Endocrinology Flashcards
1
Q
Definition of Diabetes Mellitus Type I
A
Metabolic autoimmune disorder from destruction of insulin producing beta cells in the pancreas, results in absolute insulin deficiency
2
Q
Is DM Type I more common in Women or Men?
A
Women
3
Q
At what age is DM Type I most commonly diagnosed?
A
Commonly diagnosed in youth
4
Q
What causes DM Type I? (Aetiology)
A
- Environmental factors / viruses may trigger the destruction of beta cells
- HLA-DR and HLA-DQ provide protection from / increase susceptibility to it
5
Q
Name all risk factors for DM Type I.
A
- Geographic region (European >Asian)
- genetic predisposition
- infectious agents
- Dietary factors
6
Q
What are the key presentations of DM Type I?
A
Polyuria, polydipsia, blurred vision, fatigue / tiredness
7
Q
Explain the pathophysiology of DM Type I.
A
- usually develops as a result of autoimmune pancreatic beta-cell destruction
- ~90 % will have autoantibodies
8
Q
How many beta cells have to be destroyed for hyperglycaemia to develop (DM Type I) ?
A
80 - 90 %
9
Q
What does long term hyperglycaemia lead to?
A
- induces oxidative stress and inflammation
2. Oxidative stress caused endothelial dysfunction via NO
10
Q
Name the signs of DM Type I.
A
- Young age (<50)
- Weight loss
- low BMI
- FHx of autoimmune disease
- Ketoacidosis
11
Q
Name the symptoms of DM Type I.
A
- Thirst
- Dry mouth
- Lack of energy
- Blurred vision
- Hunger
- Weight loss
12
Q
Name the first-line investigations of DM Type I.
A
- Random glucose tolerance test
- Fasting plasma glucose
- 2-hour plasma glucose
- plasma/urine ketones
13
Q
Name the gold standard investigation of DM Type I and expected result.
A
- Glycated Haemoglobin A1c (HbA1c) test
2. 42 - 47 mmol/L (prediabetes), >48 mmol/L (diabetes)
14
Q
Name other investigations that can be useful in investigating DM Type I.
A
C peptide levels
15
Q
Differential diagnoses of DM Type I include…
A
DM Type II, other diabetes subtypes
16
Q
Name the first-line treatment of DM Type I.
A
- Basal - bolus insulin (glargine s/c)
- Pre-meal insulin correction dose
- Amylin analogue (pramlintide)
17
Q
Name the second-line treatment of DM Type I.
A
fixed insulin dose
18
Q
List the side effects of insulin prescribed in DM Type I.
A
- Hypoglycaemia
- Weight gain
- Lipodystrophy
19
Q
How do you monitor a patient with DM Type I?
A
- Check BP at each visit, should be <140 / 90 mmHg
2. Check lipid profile in adults with diabetes at the time of first diagnosis/initial medical evaluation / 5-yearly
20
Q
Name any microvascular complications of DM Type I.
A
- Retinopathy
- Nephropathy
- Neuropathy
21
Q
Name any macrovascular complications of DM Type I.
A
- CAD
- Cerebrovascular disease
- PAD
22
Q
What is the prognosis for a patient with DM Type I?
A
Untreated - fatal due to diabetic ketoacidosis
Poorly controlled - RF for blindness, renal failure, foot amputations and MIs
23
Q
Define DM Type II.
A
Lifelong chronic disease characterised by insulin resistance and relative insulin deficiency
24
Q
Is DM Type I or II more common in general?
A
DM Type II
25
Is DM Type II more common in younger or older people?
Older people (onset is usually >30 years)
26
Is DM Type II more common in people with a specific ethnicity?
Yes, African / Asian
27
What causes DM Type II? (Aetiology)
1. Genetic susceptibility but no HLA link
| 2. Insulin resistance aggravated by ageing, physical inactivity and being overweight
28
Name all risk factors for DM Type II.
1. older age (increasing at younger age recently)
2. Being overweight / obese
3. gestational diabetes
4. pre-diabetes
5. FHx of Type II
6. non-white ethnicity
7. physical inactivity
8. Hypertension
9. CVD
10. stress
29
What is the pathophysiology of DM Type II?
1. polygenic
2. Environmental factors trigger onset in genetically susceptible
3. Beta cell mass reduction
4. Low insulin secretion
5. Peripheral insulin resistance
30
How many beta cells have to be destroyed to cause DM Type II?
~ 50 %
31
What are the key presentations of patients with DM Type II?
Polyuria, polydipsia, fatigue, blurred vision, polyphagia, candida and skin infections, UTIs
32
What are the signs of DM Type II?
Presence of risk factors
33
What are the symptoms of DM Type II?
Thirst, Dry mouth, lack of energy, Blurred vision, neuropathy
34
Name the first-line investigations of DM Type II.
1. HbA1c test
2. fasting plasma glucose
3. random plasma glucose
35
Name the gold standard investigation of DM Type II.
Oral glucose tolerance test (OGTT)
36
Name any other investigations that can be done in patients with suspected DM Type II.
1. urine ketones
2. fasting lipid profile
3. random c peptide
4. serum creatinine and eGFR
37
Differential diagnoses of DM Type II include...
Prediabetes, DM Type I, any other subtypes of diabetes
38
What is the first-line management of DM Type II?
1. Diet and exercise changes
2. if these do not have an effect then Biguanide (Metformin)
3. +sulfonylurea (glicazide) OR DPP4 inhibitor (Sitagliptin)
4. +sulfonylurea (glicazide) AND DPP4 inhibitor (Sitagliptin)
5. +insulin
39
How do you monitor a patient with DM Type II?
1. regular monitoring and control of BP, HbA1c, tobacco use, and statin/aspirin use
2. diabetes assessment every 3-4 months
3. eye examination ever 1 - 2 years
4. Renal function assessment annually
5. Foot examinations
40
Name any complications of DM Type II.
```
Diabetic ketoacidosis, DIabetic nephropathy,
Diabetic neuropathy
Diabetic retinopathy,
Hyperosmolar hyperglycaemia,
CVD,
Stroke
```
41
What is the prognosis for someone with DM Type II?
Men lose an average of 5.8 years of life, Women an average of 6.8 years of life, excess mortality ~15% higher
42
What is the definition of Grave's disease?
It is an autoimmune thyroid condition associated with hyperthyroidism.
43
Is Grave's disease more common in women or men?
Women
44
Is Grave's disease more common at what age?
Older age (>40)
45
What ethnicity/ies is Grave's disease most commonly associated with?
White and Asian
46
In which countries is grave's disease the most common cause of hyperthyroidism?
In countries with sufficient iodine intake.
47
What causes Grave's disease? (Aetiology)
1. autoimmune condition
| 2. combination of genetic (80%) and environmental factors (20%)
48
Name all risk factors for Grave's disease.
1. FHx of autoimmune conditions
2. Female sex
3. smoking
4. High iodine intake
5. Lithium therapy
6. Stress
49
What is the pathophysiology of Grave's disease?
1. Thyroid stimulating immunoglobulins recognise and bind to the TSH receptor which stimulates T4 and T3
2. thyroxine (T4) receptors in the pituitary gland are activated by excess hormone
3. reduced release of TSH in a negative feedback look 4. Very high levels of circulating thyroid hormones, with a low TSH
50
What are the key presentations of Grave's disease?
Tachycardia, tremors, eye problems (buldging outwards and lid retraction), weight loss, onycholysis (detachment of nail from nail bed)
51
What are the signs of Grave's disease?
diffuse palpable goitre with audible bruit, high T3 and T4, lower TSH than normal, presence of risk factors
52
What are the symptoms of Grave's disease?
Rapid heartbeat, tremors, Heat intolerance (High body temp), sweating, muscle weakness
53
What are the first-line investigations for Grave's disease and expected results?
- TSH (low)
- serum free / total T4 (elevated)
- serum free or total T3 (elevated)
- total T3/T4 or FT3/FT4 ratio (high)
54
What are the gold standard investigations for Grave's disease and the expected result?
- TSH receptor antibody test (TRAb)
| - positive
55
Name any other test that can be used to investigate Grave's disease.
- Thyroid ultrasound
- CT / MRI of orbit
- Thyroid isotope scan
- Radioactive Iodine uptake
56
Differential diagnoses for Grave's disease include...
- Toxic nodular goitre
- gestational hyperthyroidism
- iodine-induced hyperthyroidism
57
What is the first-line treatment of Grave's disease?
1. Antithyroid drugs (carbimazole/thiamayzole) with dose titration or 'block and replace'.
2. Radioactive iodine +/- corticosteroid Thyroidectomy
58
What are adjunct treatments for Grave's disease?
1. Treatment for orbitopathy (methylprednisolone) and dermopathy (triamcinolone acetonide topical)
59
How do you monitor a patient with Grave's disease?
serum TSH at 6-week intervals until stable, then with serum TSH at least annually, orbitopathy follow-up
60
Name complications associated with Grave's disease and its treatment.
- Thyroid storm – high heart rate, BP and Body temp (treat with propylthiouracil)
- bone mineral loss
- atrial fibrillation
- congestive heart failure
61
What is the prognosis for a patient with Grave's disease?
- Increased mortality (CV)
- high degree of relapse
- excellent prognosis following antithyroid medication therapy
62
Define Hashimoto's thyroiditis (long)
Autoimmune mediated inflammation of thyroid gland with release of TH resulting in transient hyperthyroidism (very rare usually straight hypo), frequently followed by hypothyroid phase before recovery of normal thyroid function
63
Give a simple definition of Hashimoto's thyroiditis
Hypothyroidism due to aggressive destruction of thyroid cells
64
Is Hashimoto's thyroiditis more common in men or women?
Women
65
At what age is Hashimoto's thyroiditis most common?
older age (~60 - 70)
66
In which areas is Hashimoto's thyroiditis the most prevalent?
In areas with excess iodine intake.
67
What causes Hashimoto's thyroiditis? (Aetiology)
- Unknown cause
- Autoimmune condition
- some genetic element
- Triggers: iodine, infection, smoking
68
Name all the risk factors for Hashimoto's thyroiditis.
1. postnatal thyroiditis
2. thyroid peroxidase antibodies (TPO)
3. Female sex
4. FHx
5. Lithium therapy
6. immune-modulatory therapy
69
What is the pathophysiology of Hashimoto's thyroiditis?
1. Aggressive destruction of thyroid cells by various cell and antibody mediated immune processes
2. Antibodies bind and block TSH receptors
3. inadequate thyroid hormone production and secretion
70
What are the key presentations of Hashimoto's thyroiditis?
```
- heat intolerance
weight loss / gain,
- excessive fatigue
- small non-tender goitre
- bloating
- muscle cramps,
- Thyroid gland may enlarge rapidly
```
71
What are the signs of Hashimoto's thyroiditis?
- small non-tender goitre
- palpitations
- tachycardia
72
What are the symptoms of Hashimoto's thyroiditis?
- nervousness
- excessive fatigue
- bloating
- poor concentration
73
What are the first-line investigations for Hashimoto's thyroiditis and the expected results?
- serum-free T3 and T4 (elevated = thyrotoxicosis, low = hypothyroid phase)
- TPO antibodies (positive)
74
What is the gold standard investigation for Hashimoto's thyroiditis?
- TSH
- low = thyrotoxicosis
- elevated = hypothyroid phase
75
Name any other tests used to investigate Hashimoto's thyroiditis.
Thyroid biopsy, total T3 / T4 ratio
76
Differential diagnoses for Hashimoto's thyroiditis include...
Grave's disease, toxic multinodular goitre
77
What is the first-line treatment for Hashimoto's thyroiditis?
Thyroid hormone replacement (Levothyroxine) and resection of obstructive goitre
78
How do you monitor a patient with Hashimoto's thyroiditis?
monitored with period thyroid-stimulating hormone measurements
79
List any complications of Hashimoto's thyroiditis.
Hyperlipidaemia and consequences
80
Define primary Hypothyroidism
Underproduction of thyroid hormone T3, T4 specifically failure to produce thyroid hormones by the thyroid gland
81
Is primary hypothyroidism more common in women or men ?
Women
82
At what age is primary hypothyroidism more common?
Older age
83
What causes primary hypothyroidism? (Aetiology)
Autoimmune hypothyroidism (Hashimoto's), iodine deficiency, congenital defects
84
Name all risk factors for primary Hypothyroidism.
- Iodine deficiency
- Female sex
- Age
- FHx
- autoimmune disorder
- Grave's disease
85
What is the pathophysiology of primary hypothyroidism?
1. Aggressive destruction of thyroid cells by various cell and antibody-mediated immune processes.
2. Antibodies bind and block TSH receptors
3. inadequate thyroid hormone production and secretion
86
What are the key presentations of primary Hypothyroidism?
presence of risk factors, non-specific symptoms
87
What are the symptoms of primary hypothyroidism?
weakness, lethargy, cold sensitivity, constipation, weight gain, depression, myalgia, dry or coarse skin, eyelid oedema, facial oedema, coarse hair
88
What is the first-line investigation for primary Hypothyroidism and the expected results?
- TSH (low = thyrotoxicosis, elevated = hypothyroid phase)
89
What is the gold standard investigation for primary Hypothyroidism and the expected results?
- TSH (low = thyrotoxicosis, elevated = hypothyroid phase)
90
Name any other investigations that can be used to investigate primary Hypothyroidism.
Free serum T4, serum cholesterol, antithyroid peroxidase antibodies
91
Name the differential diagnoses of primary Hypothyroidism.
Central/secondary hypothyroidism, depression, Alzheimer's dementia, Anaemia
92
What is the first-line treatment of primary Hypothyroidism?
Thyroid hormone replacement (Levothyroxine)
93
How do you monitor a patient with primary hypothyroidism?
- thyroid-stimulating hormone (TSH) should be measured 4-6 weeks after initiation of therapy or dosage change
- Stable patients with normal serum TSH should have TSH measured every 12 months
94
List any complications of primary Hypothyroidism.
Myxoedema coma:
- 20-50% mortality
- Reduced level of consciousness
- seizures
- hypothermia
95
What is the prognosis for a patient with primary hypothyroidism?
generally excellent with full recovery upon adequate replacement of thyroid hormones
96
Define s/c hypothyroidism.
Decreased TSH causing low TH synthesis resulting from hypofunction of Anterior pituitary or Hypothalamus
97
Does s/c hypothyroidism have a sex / age predominance.
No.
98
Is s/c hypothyroidism very common?
No, it is rare and accounts for <1% of hypothyroidism.
99
What causes s/c hypothyroidism? (Aetiology)
Hypopituitarism - pituitary adenomas / infection
| hypothalamic disorders - neoplasms, trauma
100
List all risk factors for s/c hypothyroidism
Multiple endocrine neoplasia (Type I), head and neck irradiation, traumatic brain injury
101
What is the pathophysiology of s/c hypothyroidism?
1. Reduced release or production of TSH or decreased stimulation of anterior pituitary by TRH causing deficiency of TSH
2. reduced T3 and T4 release
102
What are the key presentations of s/c hypothyroidism?
Dry/ coarse skin, reduced body and scalp hair, muscle cramps, Presence of risk factors, fatigue, cold intolerance, weakness
103
What are the signs of s/c hypothyroidism?
Bradycardia
104
What are the symptoms of s/c hypothyroidism?
Weight gain, constipation, dry skin
105
What are the first-line investigations of s/c hypothyroidism and the expected results?
Free serum T4 (low),
| TSH (low / normal)
106
What are the gold standard investigations of s/c hypothyroidism and the expected results?
Free serum T4 (low),
| TSH (low / normal)
107
Name any other tests that might be done to investigate s/c hypothyroidism.
Brain MRI, head CT
108
Name the differential diagnoses of s/c hypothyroidism.
primary hypothyroidism, non-thyroidal illness, iodine deficiency, chronic fatigue syndrome, depression
109
What is the first-line management of s/c hypothyroidism?
Thyroid hormone replacement (Levothyroxine)
110
Name adjunct treatments of s/c hypothyroidism.
treatment of underlying pituitary tumour, if adrenal insufficiency then corticosteroids
111
How do you monitor a patient with s/c hypothyroidism?
Measurement of serum free thyroxine (T4) should be performed 4 to 8 weeks after new levothyroxine dose, then yearly
112
List complications of s/c hypothyrodism.
Myxoedema coma:
- 20-50% mortality
- Reduced level of consciousness
- seizures
- hypothermia
113
What is the prognosis for a patient with s/c hypothyroidism?
Prognosis dependent on underlying aetiology, for pituitary adenomas is dependent on the size and functionality
114
Define papillary thyroid cancer.
Cancer that forms in follicular cells in the thyroid and grows in finger-like shapes, Named for the papillae among its cells on microscopy
115
What % of thyroid cancers are classed as papillary?
~70%
116
Is papillary thyroid cancer more prevalent in women or men?
It is 3 x more common in women
117
Is papillary thyroid cancer more common in younger or older people?
Young people
118
What causes papillary thyroid cancer? (Aetiology)
- Mutation
| - usually well differentiated with a tendency towards multi-centricity and lymph node involvement
119
What are the risk factors for papillary thyroid cancer?
- head and neck irradiation
- female sex
- FHx of thyroid cancer
120
What is the pathophysiology of papillary thyroid cancer?
- tends to spread locally in the neck especially local lymph nodes
- often compresses the trachea
121
What are the key presentations of papillary thyroid cancer?
- presence of risk factors
- asymptomatic palpable thyroid nodule (hard and fixed)
- (possibly) enlarged lymph nodes on examination
- young age
FHx
122
What are the signs of papillary thyroid cancer?
tracheal deviation, palpable thyroid nodule
123
What are the symptoms of papillary thyroid cancer?
Hoarseness, dyspnea, dysphagia
124
What are the first-line investigations for papillary thyroid cancer and expected results?
- TSH (normal)
| - Ultrasound of the neck (nodule-no / characteristic)
125
What is the gold standard investigation for papillary thyroid cancer and expected results?
- Fine-needle aspiration biopsy (intranuclear holes and grooves)
126
What other tests can be used to investigate papillary thyroid cancer?
Free T4 and T3, CT of neck
127
Name the differential diagnosis of papillary thyroid cancer.
Benign thyroid nodule
128
What is the first-line management of papillary thyroid cancer?
1. surgery
2. radioactive iodine ablation
3. TSH suppression (levothyroxine)
129
How do you monitor a patient with papillary thyroid cancer?
- radioactive iodine scan post-operatively when the patient becomes hypothyroid (generally in 4 to 6 weeks)
- The scan detects residual thyroid tissue in the neck and also metastases, followed by ablation of residual cells with radioiodine
130
Name complications of the treatment of papillary thyroid cancer.
TSH suppression related atrial fibrillation
131
What is the prognosis of a patient with papillary thyroid cancer?
Best when young and female
132
Define anaplastic thyroid cancer.
Uncontrolled growth of cells in the thyroid gland, “one of the most aggressive cancers in humans”
133
What % of thyroid cancers are classed as anaplastic?
It is very rare, <5%
134
Does anaplastic thyroid cancer respond well to treatment?
No, usually poor response to treatment
135
Is anaplastic thyroid cancer more common in younger or older patients?
More common in elderly patients
136
List the risk factors for anaplastic thyroid cancer.
- Head and neck irradiation
- Female sex
- FHx of thyroid cancer
137
What is the pathophysiology of anaplastic thyroid cancer?
- affects the Follicular cells of the thyroid, but does not retain original cell features like iodine uptake or synthesis of thyroglobulin. - undifferentiated carcinoma with a high propensity for local invasion (recurrent laryngeal nerve and trachea, muscle, and/or oesophagus)and metastatic spread.
138
What are the key presentations of anaplastic thyroid cancer?
- presence of risk factors
- asymptomatic palpable thyroid nodule (hard and fixed)
- (possibly) enlarged lymph nodes on examination
139
What are the signs of anaplastic thyroid cancer?
Tracheal deviation, palpable thyroid nodules
140
What are the symptoms of anaplastic thyroid cancer?
Hoarseness, dyspnea, dysphagia
141
What are the first-line investigations for anaplastic thyroid cancer and expected results?
- TSH (normal)
| - Ultrasound of the neck (nodule-no / characteristic)
142
What is the gold-standard investigation for anaplastic thyroid cancer and expected results?
- Fine-needle aspiration biopsy (wide variations in appearance)
143
What other tests can be used to investigate anaplastic thyroid cancer?
Free T4 and T3, CT of the neck
144
The differential diagnosis for anaplastic thyroid cancer is?
Benign thyroid nodule
145
What is the first-line management of anaplastic thyroid cancer?
total thyroidectomy done when possible otherwise palliative care + chemoradiation
146
What are adjunct managements of anaplastic thyroid cancer?
Thyroid replacement (medication)
147
Name the complications of the treatment of anaplastic thyroid cancer.
TSH suppression related atrial fibrillation
148
What is the prognosis for a patient with anaplastic thyroid cancer?
Average survival a few months, high propensity for local invasion and metastatic spread
149
Define follicular thyroid cancer.
Well-differentiated thyroid cancer like papillary thyroid cancer but more malignant
150
What percentage of thyroid cancers are classified as follicular?
20%
151
In what areas is follicular thyroid cancer more prevalent?
areas of low iodine intake
152
In patients at what age is follicular thyroid cancer most common?
Middle-aged patients
153
What causes follicular thyroid cancer? (Aetiology)
chromosomal translocation
154
List all risk factors for follicular thyroid cancer.
1. Head and neck irradiation
2. Female sex
3. FHx of thyroid cancer
155
What is the pathophysiology of follicular thyroid cancer?
- early forms indolent but invasive forms aggressive
- May infiltrate neck, but greater propensity to metastasise to lung and bones
- spreads haematogenously
156
What are the key presentations of follicular thyroid cancer?
- presence of risk factors
- asymptomatic palpable thyroid nodule (hard and fixed)
- (possibly) enlarged lymph nodes
157
What are the signs of follicular thyroid cancer?
- tracheal deviation
| - palpable thyroid nodule
158
What are the symptoms of follicular thyroid cancer?
- Hoarseness
- dyspnea
- dysphagia
159
What are the first-line investigations for follicular thyroid cancer and expected results?
- TSH (normal)
| - Ultrasound of the neck (nodule-no / characteristic)
160
What is the gold standard investigation for follicular thyroid cancer and the expected result?
- Fine-needle aspiration biopsy (hypercellularity, micro follicles)
161
Name any other test used to investigate follicular thyroid cancer.
Free T4 and T3, CT of the neck
162
Name the differential diagnosis for follicular thyroid cancer.
Benign thyroid nodule
163
What is the first-line management of follicular thyroid cancer?
1. surgery
2. radioactive iodine ablation
3. TSH suppression (levothyroxine)
164
How do you monitor a patient with follicular thyroid cancer?
- radioactive iodine scan post-operatively when the patient becomes hypothyroid (generally in 4 to 6 weeks)
- The scan detects residual thyroid tissue in the neck and also metastases, followed by ablation of residual cells with radioiodine
165
Name the complications of the treatment of follicular thyroid cancer.
TSH suppression related atrial fibrillation
166
What is the prognosis for a patient with follicular thyroid cancer?
- worse than papillary
| - tends to have systemic metastases
167
Define medullary thyroid cancer.
Cancer that develops in the c cells of the thyroid – cells that make calcitonin to maintain healthy level of calcium in the blood
168
What percentage of thyroid cancers is classified as medullary?
5%
169
What causes medullary thyroid cancer? (Aetiology)
Mutations
170
List the risk factors for medullary thyroid cancer.
1. Head and neck irradiation
2. Female sex
3. FHx of thyroid cancer (25% of medullary cancers as part of familial syndrome)
171
What is the pathophysiology of medullary thyroid cancers?
- Parafollicular calcitonin-producing C cells.
- Produce large amounts of peptide such as calcitonin, occurs in sporadic and familial forms
- tendency to multi-centricity and early lymph node spread
172
What are the key presentations of medullary thyroid cancer?
- Presence of risk factors
- palpable thyroid nodule
- young age
- Diarrhoea
- flushing epidoses
- itching
- FHx
173
Is medullary thyroid cancer more common in younger or older people?
younger people
174
What are the signs of medullary thyroid cancer?
tracheal deviation, palpable thyroid nodule
175
What are the symptoms of medullary thyroid cancer?
Hoarseness, dyspnea, dysphagia
176
What are the first-line investigations for medullary thyroid cancer and expected results?
- TSH (normal)
- Ultrasound of the neck (nodule-no / characteristic)
- serum calcitonin (postive)
177
What is the gold standard investigation for medullary thyroid cancer and expected result?
- Fine-needle aspiration biopsy (eosinophilic cells arranged in nests or sheets separated by amyloid and vascular stroma, staining +ve for calcitonin)
178
Name any other tests that can be used to investigate medullary thyroid cancer.
- Free T4 and T3, CT of neck
179
Name the differential diagnosis for medullary thyroid cancer.
Benign thyroid nodule
180
What is the first-line management for medullary thyroid cancer?
- total thyroidectomy
| - ± lymph node dissection / radical neck dissection on site of metastasis
181
What is an adjunct teatment of medullary thyroid cancer?
Thyroid replacement (levothyroxine)
182
How do you monitor a patient with medullary thyroid cancer?
- monitored with serum calcitonin every 3 months for 2 years, followed by every 6 months for 3 years, - if levels undetectable then annual follow up
183
Name the complications of the treatment of medullary thyroid cancer.
TSh suppression related atrial fibrillation.
184
What is the prognosis for a patient with medulalry thyroid cancer?
5 year survival for medullary cancer is 80%. (with correct treatment)
185
Define lymphoma thyroid cancer.
Lymphoma (cancer of lymphatic system) that arises from lymphocytes that are present within the thyroid gland
186
What percentage of thyroid cancers is classified as lymphoma?
2%
187
Which thyroid cancer is often associated with Hashimoto's thyroiditis?
Lymphoma
188
What causes lymphoma? (Aetiology)
Rapidly grwing mass in the neck.
189
List the risk factors for lymphoma thyroid cancer.
- head and neck irradiation
- female sex
- FHx of thyroid cancer
190
What is the pathophysiology of lymphoma thyroid cancer?
almost always non-hodkins lymphoma
191
What are the key presentations of lymphoma thyroid cancer?
Presence of risk factors, palpable thyroid nodule
192
What are the signs of lymphoma thyroid cancer?
tracheal deviation, palpable thyroid nodule
193
What are the symptoms of lymphoma thyroid cancer?
Hoarseness, dyspnea, dysphagia
194
What are the first-line investigations for lymphoma thyroid cancer and expected results?
- TSH (normal)
| - Ultrasound of the neck (nodule-no / characteristic)
195
What is the gold standard investigation for lymphoma thyroid cancer?
Fine-needle aspiration biopsy (may be identified by flow cytometry and nuclear atypia)
196
Name any other test that can be used to investigate lymphoma thyroid cancer.
Free T3 and T4, CT of neck
197
Name the differnetial diagnosis of lymphoma thyroid cancer.
Benign thyroid nodule
198
What is the first line management of lymphoma thyroid cancer?
Chemotherapy + external radiation
199
Name the complications of the treatment of lymphoma thyroid cancer.
TSH suppression related atrial fibrillation
200
What is the prognosis for a patient with lymphoma thyroid cancer?
5 year survival <50%
201
Define Cushing's syndrome.
metabolic disorder caused by overproduction of corticosteroid hormones by the adrenal cortex and often involving obesity and high blood pressure – persistently and inappropriately elevated circulating glucocorticoid (cortisol)
202
What is the incidence rate of cushing's syndrome?
1/100,000
203
How many cases of cushing's syndrome are cushing's disease?
2 / 3 of cases
204
Are cushing's syndrome and disease more common in men or women?
Women
205
What are the two types of cushing's syndrome?
ACTH (adrenocorticotropic hormone) dependent disease and Non-ACTH dependent disease
206
What causes ACTH dependent cushing's syndrome? (Aetiology)
- excessive ACTH from pituitary
- ACTH producing tumour (most common)
- excess ACTH administration
207
What causes Non-ACTH dependent cushing's syndrome? (Aetiology)
- adrenal adenomas
- adrenal carcinomas
- excess glucocorticoid administration
208
List the risk factors for Cushing's syndrome.
- Exogenous corticosteroid use
- pituitary adenoma
- adrenal adenoma
- adrenal carcinoma
209
What is the pathophysiology of Cushing' syndrome?
- Many features due to protein-catabolic effects of cortisol; thin skin, easy bruising, striae.
- Excessive alcohol consumption can mimic the clinical and biochemical signs (Pseudo-Cushings's), but resolves on alcohol recession
210
What are the key presentations of Cushing's syndrome?
- Presence of risk factors
- Obesity (fat distribution centrally, buffalo hump)
- plethoric complexion
- rounded 'moon' face
- thin skin
- pathological fractures
- hypertension
211
What are the signs of Cushing's syndrome?
- pathological fractures
| - hypertension
212
What are the symptoms of Cushing's syndrome?
- Acne
- weight gain
- easy bruisability
- weakness
- unexplained fractures
- striae
213
What are the first-line investigations for cushing's syndrome and expeced results?
- Serum glucose (elevated)
- late night salivary cortisol (elevated)
- 48h low dose dexamethasone 2mg test (elevated)
- Urine preg test (negative)
- 24h urinary free cortisol (raised)
214
What is the gold standard test for cushing's syndrome and expected result?
- Petrosal snus sampling
| elevated central / peripheral ACTH ratio indicates pituitary source
215
Name any other test that can be used to investigate Cushing's syndrome.
Renal / pituitary CT or MRI, morning plasma ACTH
216
DIfferential diagnoses of cushing's syndrome include...
Obesity and metabolic syndrome
217
What is the first line management of Cushing's syndrome?
Tumour: surgical removal
| Cortisol synthesis inhibition: metyrapone, ketoconazole
218
How do you monitor a patient with cushing's syndrome?
Periodical screening for recurrence of the disease
219
What are the complications of Cushing's syndrome?
1. Hypertension
2. Obesity
3. CVD
4. DM
5. Death
6. Adrenal insufficiency
220
What is the prognosis for a patient with Cushing's syndrome?
- Untreated survival rate is 50% at 5 years
| - Cushing's syndrome generally has rare remission
221
Define Cushing's disease.
When elevated glucocorticoid is attributed to inappropriate ACTH secretion from the pituitary
222
Define Acromegaly.
Overgrowth of all organ systems due to excess GH being secreted 99% due to pituitary tumour
223
What is the no of cases of Acromegaly in the UK per eyar?
~3 million cases / year
224
Is Acromegaly more prevalent in women or men?
M = W
225
At what age is Acromegaly usualy diagnosed?
Middle age
226
What causes Acromegaly? (Aetiology)
- 99% of cases due to pituitary adenoma
| - other: hyperplasia due to neuroendocrine carcinoid tumour that overproduced GH-releasing hormone
227
What are the risk factors for Acromegaly?
Multiple endocrine neoplasia Type 1 syndrome, Carney's complex
228
What is the pathophysiology of Acromegaly?
- Pituitary cells physiologically regulated by hormones, transcription factors, growth factors that stimulate their proliferation and hormone production throughout life.
- Dysregulation of these signalling pathways can promote tumour development.
- Pituitary somatotroph adenomas chronically secrete excessive growth hormone, which stimulates insulin-like growth factor 1 production leading to the majority of the clinical manifestations of the disease
229
What are the key presentations of Acromegaly?
- Coarsening of face
- carpal tunnel syndrome
- joint pain
230
What are the signs of Acromegaly?
- Increased growth of hand
- Coarsening face
- Wide nose
- Macroglossia
- Widely spaced teeth
- puffy lips/eyelids/ skin
231
What are the symptoms of Acromegaly?
- Acroparaesthesia
- Amenorrhoea
- Headache
- increased sweating
- snoring
- arthralgia
- back ache
- alterations in sexual functioning
232
What are the first-line investigations for Acromegaly and expected results?
- OGTT (GH value >1 microgram/L)
- IGF-1 (elevated)
- random serum GH (elevated)
233
What is the Gold standard test for Acromegaly and expected result?
OGTT (GH value >1 microgram/L)
234
Name any other tests that can be used to investigate Acromegaly.
Pituitary MRI, prolactin, Visual field testing (deficit if pressing on optic chiasm)
235
Differential diagnoses for Acromegaly include...
Pseudo-acromegaly
236
What is the first-line management of Acromegaly?
Transsphenoidal resection surgery
237
List adjunct treatments for Acromegaly.
1. Dopamine agonist (Cabergoline)
2. somatostatin analogues (Ocreotide)
3. GH receptor antagonist (Pegvisomant)
238
How do you monitor a patient with Acromegaly?
Lifelong monitoring of growth hormone and IGF-1
239
List the complications of Acromegaly.
- Hypertension
- DM
- untreated adenoma can impact optic chiasm (blidness)
240
What is the prognosis for a patient with Acromegaly?
May return to normal.
241
What differentiates gigantism from acromegaly?
Gigantism happens when the condition happens before the fusion of epiphyseal plates.
242
Define Conn's syndrome.
Excessive production of aldosterone, independent of the renin-angiotensin system
243
What causes Conn's syndrome? (Aetiology)
Solitary aldosterone-producing adenoma – linked to mutations in K+ channels
244
List the risk factors for Conn's syndrome.
1. FHx of primary aldosteronism
| 2. FHx of early onset Hypertension and/or stroke
245
What is the Pathophysiology of Conn's syndrome?
- Aldosterone causes exchange of transport of sodium & potassium in the distal renal tubule.
- hyperaldosteronism causes increased reabsorption of sodium & excretion of potassium
246
What are the key presentations of Conn's syndrome?
- presence of risk factors
| - Hypertension
247
What are the signs of Conn's syndrome?
Muscle cramps, muscle weakness, palpitations, polyuria, lethargy
248
What are the symptoms of Conn's syndrome?
Nocturia, polyuria, lethargy, mood disturbance, difficulty concentrating
249
What are the first-line investigations of Conn's syndrome and expected results?
- Plasma K+ (normal / low)
| - Aldosterone / renin ratio
250
What is the gold standard investigation for Conn's syndrome and expected result?
Selective adrenal vein sampling
| - > unilateral (most common in conn’s)or bilateral production
251
What are the differential diagnoses of Conn's syndrome?
- Essential hypertension
- secondary HTN
- Thiazide induced hypokalaemia
- Liddle syndrome
252
What is the first line management of Conn's syndrome?
Laparoscopic adrenalectomy
253
Name adjunct treatments of Conn's syndrome.
pre operative aldosterone antagonist (Spironolactone)
254
How do you monitor a patient with Conn's syndrome?
BP, plasma electrolytes, and aldosterone and renin levels should be monitored every 6 to 12 months for clinical and biochemical evidence of recurrence
255
What are the complications of Conn's syndrome?
Heart failure, MI, stroke, atrial fibrillation, impaired renal function
256
What is secondary Hyperaldosteronism (NOT Conn's)?
Hyperaldosteronism due to high renin levels
257
Define Addison's disease. (Primary Adrenal insufficiency)
Decreased secretion of hormones (cortisol, aldosterone, dehydroepiandrosterone) by adrenal glands
258
What is the Incidence of Addison's disease?
1 / 10,000
259
What causes Addison's disease? (Aetiology)
Organ-specific autoantibodies in 90% of cases. Rarely: adrenal gland tuberculosis, surgical removal or haemorrhage
260
List all risk factors for Addison's disease.
1. Female sex
2. adrenocortical autoantibodies
3. adrenal haemorrhage
4. TB
5. Autoimmune disease
6. use of anticoagulants
261
What is the pathophysiology of Addison's disease?
- Destruction of adrenal cortex (≥ 90%) leads to cortisol and aldosterone deficiency,
- Excess ACTH stimulates melanocytes
- hyperpigmentation
262
What are the key presentations of Addison's disease?
Presence of risk factors, fatigue, anorexia, weight loss, hyperpigmentation
263
What are the signs of Addison's disease?
Anorexia, hyperpigmentation
264
What are the symptoms of Addison's disease?
Lean, tired, tanned, tearful, dizzy, faints, unexplained abdominal pain and vomiting
265
What are the first-line investigations of Addison's disease and expected results?
- serum electrolytes (low Na+, elevated K+)
- blood urea (may be elevated)
- FBC (anaemia)
- morning serum cortisol (v low levels)
266
What is the gold standard investigation of Addison's disease and expected result?
- ACTH stimulation test (serum cortisol low)
267
What other tests can be used to investigate Addison's disease?
serum ACTH, plasma renin activity, adrenal antibodies
268
Name all differential diagnoses of Addison's disease.
- 2°/ 3° adrenal insufficiency
- Hyperthyroidism
- adrenal suppression due to corticosteroid therapy
269
What is the first-line management of Addison's disease?
Hormone replacement (glucocorticoid (hydrocortisone) and mineralocorticoid (fludrocortisone))
270
How do you monitor a patient with Addison's disease?
Yearly follow up (U&E, BP), regular measurements of bone density
271
List all complications of Addison's disease.
Adrenal crisis can lead to death, secondary Cushing's syndrome, osteopenia/porosis
272
Define secondary adrenal insufficiency.
Condition where pituitary gland does not produce enough ACTH meaning adrenal gland does not produce enough cortisol
273
What is the incidence of secondary adrenal insufficiency.
2 / 10,000
274
What causes secondary adrenal insufficiency? (Aetiology)
Usually caused by long term steroid therapy (or hypothalamic – pituitary disease) leading to suppression of pituitary – adrenal axis
275
What is the pathophysiology of secondary adrenal insufficiency?
- Reduction of adrenal cortex stimulation by pituitary
- Less cortical products. Low ACTH
- less melanocytes stimulation
- no pigmentation
276
What are the key presentations of secondary adrenal insufficiency?
- Presence of risk factors
- fatigue
- anoxeria / weight loss
277
What are the signs of secondary adrenal insufficiency?
Anorexia
278
What are the symptoms of secondary adrenal insufficiency?
Lean, tired, dizzy, faints
279
What are the first-line investigations of secondary adrenal insufficiency and expected results?
- Long ACTH test = synacthen test (to distinguish from primary - ACTH raised in primary, lowered in secondary)
- serum electrolytes (low Na+, elevated K+)
- blood urea (may be elevated)
- FBC (anaemia)
- morning serum cortisol (v low levels)
280
What is the gold standard investigation of secondary adrenal insufficiency and expected results?
ACTH stimulation test (serum cortisol low)
281
What are the differential diagnoses of secondary adrenal insufficiency?
Addison's disease, adrenal suppression due to corticosteroid therapy
282
What is the first-line management of secondary adrenal insufficiency?
Hormone replacement glucocorticoid (hydrocortisone), if from steroid therapy then remove steroids very slow
283
How do you monitor a patient with secondary adrenal insufficiency?
- Yearly follow up (U&E, BP), regular measurements of bone density
284
Define adrenal hyperplasia (congenital).
Defective enzymes mediating the production of adrenal cortex products
285
What causes adrenal hyperplasia? (aetiology)
Genetic 21-hydroxylase deficiency is the cause of about 95% of cases.
286
What is a risk factor for adrenal hyperplasia?
Genetic predisposition
287
What is the pathophysiology of adrenal hyperplasia?
- Defective 21-hydroxylase
- disruption of cortisol biosynthesis
- causes cortisol deficiency, with or without aldosterone deficiency and androgen excess
- severe forms = aldosterone deficiency -> salt loss
288
What are the key presentations of adrenal hyperplasia?
Genetic predisposition, weight loss, failure to thrive, vomiting, hypotension, ambiguous genitalia
289
What are the signs of adrenal hyperplasia in a female patient?
Ambiguous genitalia with common urogenital sinus
290
What are the signs of adrenal hyperplasia in a male patient?
no signs at birth, bar subtle hyperpigmentation and possible penile enlargement
291
What are the symptoms of adrenal hyperplasia?
Weight loss, vomiting, hypotension, failure to thrive
292
What are the first-line investigations for adrenal hyperplasia and expected results?
- serum11-deoxycortisol (elevated)
- serum chem (low Na+, low K+)
- genetic analysis (mutation)
293
What is the gold standard investigation for adrenal hyperplasia and expected result?
- serum17-hydroxyprogesterone (precursor to cortisol) levels = high
294
Name any other tests that can be used to investigate adrenal hyperplasia.
plasma renin activity, pelvic / adrenal ultrasound
295
Name the differential diagnoses of adrenal hyperplasia.
Addison’s disease, Gender identity disorder, renal salt-wasting
296
What is the first-line management of adrenal hyperplasia?
Glucocorticoids: Hydrocortisone
297
Name any adjunct management of adrenal hyperplasia.
Mineralocorticoids: fludrocortisone, If salt loss: NaCl supplement, genital surgery
298
How do you monitor a patient with adrenal hyperplasia?
Children – follow up every 3 months, adults – follow up every 6 months
299
List complications of adrenal hyperplasia.
Adrenal crisis, testicular adrenal rests, short stature
300
What is the prognosis for a patient with adrenal hyperplasia?
Proper treatment – good prognosis and normal life expectancy
301
Define SIADH.
Excessive ADH secretion leading to hypotonic hyponatraemia and conc urine
302
What causes SIADH? (Aetiology)
Disordered hypothalamic-pituitary secretion, or ectopic production of ADH, - Neurological: Tumour, trauma, infection, , CNS disorders
- Pulmonary: Lung small cell cancer (common), mesothelioma, cystic fibrosis, Drugs
303
List all risk factors for SIADH.
- >50
- pulmonary condition
- nursind home residence
- malignancy
- drugs associated with SIADH induction
- CNS disorders
304
What is the pathophysiology of SIADH?
Ectopic production increases the amount of ADH produced, beyond mechanisms of control
305
What are the key presentations of SIADH?
presence of risk factors, nausea, irritability and headache with mild dilutional hyponatraemia, Fits and coma with severe hyponatraemia
306
What are the signs of SIADH?
Absence of hypo/hypervolaemia, absence of signs of adrenal insufficiency / hypothyroidism
307
What are the symptoms of SIADH?
Nausea, vomiting, altered mental status, headache, seizure, coma
308
What is the first-line investigation for SIADH and expected results?
Serum sodium (low), Serum osmolality (low), serum urea (low)
309
What is the gold standard investigation for SIADH and expected results?
Serum sodium (low)
310
Name any other tests that can be used to investigate SIADH.
DIagnostic trial with normal saline, serum TSH
311
Name the differential diagnoses of SIADH.
- Pseudohyponatraemia
- hypo/hypervolaemia
- renal failure
- addison’s disease
- cerebral salt-wasting
312
What is the first-line management of SIADH.
treat underlying cause + restrict fluids , if chronic – ADH suppression
313
How do you monitor a patient with SIADH?
Monitor serum sodium daily until stabilised, regular monitoring after (eg every 6 months)
314
What is the prognosis for SIADH?
If underlying course found and treated, SIADH typically resolves
315
Define central / cranial diabetes insipidus?
Disease that occurs when the body has lower than normal amounts of ADH due to reduced synthesis or release of ADH (= Arginine vasopressin, AVP)
316
Is central / cranial diabetes insipidus more prevalent in men or women?
M = W
317
Is central / cranial diabetes insipidus very common?
No, generally uncommon (1 in 25,000)
318
What causes central / cranial diabetes insipidus? (Aetiology)
- Acquired – Pituitary surgery, post traumatic head injury, Craniopharygioma, idiopathic (Phenytoin, temozolomide), autoimmune disorder,
- Genetic – Mutations in the ADH gene
319
What are the risk factors for central / cranial diabetes insipidus?
- Pituitary surgery
- craniopharyngioma
- pituitary stalk lesions
- traumatic brain injury
- medication
- autoimmune disease
- FHx
- genetic mutations
320
What is the pathophysiology of central /cranial diabetes insipidus?
- Results from any condition that impairs the production, transportation, or release of AVP.
- Disease of the hypothalamus, where ADH is produced -> Insufficient ADH production. Interestingly, damage to the Posterior Pituitary gland, does not lead to ADH deficiency, as it can still 'leak' out.
321
What are the key presentations of central / cranial diabetes insipidus?
polyuria, compensatory polydispsia
322
What are the signs of central / cranial diabetes insipidus?
FHx, genetic mutations, history of pituitary / hypothalamic disease, history of autoimmune disorders
323
What are the symptoms of central / cranial diabetes insipidus?
Nocturia, polydipsia, polyuria
324
What are the first-line investigations for cranial / central diabetes insipidus and expected results?
1. urine osmolality (low)
2. serum glucose (normal)
3. 24h urine collection (high)
4. U&E's (confirm that there is not a more common cause of polyuria)
325
What is the gold standard investigation for cranial / central diabetes insipidus and expected results?
8h water deprivation test (confirm DI)
326
Name any other tests that can be used to investigate cranial / central diabetes insipidus.
- Cranial MRI
| - desmopressin stimulation test (distinguish between central / nephrogenic DI)
327
Name the differential diagnoses of central / cranial diabetes insipidus.
DM, Diuretics, psychogenic polydipsia, Hypercalcaemia
328
What is the first-line management for central / cranial diabetes insipidus?
Desmopressin (synthethic analogue of ADH)
329
Name any adjunct managements for central / cranial diabetes insipidus?
Oral / intravenous fluids
330
How do you monitor a patient with central / cranial diabetes insipidus?
Follow up imaging to detect pathology if previously undetected, follow up serum electrolytes
331
What is the prognosis for a patient with Central / cranial diabetes insipidus?
usually well controlled on desmopressin
332
Define nephrogenic diabetes insipidus.
Disease with defect in kidney tubules so that kidneys are unable to properly respond to ADH
333
Is nephrogenic diabetes insipidus more prevalent in men or women?
M = W
334
Is nephrogenic diabetes insipidus very common?
No, generally uncommon (1 in 25,000)
335
What causes nephrogenic diabetes insipidus? (Aetiology)
- Acquired – Hypokalaemia, hypercalcaemia, drugs: lithium therapy, renal tubular acidosis, sickle cell, prolonged polyuria, chronic kidney disease
- Genetic – Mutation in ADH receptor (90%)
336
List the risk factors of nephrogenic diabetes insipidus.
1. FHx
2. genetic mutations
3. medication (lithium therapy)
337
What is the pathophysiology of nephorgenic diabetes insipidus?
depends on the aetiology, Can be due to disruption of the channels, damage to the kidney -> Lack of appropriate response to ADH, results from conditions that impair the renal collecting ducts' ability to respond to AVP
338
What are the key presentations of nephrogenic diabetes insipidus?
Polyuria, compensatory polydipsia
339
What are the signs of nephrogenic diabetes insipidus?
Hx of Lithium therapy, FHx, genetic mutations
340
What are the symptoms of nephrogenic diabetes insipidus?
Polyuria, compensatory polydipsia
341
What are the first-line investigations for nephrogenic diabetes insipidus and expected results?
1. urine osmolality (low)
2. serum glucose (normal)
3. 24h urine collection (high)
4. U&E's (confirm that there is not a more common cause of polyuria)
342
What is the gold standard investigation for nephrogenic diabetes insipidus and expected results?
8h water deprivation test (confirm DI)
343
Name any other tests that can be used to investigate nephrogenic diabetes insipidus.
Desmopressin stimulation test - distinguish between central/cranial and nephrogenic DI
344
What are the differential diagnoses of nephrogenic diabetes insipidus?
DM, Diuretics, psychogenic polydipsia, Hypercalcaemia
345
What is the first-line management of nephrogenic diabetes insipidus?
maintenance of adequate fluid intake + treatment of underlying cause
346
Name any adjunct treatments for nephrogenic diabetes insipidus.
sodium restriction and/or pharmacotherapy
347
How do you monitor a patient with nephorgenic diabetes insipidus?
Periodic renal and bladder ultrasonography and regular serum creatinine
348
Define hyperkalaemia.
Excess potassium, if >6.5mmol/L then potential EMERGENCY
349
What causes hyperkalaemia? (Aetiology)
Renal impairment (most common), Metabolic acidosis, drug interference with potassium excretion, massive blood transfusion, Elevated without any of these may be artefactual (eg venepuncture problems, delayed analysis due to problems in lab)
350
List the risk factors for hyperkalaemia.
1. Renal impairment
2. DM
3. Burns
4. Addison's disease
351
What is the pathophysiology of hyperkalaemia?
Renal impairment can lead to retention of potassium in the nephron. This is possible with potassium sparing diuretic.
352
What are the key presentations of hyperkalaemia?
Few symptoms until MI, impaired neuromuscular transmission (muscle weakness and paralysis)
353
What are the signs of hyperkalaemia?
Tall tented T waves on ECG
354
What are the symptoms of hyperkalaemia?
Irregular fast pulse, chest pain, weakness, palpitations, light-headedness
355
What are the first line investigations for hyperkalaemia?
U&E
serum calcium
FBC
ECG (peaked T waves, prolonged PR, widened QRS and reduced P)
356
What is the gold standard investigation for hyperkalaemia?
Serum potassium (recheck if unexpected result)
357
What are the differential diagnoses of hyperkalaemia?
- CKD
- diabetic ketoacidosis
- potassium supplementation with underlying renal dysfunction
- drug-related reduced urinary potassium excretion
358
What is the first-line management of hyperkalaemia?
dietary potassium restriction and loop diuretic (acts on loop of Henle – furosemide)
359
Name any adjunct treatment for hyperkalaemia.
treat underlying condition and review meds
360
What is a serious complication of hyperkalaemia?
MI -> Death
361
Define hypokalaemia.
Deficiency of potassium (serum potassium <3.5mmol/L), if <2.5 then EMERGENCY
362
What causes hypokalaemia? (Aetiology)
- Diuretic treatment
- hyperaldosteronism (Conn’s)
- GI fluid loss by vomiting/diarrhoea
- pyloric stenosis
- Cushing’s
- Alkalosis
- Renal tubular failure
363
List all risk factors of hypokalaemia.
1. Diuretic treatment
2. Conn's syndrome
3. V / D
364
What is the pathophysiology of hypokalaemia?
Excessive loss of potassium through the kidneys in response to aldosterone or diuretic therapy. GI fluid loss -> less chloride -> increase in aldosterone -> Decreased potassium reabsorption
365
What are the key presentations of hypokalaemia?
Usually asymptomatic, possibly muscle weakness, increased risk of cardiac arrhythmias, polyuria
366
What are the signs of hypokalaemia?
Polyuria, T wave inversion, possible prominent U wave
367
What are the symptoms of hypokalaemia?
Possible muscle weakness, polyuria
368
What are the first-line investigations of hypokalaemia?
U&E, serum calcium, FBC, ECG (Flat T waves, ST depression, prominent U waves)
369
What is the gold standard investigation of hypokalaemia and expected results?
Serum potassium & magnesium (both low)
370
Name the differential diagnoses of hypokalaemia.
- severe V / D
- Bulimia / anorexia nervosa
- laxative
- drug-induced
- alcoholism
- diabetic ketoacidosis
371
What is the first-line management of hypokalaemia?
K+ and Mg+ supplement
372
Name any adjunct managements of hypokalaemia.
treat underlying cause, withdraw harmful medication
373
Name any complications of hypokalaemia.
Cardiac arrhythmia and sudden death
374
Define hypercalcaemia.
Excess calcium, if serum levels > 3.5mmol/L then potential EMERGENCY
375
What is the incidence of hypercalcaemia?
3 / 10,000
376
What causes hypercalcaemia? (Aetiology)
>90% caused by primary hyperparathyroidism or malignancy (eg bone metastases), other (Vit D intoxication, thyrotoxicosis, lithium)
377
List the risk factors of hypercalcaemia.
1. Non-metastatic malignancy
2. metastatic skeletal involvement
3. lymphoma
4. primary hyperparathyroidism
378
What is the pathophysiology of hypercalcaemia?
Ectopic secretion of PTH is very rare. Tumour related hypercalcaemia tends to work by a secretion of a peptide with PTH-like activity, direct invasion of bone and production of local factors for calcium mobilisation
379
What are the key presentations of hypercalcaemia?
“painful Bones, renal stones, abdominal groans and psychic moans” Occasionally: renal calculi and CKD
380
What are the signs of hypercalcaemia?
- renal failure
- ectopic calcification
- Cardiac Arrest
- shortening of QT interval
381
What are the symptoms of hypercalcaemia?
- Abdominal pain
- Vomiting
- constipation
- polyuria
- polydipsia
- depression
- weight loss
- hypertension
- confusion
- weakness
- tiredness
382
What are the first-line investigations of hypercalcaemia and expected results?
- serum calcium (elevated)
- serum albumin (low in malignancy)
- U&E (high urea and bicarbonate)
- serum intact PTH (high in 1° hyperparathyroidism)
383
What is the gold standard investigation of hypercalcaemia and expected results?
- serum calcium (elevated)
384
Name any other tests used to investigate hypercalcaemia.
Chest Xray, isotope bone scan, FBC
385
Name all differential diagnoses of hypercalcaemia.
- Primary hyperparathyroidism
- Hyperthyroidism
- adrenal insufficiency
- Phaeochromocytoma
- sarcoidosis
- med-related hypercalcaemia
- TB
386
What is the first-line management of hypercalcaemia?
IV saline + Biphosphate (palmidronate disodium), If primary hyperparathyroidism – surgery
387
Name any adjunct treatment of hypercalcaemia.
calcitonin, loop diuretic (furosemide), treatment of underlying malignancy
388
What is the prognosis for a patient with hypercalcaemia?
Eradication of underlying malignancy crucial for permanent reversal of hypercalcaemia
389
What is PTH?
PTH = parathyroid hormone that regulates serum calcium conc through its effects on bone, kidney and intestine
390
Define hypocalcaemia.
Deficiency of calcium, if serum levels <2mmol/L then potential EMERGENCY
391
What causes hypocalcaemia?
1. increased serum phosphate: Chronic kidney disease (most common), Phosphate therapy
2. Reduced PTH function: Post thyroidectomy and parathyroidectomy
3. Vitamin D deficiency: Reduced exposure to sunlight
4. Other: osteomalacia, acute pancreatitis, over-hydration, hypomagnesaemia
392
List all risk factors for hypocalcaemia.
CKD, primary hyperparathyroidism, Vit D deficiency
393
What is the pathophysiology of hypocalcaemia?
CKD -> Increased phosphate -> Microprecipitation of calcium phosphate in tissues -> Low serum level of calcium, CKD -> Inadequate production of active vitamin D
394
What are the key presentations of hypocalcaemia?
anxious / irritable / irrational, confused, seizures/spasms
| Severe / chronic: Trousseau’s sign, Chovtek’s sign, cataract
395
What are the signs of hypocalcaemia?
Increased muscle tone in smooth muscle, cardiomyopathy (long QT interval)
396
What are the symptoms of hypocalcaemia?
perioral paraesthesiae, spasms, anxious / irritable / irrational, seizures, confusion / impaired orientation, dermatitis, impetigo
397
What are the first-line investigations for hypocalcaemia and expected results?
- History (age of occurance, neck surgery, DHx)
- eGFR (search for CKD)
- serum PTH (elevated)
- Vit D (low)
398
What is the gold standard investigation for hypocalcaemia and expected results?
serum calcium (low)
399
List all differential diagnoses of hypocalcaemia.
- Vit D deficiency
- hypomagnesaemia
- hyperventilation
- postsurgical hypoparathyroidism
400
How do you manage acute hypocalcaemia?
IV calcium
401
How do you treat persistent hypocalcaemia?
if Vit D deficient: supplement, if hypoparathyroidism: alfacalcidol
402
What are the complications of hypocalcaemia?
Death
403
Define Primary Hyperparathyroidism.
Excessive secretion of PTH as one parathyroid gland produces excess PTH
404
Is primary hyperparathyroidism more common in men or women?
W>M
| - 1 in 500W and 1 in 2000M
405
At what age is primary hyperparathyroidism more common?
Aged >40
406
What causes primary hyperparathyroidism? (Aetiology)
Single parathyroid adenoma (~80%) or hyperplasia (~20%)
407
List all risk factors for primary hyperparathyroidism.
- female sex
- age >50
- FHx of PHPT
- endocrine neoplasia
- lithium treatment
- hyperparathyroidism -jaw tumour syndrome
408
What is the pathophysiology of primary hyperparathyroidism?
Adenoma or hyperplasia provides additional secretive tissue to provide excess PTH
409
What are the key presentations of primary hyperparathyroidism?
70 – 80 % asymptomatic presentation, bone pain, poor sleep, fatigue, anxiety, memory loss, myalgias, muscle cramps, constipation
410
What are the signs of primary hyperparathyroidism related to increased calcium?
- weak, tired, depressed, thirsty
411
What are the signs of primary hyperparathyroidism related to bone resorption?
bone pain, fractures, osteoporosis
412
What are the symptoms of primary hyperparathyroidism?
Fatigue, poor sleep, pain, depression, fractures
413
What is the first-line investigation for primary hyperparathyroidism and expected result?
serum calcium (high in normal range or elevated)
414
What is the gold standard investigation for primary hyperparathyroidism and expected result?
Serum intact PTH with immunoradiometric / immunochemical assay ( high in normal range or elevated) (inappropriate elevation)
415
Name any other tests that can be used to investigate primary hyperparathyroidism.
Vit D, serum phosphorus, 24h urinary calcium, DEXA scan (osteoporosi/penia)
416
What are the differential diagnoses of primary hyperparathyroidism?
- Familial hypocalciuric Hypercalcaemia
- multiple myeloma
- milk-alkali syndrome
- sarcoidosis
- Thiazides
- Immobilisation
- Hypervitaminosis D
- humoral hypercalcaemia of malignancy
417
What is the first-line management of primary hyperparathyroidism?
parathyroidectomy / monitoring (if surgery declined / not candidate for surgery)
418
Name any adjunct treatments of primary hyperparathyroidism.
bisphosphonate (alendronic acid) + Vit D supplementation (ergocalciferol)
419
How do you monitor a patient with primary hyperparathyroidism?
Monitoring of serum calcium levels for 6 months then annual checks, bone density check every 1-2 years
420
What are the complications of primary hyperparathyroidism?
Hypercalcaemia, osteoporosis, bone fractures, recurrent laryngeal nerve damage (hoarse voice)
421
What is the prognosis for a patient with primary hyperparathyroidism?
Parathyroidectomy has cure rate of >95%, most common cause of mortality in PHPT patient is stroke/MI
422
Define secondary hyperparathyroidism.
Disease outside of glands leads to enlargement of parathyroid glands usually –> Hypocalcaemia leads to increased secretion of PTH to compensate
423
What causes secondary hyperparathyroidism? (Aetiology)
CKD, intestinal malabsorption or chronic inadequate sunlight exposure which gives rise to alterations in Vit D, phosphorus and calcium
424
List all risk factors for secondary hyperparathyroidism.
1. Ageing
2. Chronic renal failure (>60% of patients with CKD at risk of developing secondary HPTH)
2. low Vit D (malabsorption/inadequate light exposure/nutritional deficiency)
425
What is the pathophysiology of secondary hyperparathyroidism?
Parathyroid gland becomes hyperplastic in response to chronic hypocalcaemia as PTH acts to increase ionised calcium in blood
426
What are the key presentations of secondary hyperparathyroidsm?
Presence of risk factors, muscle cramps and bone pain, Chovstek’s sign, Trousseau’s sign, fractures
427
What are the signs of secondary hyperparathyroidism?
Chovstek’s sign, Trousseau’s sign, fractures, features of chronic renal failure
428
What are the symptoms of secondary hyperparathyroidism?
Muscle cramps and bone pain
429
What are the first-line investigations of secondary hyperparathyroidism and expected results?
- serum intact parathyroid hormone (elevated)
- serum calcium (low)
- serum creatinine (elevated)
- serum urea nitrogen (elevated)
430
What is the gold standard investigation for secondary hyperparathyroidism and expected result?
Serum intact parathyroid hormone (elevated) (appropriate elevation)
431
Name any other tests that can be used to investigate secondary hyperparathyroidism.
Neck Ultrasound / CT / MRI, serum Vit D (low)
432
What is the differential diagnosis of secondary hyperparathyroidism?
Primary hyperparathyroidism
433
What is the first-line management of secondary hyperparathyroidism?
treat underlying condition (ie if lack of sunlight – UV radiation exposure, malabsorption – different diet / supplements, CKD – dietary phosphate restriction / parathyroidectomy)
434
Name any adjunct treatments of secondary hyperparathyroidism.
calcium supplementation (calcium carbonate), Vit D supplementation (ergocalciferol)
435
How do you monitor a patient with secondary hyperparathyroidism?
Regular electrolyte examinations , bone densitometry measurements every 2nd year
436
What are the complications of secondary hyperparathyroidism?
Development into tertiary hyperparathyroidism, osteodystrophy, osteoporosis
437
What is the prognosis for a patient with secondary or tertiary hyperparathyroidism?
prognosis depends on underlying disease
438
Define tertiary hyperparathyroidism.
Excess production of Parathyroid hormone that does not follow normal body feedback controls and persists even if initial cause (low Ca2+) has been corrected
439
What causes secondary hyperparathyroidism? (Aetiology)
Occurs after prolonged secondary hyperparathyroidism
440
What are the risk factors for tertiary hyperparathyroidism?
CKD, secondary hyperparathyroidism
441
What is the pathophysiology of tertiary hyperparathyroidism?
Glands become autonomous, producing excess of PTH even after the correction of calcium deficiency
442
What are the key presentations of tertiary hyperparathyroidism?
bone pain, poor sleep, fatigue, anxiety, memory loss, myalgias, muscle cramps, constipation, bone pain, fractures, osteoporosis, Hypertension
443
What are the signs of tertiary hyperparathyroidism related to increased calcium?
weak, tired, depressed, thirsty
444
What are the signs of tertiary hyperparathyroidism related to bone resorption?
bone pain, fractures, osteoporosis
445
What are the symptoms of tertiary hyperparathyroidism?
Fatigue, poor sleep, pain, depression, fractures
446
What are the first-line investigations of tertiary hyperparathyroidism and expected results?
- Serum intact parathyroid hormone (elevated)
- serum calcium (elevated)
- serum creatinine (elevated)
- serum urea nitrogen (elevated)
447
What is the gold standard investigation for tertiary hyperparathyroidism and expected results?
- serum intact parathyroid hormone (elevated) (inappropriate elevation)
448
Name any other test that can be used to investigate tertiary hyperparatroidism.
Neck Ultrasound / CT / MRI, serum Vit D (low)
449
What is the first-line management of tertiary hyperparathyroidism?
Calcium mimetic (Cinacalcet) + total / subtotal parathyroidectomy
450
Name any adjunct treatments of tertiary hyperparathyroidism.
treat underlying cause (chronic kidney failure)
451
What are the complications of tertiary hyperparathyroidism?
Transient hypocalcaemia follows parathyroidectomy
452
Define hypoparathyroidism.
Disease with low synthesis and secretion of parathyroid hormone in blood causing deficiencies of calcium and elevated serum phosphorus
453
What is the epidemiology of hypoparathyroidism?
It is rare and usually occurs postoperatively
454
What causes hypoparathyroidism? (Aetiology)
Postsurgical hypoparathyroidism, can be genetic: due to defects in PTH gene, can be autoimmune
455
List the risk factors for hypoparathyroidism.
1. Thyroid / parathyroid surgery
2. hypomagnesaemia
3. moderate/chronic maternal Hypercalcaemia (leads to neonatal hypocalcaemia)
4. autosomal dominant conditions (mutations)
456
What is the pathophysiology of hypoparathyroidism?
1. PTH stimulates the activation of vitamin D
2. Vit D facilitates intestinal calcium absorption, renal reabsorption of calcium as well as calcium release from bone
3. Phosphate reabsorption is inhibited by PTH
4. In disease, these processes do not occur.
457
What are the key presentations of hypoparathyroidism?
- History of thyroid/parathyroid/laryngeal surgery
- muscle twitches/spasms/cramps
- paraesthesias/numbness/tingling
- malnutrition/malabsorption
- chronic alcoholism
458
What are the signs of hypoparathyroidism?
Increased excitability of muscles, malnutrition/malabsorption, poor memory
459
What are the symptoms of hypoparathyroidism?
Numbness around mouth/extremities, cramps, tetany, convulsions, Chvostek/Trousseauu’s sign
460
What are the first-line investigations of hypoparathyroidism and expected results?
- Serum calcium (low)
- ECG (prolonged QT interval)
- plasma intact PTH ( low / normal)
- serum magnesium (may be low)
- serum phosphorus (elevated)
461
What is the gold standard investigation for hypoparathyroidism and expected results?
- Serum calcium (low)
462
Name any other investigations used to investigate hypoparathyroidism.
Liver function test, 24h urine calcium / creatinine, 24 h magnesium, ABGs, ophthalmological examination, renal imaging, audiology
463
List the differential diagnoses of hypoparathyroidism.
- Hypovitaminosis D
- Hypomagnesaemia/hypoalbuminaemia
- Pseudohypoparathyroidism
- CKD/renal failure
464
What is the first-line management of acute hypoparathyroidism?
IV calcium
465
What is the first-line management of persistent hypoparathyroidism?
Vit D analogue (calcitriol)
466
How do you monitor a patient with hypoparathyroidism?
Serum calcium/albumin and plasma PTH level monitoring every 6 months
467
What are the complications of hypoparathyroidism?
Overtreatment with Vit D –> hypercalcaemia, cataract, renal stones
468
What is the prognosis for a patient with hypoparathyroidism?
Prognosis dependents on aetiology and severity
469
Define phaeochromocytoma.
Rare, usually benign tumour that develops in adrenal gland causing increase in adrenaline production
470
What is the epidemiology of phaechromocytoma?
- Incidence: 0.6/100,000
- M=W
- equal incidence across all races
- usually >40s
471
What is the aetiology of phaeochromocytoma?
- 90% arise in adrenal medullary catecholamine-producing chromaffin cells
- can be inherited (more noradrenaline) or spontaneous (more adrenaline)
- can be associated with multiple endocrine neoplasia
472
What are the risk factors for phaeochromocytoma?
- multiple endocrine neoplasias
- Von hippel-lindau disease
- succinate dehydrogenase gene mutations
473
What is the pathophysiology of phaeochromocytoma?
1. Catecholamine (adrenaline, noradrenaline) producing tumours of the chromafin cells of the medulla
2. can be adrenal-origin or extra-adrenal origin as well as benign(90%) or malignant(10%)
474
What are the key presentations of phaeochromocytoma?
1. Presence of risk factors
2. headache
3. palpitations
4. diaphoresis
5. hypertension
6. hypertensive retinopathy
7. pallor
8. impaired glucose tolerance/DM, EPISODIC
475
What are the signs of phaeochromocytoma?
- tachycardia
- pallor
- hypertension
476
What are the symptoms of phaeochromocytoma?
- Headaches
- palpitations
- sweating
- tremors
- anxiety
- nausea
- weight loss
477
Name the first line investigations for phaeochromocytoma and the expected results.
1. 24h urine for metanephrine/normetanephirnes / catecholamines / creatinine (elevated)
2. abdominal/pelvis CT (localisation)
3. genetic testing (familial disorders)
4. Plasma catecholamines (may be elevated)
478
Name the gold standard investigation for phaeochromocytoma and the expected results.
1. Serum free metanephrines/normetanephirnes (elevated)
479
Name any other investigations for phaeochromocytoma.
1. serum calcium (elevated)
| 2. Serum potassium (may be low)
480
What are the differential diagnoses of phaeochromocytoma?
- Anxiety/panic attack
- hypertension
- hyperthyroidism
- consumption of illicit substance
- carcinoid syndrome
- cardiac arrhythmias
- menopause
- pre-eclampsia
481
What is the first line management of phaeochromocytoma?
Alpha blockers (phenoxybenzamine) + beta blockers (after alpha, tenolol) + surgical excision
482
What are the adjunct treatments for phaeochromocytoma?
if malignant tumour then postsurgical chemotherapy / radiotherapy
483
How do yo monitor a patient with phaeochromocytoma?
Post-operative 24h urine metanephrine after 2 weeks, monitor BP
484
What are the complications of phaeochromocytoma?
- stroke during surgery due to rapid effect of adrenaline on BP
- neurological/postoperative complications
485
What si he prognosis of a patient with phaeochromocytoma?
Surgery curative method in >85% of cases, 95% 5year survival with benign disease
486
Define carcinoid syndrome.
Disease occurring due to release of serotonin and other vasoactive peptides into systemic circulation from carcinoid tumours which are commonly found in GI tract or lungs
487
What is the epidemiology of carcinoid syndrome?
M>W, aged >60, incidence: 35 per 100,000,
488
What is the Aetiology of carcinoid syndrome?
Caused by Neuroendocrine tumours, Derived from enterochromaffin cells,
seen in 95% of patients with liver metastases,
489
What is the classification of carcinoid tumours?
Classified as Foregut, Midgut or Hindgut tumours, carcinoid syndrome occurs in 20-30% of patients with midgut tumours, 1% of foregut and rarely hindgut tumours,
490
What are the risk factors for carcinoid syndrome?
Functional (secreting) carcinoid tumour
491
What is the pathophysiology of carcinoid syndrome?
1. GI tumours symptomless unless liver metastases present
2. tumours tend to secrete bioactive compounds including serotonin and Kallikrein (lead to ↑ bradykinin), which cause carcinoid syndrome.
492
What are the key presentations of carcinoid syndrome?
1. Initially symptomless
2. diarrhoea
3. flushing
4. palpitation
5. hepatic metastases might cause RUQ pain
6. bronchoconstriction
7. Severe: Carcinoid crisis (EMERGENCY)
493
What are the signs of carcinoid syndrome?
1. Palpitation
2. signs of right heart failure (CCF)
3. cardiac murmurs
4. hepatomegaly
494
What are the symptoms of carcinoid syndrome?
1. hepatic metastases might cause RUQ pain
2. abdominal cramps
3. bronchoconstriction
495
Name the first line investigations of carcinoid syndrome and expected results.
1. 24h urinary 5-hydroxyindoleacetic acid (elevated)
2. CXR + pelvis / chest MRI/CT (tumour location)
3. metabolic panel (elevated creatinine if dehydrated)
496
Name the gold standard investigation of carcinoid syndrome and exected results.
Serum chromogranin A/B (CGA): elevated
497
Name any other investigation that can be used to investigate carcinoid syndrome.
1. Bronchoscopy (if lung tumour)
2. endoscopy
3. histology
4. Octreoscan
498
What are the differential diagnoses of carcinoid syndrome?
1. Irritable bowel syndrome
2. Crohn’s disease
3. Menopause
4. Asthma
499
What is the first line management of carcinoid syndrome?
Surgical resection (if possible – only cure for carcinoid tumours!) + somatostatin analogue (octreotide)
500
How do you monitor a patient with carcinoid syndrome?
Review ever 3 – 4 months including CT scan and CGA test, Octreoscan annually
501
What are the complications of carcinoid syndrome?
Carcinoid heart disease, bowel obstruction or intestinal bleeding, carcinoid crisis
502
What is the prognosis for a patient with carcinoid syndrome?
Survival rate: 5 – 8 years unless metastases (3 years)
503
Defne prolactinoma.
Benign lactotrophs adenoma expressing and secreting prolactin
504
How are prolactinomas classified?
classified as Micro (Most common >90%) or Macro (~10%, >10mm in size)
505
What is the epidemiology of prolactinomas?
40% of all pituitary adenomas, W>M during child bearing years, then W=M
506
What is the aetiology of prolactinomas?
Cause unknown, Some genetic association
507
What are causes of Hyperprolactinaemia excluding prolactinomas?
Non-functioning pituitary tumour; compress pituitary stalk -> no inhibition of prolactin release, Antidopaminergic drugs, Head injury -> damage to the pituitary stalk
508
What are the risk factors of prolactinomas?
1. Female gender
| 2. 20 – 50 years of age
509
What is another name for prolactinoma?
anterior pituitary lactotroph tumours
510
What is the pathophysiology of prolactinomas?
1. Increased release of prolactin can cause galactorrhoea by stimulating milk production from mammary gland, as well as inhibit FSH and LH
2. causes secondary hypogonadism, reduced libido and sexual dysfunction in men
3. Dopamine has an inhibitory effect on prolactin
4. Pituitary tumour is located near to the optic chiasm -> visual field disturbances
5. Very rarely malignant.
511
What are the key presentations of prolactinomas?
- Presence of risk factors
- Effects of prolactin: amenorrhoea / oligomenorrhoea, infertility, galactorrhoea, loss of libido, erectile dysfunction
- Local effect of tumour: visual deterioration, headache
512
What are the signs of prolactinomas?
Osteoporosis
513
What are the symptoms of prolactinomas?
amenorrhoea / oligomenorrhoea, infertility, galactorrhoea, loss of libido, erectile dysfunction, visual deterioration
514
Name the first line investigations for prolactinomas and the expected results.
1. Serum prolactin (elevated)
2. pituitary MRI (detect small micro adenomas)
3. computerised visual field examination (visual field defects )
515
Name the gold standard investigation for prolactinomas and the expected result.
Serum prolactin (elevated)
516
Name the differential diagnoses of prolactinomas.
1. Non-functioning pituitary macro-adenomas
2. drug-induced hyperprolactinaemia
3. primary hypothyroidism
4. renal insufficiency
5. pregnancy
6. polycystic ovarian syndrome
517
What is the first-line management of prolactinomas?
Dopamine agonist (cabergoline) or trans-sphenoidal surgery (if intolerant to dopamine agonist)
518
How do you monitor a patient with prolactinoma?
Periodic measurement of serum prolactin, regular visual field examination, pituitary MRI annualy
519
What are the complications of prolactinomas?
- Visual field impairment
- anterior pituitary failure +/- diabetes insipidus
- hypopituitarism
520
What is the prognosis for a patient with prolactinoma?
good prognosis with dopamine agonist treatment
521
What is the classification of pituitary adenomas?
- Clinically functional (eg Cushing’s, Prolactinomas)
| - clinically non-functional adenomas
522
How many intra-cranial tumours are non-functional pituitary adenomas?
10%
523
What is the epidemiology of non-functional pituitary adenomas?
- no sex / race prevalence
- Incidence: 28 per 100,000
- more common in W aged 20 – 45 or M aged 35 – 60
524
What is the aetiology of non-functional pituitary adenomas?
Unknown, maybe intrinsic genetic alterations
525
What are the risk factors of non-functional pituitary adenomas?
- Multiple endocrine neoplasisa
- familial isolated pituitary adenomas
- carney complex
526
What is the pathophysiology of non-functional pituitary adenomas?
1. Hypermethylation of specific gene locus
| 2. histopathological subtype knowledge important for clinical course of adenoma
527
What are the signs of non-functional pituitary adenoma?
anorexia, gynaecomastia, breast atrophy, visual defect, soft small testicles,
528
What are the symptoms of non-functional pituitary adenoma?
headaches, erectile dysfunction, amenorrhoea, infertility, weight gain, fatigue, nausea / vomiting, weakness, diaphoresis, hot flushes, loss of libido,
529
What are the first line investigations of non-functional pituitary adenomas?
Different tests to see which specific adenoma eg ACTH, IGF-1, insulin tolerance test
530
What is the gold standard nvestigation of non-functional pituitary adenomas?
MRI – location of adenoma
531
Name the differential diagnoses of non-functional pituitary adenomas.
- Prolactinoma
- Acromegaly
- Cushing’s syndrome
- Meningioma
- Craniopharyngioma
532
What is the management of non-functional pituitary adenomas?
Treatment depends on adenoma – could be surgery, hormone replacement, observation etc
533
How do you monitor a patient with non-functional pituitary adenomas?
No available evidence based guidance on monitoring!, recommendation of follow up MRI
534
What are the complications of non-functional pituitary adenomas?
Diabetes insipidus, Meningitis, hypopituitarism
535
What is the prognosis for a patient with non-functional pituitary adenomas?
Generally good prognosis, 10 year progression free survival ~80 – 94%
