WK 7: Endocrine Disorders Flashcards
1
Q
Identify the 3 body parts included within the endocrine system
A
Pancreas
Adrenal Glands
Thyroid
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
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
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
5
Q
What is insulin secreted from?
A
Beta cells
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
7
Q
Identify the cause of T1DM
A
Strong link between genetic susceptibility and environmental factors e.g. virus exposure
8
Q
Identify the typical onset of T1DM
A
Usually <30 most commonly around puberty
9
Q
Identify the cure for T1DM
A
No cure, lifelong disorder
10
Q
Identify the characteristics of T1DM
A
Decreased/Absent blood insulin levels
Decreased secretion of amylin
11
Q
What is amylin?
A
Co released with insulin from beta cells to suppress the release of glucagon from alpha cells
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
13
Q
Identify 3 clinical manifestations associated with T1DM
A
Polyphagia (Increased hunger) Polydipsia (Increased thirst) Poly uria (Incraesed urine production) Weight loss Lethargy
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
15
Q
What is T2DM
A
Life long chronic condition, considered “silent” as it is a progressive disorder developing over many years
16
Q
Identify the cause of T2DM
A
Strong link to modifiable factors e.g. smoking, obesity, poor diet
17
Q
Identify the typical onset of T2DM
A
Usually in adults >45 years, more frequently these days in younger age groups
18
Q
Identify the cure for T2DM
A
No cure, lifelong disorder
19
Q
Identify the characteristics of T2DM
A
Normal to increased blood insulin levels (Gradually deteriorates)
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
21
Q
Identify the 2 pathological reasons for T2DM
A
- Insulin deficiency: Relative shortage of insulin
2. Insulin resistance: Ineffective response to insulin from target cells = Loss of insulin sensitivity
22
Q
Identify 3 clinical manifestations associated with T2DM
A
People often asymptomatic and undiagnosed until an AMI or DFU develops
23
Q
Identify the typical treatment for T2DM
A
Lifestyle changes especially modifiable risk factors, oral DM management by glucose lowering medications
24
Q
Identify the 5 characteristics which contribute to a diagnosis of DM
A
- Symptoms
- Fasting BGL 7mmol/l>
- Random BGL 11mmol/l>
- Oral glucose tolerance test 11.1mmol/l>
- HbA1c 7.0%>
25
Identify the normal range for Hb1Ac
4-5.5%
26
Describe the concept of Hb1Ac
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
27
Identify the range for severe hypoglycaemia
<2.5mmol/L
28
Identify the range for moderate hypoglycaemia
>2.5-3.9mmol/L
29
Identify the range for hypoglycaemia
<3.9mmol/L
30
Identify the normal range pre meals for T1DM
6-8mmol/L
31
Identify the normal range pre meals for T2DM
6-10mmol/L
32
Identify the range for hyperglycaemia
>14mmol/L
33
How often should BGL be tested
QID unless specificed by medical officer, immediately pre meals and before bed
34
What are the 3 reasons when ketones should be tested?
1. T1DM is suspected
2. DKA suspected
3. Hyperglycaemia is persistent
35
How often should BGL be tested for patients recieiving continuous feeds
4-6 hourly
36
How often should BGL be tested in fasting patients unable to recommence food and fluids
2 hourly
37
How often should BGL be tested if on continuous infusion
Hourly until 3 consecutive stable readings are obtained
38
How often should BGL be tested during a hypo
Every 10-15 mins until stablised
39
What is glycemic index?
Ranks carbohydrates according to their effect on BGL, the lower the GI, the slower the rise in BGL when food is consumed
40
What types of foods are reccomned for DM patients in terms of GI?
Moderate amounts of carbohydrates and high fibre foods with a low GI
41
Identify the two overall management goals for Dm
1. Restore normal BGl (euglycaemia)
| 2. Correct related metabolic disorders
42
Identify the 3 acute complications of DM
Hypoglycaemia
Hyperglycaemia
Hypersmolar hyperglycaemic state (HHS)
43
Describe hypoglycaemia (Complication)
Occurs when there is too much insulin relative to glucose levels (<4mmol/L)
44
Identify 2 causes of hypoglycaemia
Reduced or poor timing intake of food
Increased exercise
Dehydration
45
Identify 2 clinical manifestations associated with hypoglycaemia
Confusion
ACS
Visual disturbances
46
Identify the management of hypoglycaemia in a conscious state
Administration of 15-20g of quick acting carbs
Check BGL after 15 mins
Repetition of carbs after 15 mins and administration of additional food
47
Describe Diabetic Ketoacidosis (DKA)
Occurs in T1DM Severe hyperglycaemia or ketoanaemia, acidosis or severe dehydration
48
Identify 2 clinical manifestations associated with DKA
```
Deep RR (Kussmali breathing)
Fruity breath (acetone blowout)
```
49
Describe the pathophysiology of DKA
Increased metabolism of fat and protein as glucose cannot be used, fat releases ketones into blood, pH drops, respiratory compensation
50
Describe Hyperosmolar Hyperglycaemic State (HHS)
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
51
Identify 2 complications of HHS
Extreme dehydration, lethargy, cofusion leading to seizures
52
Identify a chronic complication of DM
Diabetic foot disease
53
Describe diabetic foot disease
Peripheral neuropathy results in paraesthesia of hans and feet and can lead to the development of diabetic foot ulcers
54
What are diabetic foot ulcers
Ulceration, infection or ischeamia of the foot in people with diabetes and who have developed peripheral neuropathy
55
Identify the classification of DFU
Graded as present (0), or absent (1)
56
Identify 2 nursing considerations in the care of DFU
Education in routine wearing of appropriate footwear
| Treatment of pre ulcerative signs
57
What role do the adrenal glands play in the body
Metabolism, stress response, sex function, immune response and blood pressure regulation
58
Identify the 2 disorders of the adrenal glands function
Cushing's syndrome
| Adrenal Cortisol Insufficiency
59
What is cushing's syndrome
Group of clinical manifestations caused by the chronic exposure to excessive circulating levels of cortisol
60
What is the main characteristic of cushion's syndrome
Hypercortisolism
61
Identify 3 clinical manifestations associated with cushion's syndrome
Hypertension
Osteoporosis
Poor wound healing
Brusing
62
Identify 2 forms of diagnostics for cushion's syndrome
Measure cortisol levels
| 24hr urine collection
63
Identify the primary goal for treatment of cushings syndrome
To normalise hormone secretion
64
Identify 2 nursing considerations in the management of cushing syndrome
Patient/Physcial assessment
| Discharge planning and education
65
Identify a cause of cushings syndrome
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
What is adrenocortisol insufficiency
Hyposecretion of hormones from the adrenal/pituatry gland
67
Identify the 2 types of adrenocortisol insufficiency
```
Primary insufficiency (Addisons disease)
Secondary insufficiency
```
68
Describe primary insufficiency adrenocortisol insufficiency
Occurs from disorder of adrenal gland that no longer secretes adrenal hormones.
69
What is the cause of primary insufficiency adrenocortisol insufficiency
80% autoimmune 20% physical stress or trauma
70
Describe secondary insufficiency adrenocortisol insufficiency
Occurs as the pituitary gland does not make enough ACTH resulting in deficiency of corticosteroids
71
What is the cause of secondary insufficiency adrenocortisol insufficiency
Pituitary disease/Supression due to exogenous corticosteroid administration
72
Which type of adrenocortisol insufficiency is more common
Secondary adrenocortisol insufficiency
73
Identify a complication of adrenocortisol insufficiency
Addisions crisis
74
Describe Addison's crisis
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
Identify 2 clinical manifestations of Addison's crisis
Mental state changes
Fever
LOC
76
Identify 3 clinical manifestations of adrenocortisol insufficiency
Hyperpigmentation
Decraesed BP
Nausea/vomiting/diarrhoea
77
Identify 2 forms of diagnosis in adrenocortisol insufficiency
24 hr urine collection
| Serum cortisol levels/ACTH levels
78
Identify the primary goal in the management of adrenocortisol insufficiency
Normalise hormone secretion with treatment focused on underlying cause
79
Identify a treatment option in the management of adrenocortisol insufficiency
Hormone replacement therapy:
Daily glucocorticoid replacement e.g. hydrocortisone
Daily mineralocorticoid in morning e.g. fludrocortisone
80
Identify 2 nursing considerations in adrenocortisol insufficiency
Early discharge planning
| Psychological and emotional support to decrease stress levels
81
Identify the function of the thyroid gland
Uses iodine from the diet to make two main hormones that regulate vital bodily functions (metabolism, energy, growth)
82
What are the 2 hormones involved in the thyroid gland
Triodthyronine (T3)
| Thyroxine (T4)
83
How are T3/T4 levels maintained
Hypothalamus produces thyroid releasing hormone (TRH) signalling pituitary to tell the thyroid gland to produce more/less T3/T4
84
What happens when T3/T4 are low?
Pituitary gland releases more TSH to tell the thyroid gland to release more hormones
85
What happens when T3/T4 are high?
Pituitary glands releases less TSH to the thyroid gland to slow production of hormones
86
Describe hyperthyroidism
Hyperactivity of the thyroid gland resulting in sustained elevated levels of thyroid hormones resulting in changes to metabolism/use of energy
87
Identify 2 risk factors of hyperthyroidism
Females 20-40
Family history
Pregnancy in last 6 months
88
Identify the 2 types of hyperthyroidism
```
Primary hyperthyroidism (Graves disease)
Secondary hyperthyroidism
```
89
Describe primary hyperthyroidism (Graves disease
Occurs due to thyroid pathology e.g. autoimmune disorder where antibodies mimics TSH and attack thy thyroid leading to hyper secretion
90
Describe secondary hyperthyroidism
Occurs due to increased release of TSH from hypothalamus/pituatry gland leading to the thyroid gland secreting too much T3/T4
91
Identify a complication of hyperthyroidism
Thyrotoxicosis
92
What is thyrotoxicosis
Physiological effects that occur when excessive amounts of T3/T4 are in blood (All CM present in severe forms)
93
Identify 3 clinical manifestations of hyperthyroidism
Sweating
Tremor
Muscle weakness
Nausea/diarrhoea
94
What are the 3 treatment options for hyperthyroidism
1. Medication management
2. Radioactive therapy
3. Thyroid surgery
95
What is radioactive therapy
Taken as a capsule/liquid to destroy thyroid tissue, leading to decreased production of thyroid hormones
96
What is the primary goal in the management of hyperthyroidism
Normalise hormone secretion with treatment focused on management of underlying cause e.g. blocking uncomfortable CM
97
What is hypothyroidism
Undersecretion of thyroid hormones resulting in progressive general slowing of metabolic rate = body works slower
98
Identify the 3 types of hypothyroidism
Primary hypothyroidism
Secondary hypothyroidism
Hashimotos thyroiditis
99
Describe primary hypothyroidism
Destruction of the thyroid tissue/defective hormone synthesis = thyroid Gland doesn't secrete enough T3/T4
100
Describe secondary hypothyroidism
Due to decreased TRH from hypothalamus or decreased secretion of TSH from pituitary
101
Describe hashimotos thyroiditis
Autoimmune disorder where antibodies attack thyroid gland so it can not secrete enough hormones to ensure stability
102
Identify 3 clinical manifestations of hashimotos thyroiditis
Hypercholestroaemia
Heart disease
Myoxedema coma (puffy face)
103
Identify 3 clinical manifestations of hypothyroidism
Hair loss
lethargy/apathy (lack of intrest/concern)
Muscle aches/weakness
intolerance to cold
104
Identify a form of diagnosis in hypothyroidism
Serum thyroid hormone levels (increased in primary, decreased in secondary)
105
Identify the primary goal of treatment in hypothyroidism
To safely/rapidly normalise hormone secretion with hormone therapy/relief of symptoms
106
Identify 2 nursing considerations in the management of hypothyroidism
Aim for symptom relief
Stool chart (prone to constipation)
Psychological/emotional support
107
Exogenous insulin
- Class
- Indication
- Action
- Adverse effects
- Nursing consideration
- 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
Identify the 4 types of insulin and an example of each
- Ultra short acting (Rapid): Novorapid
- Short acting: Actrapid
- Intermediate: Mixtard, Protaphane
- Long acting: Optisulin
109
Oral hypoglycaemic agents
- Class
- Indication
- Action
- Adverse effects
- Nursing consideration
- 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
Identify the 5 types of OHA
```
Biguanide (First line)
SGLT2 inhibitors
Gliptins
Sulfonylureas
Thiazolidinedione
```
111
What determines what type of OHA one has?
Choice depends on the individuals weight, response to trailed drugs, pancreatic and liver functions
112
Example of Biguanide
Metformin
113
Example of SGLT2 inhibitors
Dapaglifflozin
114
Example of DPP-4 inhibitors/gliptins
Alogliptin
115
Example of Sulfonylureas
Glibenclamide
116
Example of Thiazolidinedione
Pioglitazone
117
Glucose elevating agents
- Class
- Indication
- Action
- Adverse effects
- Nursing consideration
- 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
Example of glucose elevating agent
Glucose (PO/IV)
| Glucagon (Used in unconscious) (SC, IM, IV)
119
Identify the two types of Glucocorticoids
Hydrocortisone and Prednisolone
120
Glucocorticoids
- Class
- Indication
- Action
- Adverse effects
- Nursing consideration
- 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
Mineralcorticoids
- Class
- Indication
- Action
- Adverse effects
- Nursing consideration
- 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
Antithyroid agents
- Class
- Indication
- Action
- Adverse effects
- Nursing consideration
- 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
What is an example of antithyroid agents
Carbimazole
124
Iodine
- Class
- Indication
- Action
- Adverse effects
- Nursing consideration
- Iodine
- Hyperthyroidism, relieve symptoms, maintain euthyroid state
- Transiently inhibits thryoid hormone release
- Hypersensitivity reactions
- Long term use may exacerbate hyperthyroidism
125
What is another form of medication used in the treatment of hyperthyroidism?
Beta blockers: Short term relief of symptoms, e.g. propranolol
126
Thyroxine Sodium
- Class
- Indication
- Action
- Adverse effects
- Nursing consideration
- 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
What are the 3 names for thyroxine sodium
T4
Levothyroxine
L-thyroxine sodium)
128
What is an example of thyroxine sodium
Eltoxin
| Oroxine
129
Identify the management of hypoglycaemia in a unconscious state
SC or IM injection 1mg glucagon
IV administration 50mL 50% glucose
Determine cause
