disease)
Secondary hyperthyroidism
89
Q

Describe primary hyperthyroidism (Graves disease

A

Occurs due to thyroid pathology e.g. autoimmune disorder where antibodies mimics TSH and attack thy thyroid leading to hyper secretion

90
Q

Describe secondary hyperthyroidism

A

Occurs due to increased release of TSH from hypothalamus/pituatry gland leading to the thyroid gland secreting too much T3/T4

91
Q

Identify a complication of hyperthyroidism

A

Thyrotoxicosis

92
Q

What is thyrotoxicosis

A

Physiological effects that occur when excessive amounts of T3/T4 are in blood (All CM present in severe forms)

93
Q

Identify 3 clinical manifestations of hyperthyroidism

A

Sweating
Tremor
Muscle weakness
Nausea/diarrhoea

94
Q

What are the 3 treatment options for hyperthyroidism

A
  1. Medication management
  2. Radioactive therapy
  3. Thyroid surgery
95
Q

What is radioactive therapy

A

Taken as a capsule/liquid to destroy thyroid tissue, leading to decreased production of thyroid hormones

96
Q

What is the primary goal in the management of hyperthyroidism

A

Normalise hormone secretion with treatment focused on management of underlying cause e.g. blocking uncomfortable CM

97
Q

What is hypothyroidism

A

Undersecretion of thyroid hormones resulting in progressive general slowing of metabolic rate = body works slower

98
Q

Identify the 3 types of hypothyroidism

A

Primary hypothyroidism
Secondary hypothyroidism
Hashimotos thyroiditis

99
Q

Describe primary hypothyroidism

A

Destruction of the thyroid tissue/defective hormone synthesis = thyroid Gland doesn’t secrete enough T3/T4

100
Q

Describe secondary hypothyroidism

A

Due to decreased TRH from hypothalamus or decreased secretion of TSH from pituitary

101
Q

Describe hashimotos thyroiditis

A

Autoimmune disorder where antibodies attack thyroid gland so it can not secrete enough hormones to ensure stability

102
Q

Identify 3 clinical manifestations of hashimotos thyroiditis

A

Hypercholestroaemia
Heart disease
Myoxedema coma (puffy face)

103
Q

Identify 3 clinical manifestations of hypothyroidism

A

Hair loss
lethargy/apathy (lack of intrest/concern)
Muscle aches/weakness
intolerance to cold

104
Q

Identify a form of diagnosis in hypothyroidism

A

Serum thyroid hormone levels (increased in primary, decreased in secondary)

105
Q

Identify the primary goal of treatment in hypothyroidism

A

To safely/rapidly normalise hormone secretion with hormone therapy/relief of symptoms

106
Q

Identify 2 nursing considerations in the management of hypothyroidism

A

Aim for symptom relief
Stool chart (prone to constipation)
Psychological/emotional support

107
Q

Exogenous insulin

  • Class
  • Indication
  • Action
  • Adverse effects
  • Nursing consideration
A
  • Insulins
  • When an individual has no insulin or cannot regulate BGL
  • Facilitates the metabolisation and storage of glucose through cellular transport
  • Hypo, weight gain
  • Rotation of injection sites
108
Q

Identify the 4 types of insulin and an example of each

A
  • Ultra short acting (Rapid): Novorapid
  • Short acting: Actrapid
  • Intermediate: Mixtard, Protaphane
  • Long acting: Optisulin
109
Q

Oral hypoglycaemic agents

  • Class
  • Indication
  • Action
  • Adverse effects
  • Nursing consideration
A
  • Insulin sensitisers
  • Adjunct to diet and exercise, to lower BGL in T2DM, not for T1
  • Simulates insulin release from beta cells in pancreas, lowers insulin resistance by increasing glucose uptake
  • Hypo, GI upset
  • Slow onset of effect-control may take 2 weeks to establish
110
Q

Identify the 5 types of OHA

A 
Biguanide (First line)
SGLT2 inhibitors 
Gliptins 
Sulfonylureas 
Thiazolidinedione
111
Q

What determines what type of OHA one has?

A

Choice depends on the individuals weight, response to trailed drugs, pancreatic and liver functions

112
Q

Example of Biguanide

A

Metformin

113
Q

Example of SGLT2 inhibitors

A

Dapaglifflozin

114
Q

Example of DPP-4 inhibitors/gliptins

A

Alogliptin

115
Q

Example of Sulfonylureas

A

Glibenclamide

116
Q

Example of Thiazolidinedione

A

Pioglitazone

117
Q

Glucose elevating agents

  • Class
  • Indication
  • Action
  • Adverse effects
  • Nursing consideration
A
  • Glucose elevating agents
  • Hypoglycaemia
  • Decraese insulin release and accelerate the breakdown of glycogen in the liver to release glucose
  • GI upset, vascular effects
  • Give longer acting carbohydrates after glucose/glucagon has kicked in to prevent recurrent hypo
118
Q

Example of glucose elevating agent

A

Glucose (PO/IV)

Glucagon (Used in unconscious) (SC, IM, IV)

119
Q

Identify the two types of Glucocorticoids

A

Hydrocortisone and Prednisolone

120
Q

Glucocorticoids

  • Class
  • Indication
  • Action
  • Adverse effects
  • Nursing consideration
A
  • Corticosteroids
  • Glucocorticoid replacement therapy in adrenal insufficiency, acute adrenal insufficiency (hydrocortisone)
  • Regulate gene expression resulting in glucocorticoid effects such as gluconeogenesis, proteolysis, lipolysis
  • Oedema, HTN
  • Take with food to reduce GI upset
121
Q

Mineralcorticoids

  • Class
  • Indication
  • Action
  • Adverse effects
  • Nursing consideration
A
  • Corticosteroids
  • Mineralocorticoid replacement in primary adrenal insufficiency
  • Binds to mineralocorticoid receptors = increased plasma sodium conc., increased BP
  • Oedema, HTN
  • May not be needed in high doses of glucocorticosteroids
122
Q

Antithyroid agents

  • Class
  • Indication
  • Action
  • Adverse effects
  • Nursing consideration
A
  • Thioamides
  • Hyperthyroidism (1-2yrs), pre treatment for thyroidectomy, pre/post radioactive iodine
  • Depresses thyroid hormone synthesis by inhibiting binding of iodine to tyrosine
  • Rash, fatigue
  • Education on abrupt discontinuation
123
Q

What is an example of antithyroid agents

A

Carbimazole

124
Q

Iodine

  • Class
  • Indication
  • Action
  • Adverse effects
  • Nursing consideration
A
  • Iodine
  • Hyperthyroidism, relieve symptoms, maintain euthyroid state
  • Transiently inhibits thryoid hormone release
  • Hypersensitivity reactions
  • Long term use may exacerbate hyperthyroidism
125
Q

What is another form of medication used in the treatment of hyperthyroidism?

A

Beta blockers: Short term relief of symptoms, e.g. propranolol

126
Q

Thyroxine Sodium

  • Class
  • Indication
  • Action
  • Adverse effects
  • Nursing consideration
A
  • Thyroid hormones
  • First line of drug for hypothyroidism, treatment lifelong
  • Converted to T3 (more active form of thyroid, can take 8 weeks to stabilise
  • Excess dosage (hyperthyroidism symptoms e.g. tachycardia, arrhythmia, sweating)
  • Should be taken on empty stomach
127
Q

What are the 3 names for thyroxine sodium

A

T4
Levothyroxine
L-thyroxine sodium)

128
Q

What is an example of thyroxine sodium

A

Eltoxin

Oroxine

129
Q

Identify the management of hypoglycaemia in a unconscious state

A

SC or IM injection 1mg glucagon
IV administration 50mL 50% glucose
Determine cause

NUR2226 (8 decks)

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