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!Final Year > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What is acromegaly?

A

Excessive secretion of growth hormone

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2
Q

What is the main cause of acromegaly?

A

Excess growth hormone secondary to a pituitary adenoma (95%)

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3
Q

What can also cause acromegaly?

A

Ectopic growth hormone releasing hormone (GHRH) or growth hormone producing tumours e.g. pancreatic

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4
Q

What is excess GH in childhood also known as?

A

Gigantism

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5
Q

What are the features of acromegaly?

A
  1. Coarse facial appearance
  2. Spade-like hands
  3. Interdental spaces
  4. Increase in shoe size
  5. Large tongue
  6. Prognathism (protrusion of the jaw)
  7. Excessive sweating and oily skin (sweat gland hypertrophy)
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6
Q

What other features of acromegaly may be seen on examination?

A

Pituitary tumour features:
1. Hypopituitarism
2. Headaches
3. Bilateral hemianopia
1/3 rd of people will have raised prolactin and so galactorrhoea

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7
Q

What are the investigations for acromegaly?

A
  1. Serum IGF-1 levels
  2. Oral glucose tolerance test (used as confirmation)
  3. MRI may demonstrate a pituitary tumour
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8
Q

What are the Endocrine Society guidelines for diagnosis of acromegaly?

A
  1. Measure IGF-1 levels in patient with typical clinical manifestations of acromegaly
  2. In patients with elevated or equivocal serum IGF-1, confirm diagnosis by finding a lack of suppression of GH to < 1μg/L following hyperglycaemia during an OGTT
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9
Q

What would the findings of an OGTT be for acromegaly?

A
  1. Normal = GH is suppressed to < 2 mu/L with hyperglycaemia
  2. Acromegaly = no suppression
  3. May also demonstrate impaired glucose tolerance
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10
Q

Which test can be used to monitor disease progression in acromegaly?

A

Serum IGF-1 levels

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11
Q

What is the first line management options for acromegaly?

A

Trans-sphenoidal surgery

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12
Q

What medical management is available if surgery is not successful/ inoperable in acromegaly?

A
  1. Somatostatin analogue, e.g. octreotide. Directly inhibits release of GH
  2. Pegvisomant: GH receptor antagonist, once daily s/c, very effective, does not reduce tumour volume so may still need surgery to reduce mass effect
  3. Dopamine agonists, e.g. bromocriptine, only effective in a minority of patients
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13
Q

What are the complications of acromegaly?

A

Hypertension
Diabetes (>10%)
Cardiomyopathy
Colorectal cancer
Obstructive sleep apnoea

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14
Q

What are some of the side effects of somatostatin analogues used for acromegaly?

A

Abdominal pain
Steatorrhoea
Gallstones

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15
Q

What is the prognosis for acromegaly?

A

Associated with serious complications and premature death if not treated
Physical changes are irreversible

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16
Q

What is adrenal insufficiency?

A

Deficiency of adrenal cortical hormones (mineralocorticoids, glucocorticoids and androgens)

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17
Q

What is the aetiology of adrenal insufficiency?

A

Primary (Addison’s disease): Autoimmune (>70%)
Secondary: Pituitary or hypothalamic disease.
Surgical: After bilateral adrenalectomy.
Medical: (iatrogenic) sudden cessation of long-term steroid therapy

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18
Q

What are the risk factors for adrenal insufficiency?

A

4Is:
1. Infections: Tuberculosis, meningococcal septicaemia (Waterhouse–Friderichsen syndrome), Cytomegalovirus (HIV patients)
2. Infiltration: Metastasis (lung, breast, melanoma), lymphomas, amyloidosis
3. Infarction: Secondary to thrombophilia
4. Inherited: Adrenoleukodystrophy 1, ACTH receptor mutation

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19
Q

What are the 4Is for risk factors for adrenal insufficiency?

A
  1. Infections
  2. Infiltration
  3. Infarction
  4. Inherited
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20
Q

What is the most common cause of adrenal insufficiency?

A

Most common cause is iatrogenic- sudden cessation in long term steroid therapy
Primary causes are rare

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21
Q

What are the presenting symptoms of acute adrenal insufficiency?

A

(Addisonian crisis)
Acute adrenal insufficiency with major haemodynamic collapse often precipitated by stress (e.g. infection or surgery)

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22
Q

What are the presenting symptoms of chronic adrenal insufficiency?

A

Non-specific vague symptoms such as dizziness, anorexia, weight loss, diarrhoea, vomiting, abdominal pain, lethargy, weakness, depression

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23
Q

What are the clinical features of adrenal insufficiency?

A
  1. Postural hypotension
  2. Increased pigmentation: more noticeable on buccal mucosa, scars, skin creases, nails, pressure points (resulting from melanocytes being stimulated by increased ACTH levels)
  3. Loss of body hair in women (androgen deficiency)
  4. Associated autoimmune conditions: e.g. vitiligo
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24
Q

What are the clinical features of an Addisonian crisis?

A

Hypotensive shock
Tachycardia
Pale
Cold and clammy
Oliguria

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25
Q

What are the appropriate investigations for adrenal insufficiency?

A

Definite investigation is ACTH stimulation (synACTHen) test
9am serum cortisol may also be helpful

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26
Q

What results would be seen in Addison’s disease on a synACTHen test/ 9am serum cortisol test?

A

> 500 nmol/l makes Addison’s very unlikely
< 100 nmol/l is definitely abnormal
100-500 nmol/l should prompt a ACTH stimulation test to be performed
ACTH stimulation test should show an increase in plasma cortisol levels 30 minutes after giving Synacthen 250ug IM

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27
Q

What are the appropriate investigations for an Addisonian crisis?

A

1a. Bloods- Haematology (FBC for neutrophilic, CRP and ESR for infection)
1b. Biochemistry (U&Es for hyperkalaemia, hyponatraemia, hypoglycaemia and metabolic acidosis)
1c. Microbiology (blood cultures)
2. Urine- MCS

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28
Q

What are the causes of an Addisonian crisis?

A
  1. Sepsis or surgery causing an acute exacerbation of chronic insufficiency (Addison’s, Hypopituitarism)
  2. Adrenal haemorrhage eg Waterhouse-Friderichsen syndrome (fulminant meningococcemia)
  3. Steroid withdrawal
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29
Q

What is the management for Addisonian crisis?

A
  1. Hydrocortisone 100 mg im or iv
  2. 1 litre normal saline infused over 30-60 mins or with dextrose if hypoglycaemic
  3. Continue hydrocortisone 6 hourly until the patient is stable (no fludrocortisone is required because high cortisol exerts weak mineralocorticoid action)
  4. Oral replacement may begin after 24 hours and be reduced to maintenance over 3-4 days
  5. Treat the underlying cause e.g. Abx for sepsis
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30
Q

What is the management plan for adrenal insufficiency?

A

Replacement therapy of glucocorticoid and mineralocorticoid
Combination of:
1.Hydrocortisone (usually given in 2 or 3 divided doses, 20-30 mg per day, with the majority given in the first half of the day)
2.Fludrocortisone
Patient education: importance of not missing doses, MedicAlert bracelets, hydrocortisone injection for crisis
Management of intercurrent illness: glucocorticoid dose should be doubled with fludrocortisone staying the same

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31
Q

What precaution must be taken in a patient with adrenal insufficiency and hypothyroidism?

A

Give hydrocortisone before thyroxine to avoid precipitating an Addisonian crisis

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32
Q

What are the possible complications of adrenal insufficiency?

A

Hyperkalaemia
Death during an Addisonian crisis

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33
Q

What is the prognosis for patients with adrenal insufficiency?

A

Adrenal function rarely recovers, but normal life expectancy can be expected if treated

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34
Q

What are carcinoid tumours?

A

A slow growing type of neuroendocrine tumour originating in the cells of the neuroendocrine system, but can metastasise

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35
Q

What is carcinoid syndrome?

A
  1. Usually occurs when metastases are present in the liver and release serotonin into the systemic circulation
  2. May also occur with lung carcinoid as mediators are not ‘cleared’ by the liver
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36
Q

How can carcinoid tumours be classified?

A

Fore, mid or hindgut tumours

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37
Q

What are the features of carcinoid tumours?

A
  1. Flushing (often earliest symptom)
  2. Diarrhoea
  3. Bronchospasm
  4. Hypotension
  5. Right heart valvular stenosis
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38
Q

What also might be secreted in carcinoid tumours alongside serotonin?

A

ACTH and GHRH

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39
Q

What are the investigations for carcinoid tumours?

A
  1. Urinary 5-HiAA
  2. Plasma chromogranin A y
  3. Radiolabelled octreotide scans to detect carcinoid tumours as they express somatostatin receptors
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40
Q

What is the management of carcinoid tumours?

A
  1. Somatostatin analogues e.g. octreotide
  2. Diarrhoea: cyproheptadine may help
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41
Q

What is Cushing’s syndrome?

A

The clinical manifestation of pathological hypercortisolism (chronic inappropriate elevation of free circulating cortisol) from any cause

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42
Q

What is the aetiology of Cushing’s syndrome?

A

Can be divided into exogenous and endogenous: exogenous causes of Cushing’s syndrome (e.g. glucocorticoid therapy) are far more common than endogenous ones

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43
Q

What are the endogenous causes of Cushing’s syndrome?

A
  1. ACTH-dependent (80%):
    a. Excess ACTH secreted from a pituitary adenoma: Cushing’s disease (80%).
    b. ACTH secreted from an ectopic source, e.g. small-cell lung carcinomas, pulmonary carcinoid tumours (20%)
  2. ACTH-independent (20%):
    a. Excess cortisol secreted from a benign adrenal adenoma (60%)
    b. RARE: 1% of Cushing’s syndrome cases are caused by adrenal carcinoma BUT of this 1%, adrenal overproduction of cortisol is seen in 30% to 40% of adrenal carcinomas
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44
Q

What is the epidemiology of Cushing’s syndrome?

A
  1. Relatively uncommon
  2. Exogenous Cushing’s is more common than endogenous
  3. Endogenous Cushing’s is more common in women (x4)
  4. Peak incidence is 20–40 years, although it can occur at any age
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45
Q

What are the presenting symptoms of Cushing’s syndrome?

A
  1. Weight gain and fatigue
  2. Muscle weakness, myalgia
  3. Thin skin
  4. Easy bruising
  5. Poor wound healing
  6. Fractures (resulting from osteoporosis)
  7. Hirsutism
  8. Acne
  9. Frontal balding
  10. Oligo- or amenorrhoea
  11. Depression or psychosis
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46
Q

What are the signs of Cushing’s syndrome on physical examination?

A

Specific features:
1. Facial plethora: increased perfusion, redness, one of the earliest features of Cushing’s syndrome
2. Proximal muscle weakness
3. Bruises
Other signs:
1. Facial fullness
2. Interscapular fat pad
3. Thin skin
4.Central obesity
5. Pink/purple striae on abdomen, breast, thighs
6. Kyphosis (due to vertebral fracture)
7. Poorly healing wounds
8. Hirsutism, acne, frontal balding.
9. Hypertension
10. Ankle oedema (salt and water retention as a result of mineralocorticoid effect of excess cortisol)
11. Pigmentation in ACTH-dependent cases

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47
Q

What are the two most common investigations for Cushing’s syndrome?

A
  1. Overnight dexamethasone suppression test:
    a. most sensitive test and is now used first-line
    b. Patients with Cushing’s syndrome do not have their morning cortisol spike suppressed
  2. 24 hr urinary free cortisol
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48
Q

What are the possible findings of a dexamethasone suppression test for Cushing’s syndrome?

A

If ACTH is suppressed then a non-ACTH dependent cause is likely such as an adrenal adenoma

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49
Q

What is the role of a ‘high-dose’ dexamethasone suppression test in Cushing’s syndrome?

A

Used to localise the pathology resulting in Cushing’s syndrome: Cushing’s disease and ectopic ACTH secretion

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50
Q

What are the possible findings of a high dose dexamethasone test for cushing’s syndrome?

A

Cushing’s syndrome due to other causes (e.g. adrenal adenomas):
a. Cortisol: Not suppressed
b. ACTH Suppressed
Cushing’s disease (i.e. pituitary adenoma → ACTH secretion):
a. Cortisol: Suppressed
b. Cortisol: Suppressed
Ectopic ACTH syndrome:
a. Cortisol: Not suppressed
b. ACTH: Not suppressed

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51
Q

What is the management of iatrogenic Cushing’s syndrome?

A

Discontinue administration, lower steroid dose or use an alternative steroid-sparing agent if possible

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52
Q

What is the medical management of Cushing’s syndrome?

A

Indication: Pre-operative or if unfit for surgery
1. Inhibition of cortisol synthesis with:
a. metyrapone (competitive inhibitor of 11β-hydroxylation in the adrenal cortex inhibiting cortisol production) or
b. ketoconazole (potent inhibitor of cortisol and aldosterone synthesis)
2. Treat osteoporosis and provide physiotherapy for muscle weakness

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53
Q

What is the surgical management of Cushing’s syndrome?

A
  1. Pituitary adenomas, also known as Cushing’s disease:
    a. Trans-sphenoidal adenoma resection
    b. Hydrocortisone replaced until
    pituitary function recovers
  2. Adrenal adenoma/carcinoma: Surgical removal of tumour (plus adjuvant therapy with mitotane for adrenal carcinoma)
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54
Q

What is the management of ectopic ACTH Cushing’s syndrome?

A

Investigate lung tumour: chest x-ray, bronchoscopy, CT
Treatment is directed at the tumour

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55
Q

What are some general findings in Cushing’s syndrome?

A

A hypokalaemic metabolic alkalosis may be seen, along with impaired glucose tolerance

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56
Q

What are the complications of Cushing’s syndrome?

A
  1. Diabetes
  2. Osteoporosis
  3. Hypertension
  4. Pre-disposition to infections
  5. Adrenal insufficiency secondary to adrenal suppression
  6. Complications of surgery: CSF leakage, meningitis, sphenoid sinusitis, hypopituitarism
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57
Q

What is the prognosis of Cushing’s syndrome?

A

In the untreated, 5-year survival rate is 50%, mortality is mainly from cardiovascular disease
Depression usually persists for many years following successful treatment

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58
Q

What is diabetes insipidus?

A

Characterised by either a decreased secretion of antidiuretic hormone (ADH) from the pituitary (cranial DI) or an insensitivity to antidiuretic hormone (nephrogenic DI)

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59
Q

What is the consequence of diabetes insipidus?

A

Hypotonic polyuria (production of large quantities of dilute urine)

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60
Q

What are the causes of cranial DI (decreased secretion of ADH)?

A
  1. Idiopathic
  2. Post head injury
  3. Pituitary surgery
  4. Craniopharyngiomas
  5. Infiltrative: e.g. Sarcoidosis
  6. Haemochromatosis
  7. DIDMOAD: association of cranial Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and Deafness (also known as Wolfram’s syndrome)
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61
Q

What are the causes of nephrogenic DI (insensitivity of ADH)?

A
  1. Genetic:
    a. More common form affects the vasopression (ADH) receptor
    b. Less common form results from a mutation in the gene that encodes the aquaporin 2 channel
  2. Electrolytes:
    a. Hypercalcaemia
    b. Hypokalaemia
  3. Lithium: desensitizes the kidney’s ability to respond to ADH in the collecting ducts
  4. Tubulo-interstitial disease: e.g. obstruction, sickle-cell, pyelonephritis
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62
Q

What are the two main features of diabetes insipidus?

A
  1. Polyuria
  2. Polydipsia
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63
Q

What is the pathophysiology of both forms of DI?

A
  1. Both mechanisms result in the failure of activation of aquaporins channels and the luminal membrane of the collecting duct remains impermeable to water
  2. This results in large volume hypotonic urine and polydipsia
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64
Q

What is an additional feature of DI in children?

A

Nocturia ± enuresis (involuntary urination) and sleep disturbances

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65
Q

What are the possible signs of DI on examination?

A
  1. Few signs if patients drink adequate fluids
  2. Urine output is often >3 L/24 h
  3. If fluid intake < fluid output: signs of dehydration may be present e.g. tachycardia, reduced tissue turgor, postural hypotension, dry mucous membranes
  4. Signs of the cause: e.g. visual field defect bitemporal hemianopia from pituitary tumour
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66
Q

What are the investigations for diabetes insipidus?

A
  1. Bloods and urine analysis: high plasma osmolality, low urine osmolality (if urine osmolality of >700 mOsm/kg excludes DI)
  2. Water deprivation test:
  3. Water is restricted for 8 h
  4. Plasma and urine osmolality are measured every hour over the 8 h
  5. Weigh the patient (hourly) to monitor the level of dehydration (stop the test if the fall in body weight is >3%)
  6. Desmopressin (2 mg IM) is given after 8 h and urine osmolality is measured
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67
Q

What are the findings of the water deprivation test for normal patients (without DI)?

A
  1. Water restriction causes a rise in plasma osmolality and increase in ADH secretion
  2. This leads to increased water reabsorption in the collecting ducts
  3. Urine is concentrated: (Urine osmolality > 600 mosmol/kg)
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68
Q

What are the findings of the water deprivation test for Diabetes Insipidus?

A
  1. Lack of ADH activity means that urine is unable to be concentrated by the collecting ducts (Urine osmolality < 400 mosmol/kg)
  2. Cranial: Urine osmolality rises by >50%, following administration of desmopressin (due to deficiency in vasopressin)
  3. Nephrogenic: Urine osmolality rises by <45%, following administration of desmopressin (resistance to vasopressin)
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69
Q

What is the main difference in the water deprivation test findings for the two types of DI?

A

With desmopressin administration, there will be an increase in urine osmolality in patients with cranial DI (not in nephrogenic because are insensitive to it)

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70
Q

What is the management of DI?

A

Cranial DI: desmopressin
Nephrogenic DI: thiazides and a low salt/protein diet

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71
Q

What are the complications of DI?

A

Hypernatraemic dehydration:
1. Mild to moderate hypernatraemia may present with irritability, restlessness, lethargy, muscle twitching, spasticity, or hyper-reflexia
3. Severe hypernatraemia may present with delirium, seizures, or coma
Excess desmopressin therapy may cause hyponatraemia

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72
Q

What is the prognosis of Diabetes Insipidus?

A

Variable depending on cause:
1. While DI is often a lifelong condition cranial DI may be transient following head trauma
2. Cure of cranial or nephrogenic diabetes insipidus may be possible on removal of cause, e.g. tumour resection, drug discontinuation

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73
Q

What is Diabetes Mellitus?

A

A chronic condition characterised by abnormally raised levels of blood glucose

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74
Q

What is Type 1 DM?

A
  1. Autoimmune disorder where the insulin-producing beta cells of the islets of Langerhans in the pancreas are destroyed by the immune system
  2. This leads to an absolute deficiency of insulin resulting in raised glucose levels
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75
Q

What is the epidemiology of Type 1 DM?

A

Tends to develop in childhood/early adult life and typically present unwell, possibly in diabetic ketoacidosis

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76
Q

What is Type 2 DM?

A
  1. Caused by a relative deficiency of insulin due to an excess of adipose tissue
  2. In simple terms there isn’t enough insulin to ‘go around’ all the excess fatty tissue, leading to blood glucose creeping up
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77
Q

What is the epidemiology of Type 2 DM?

A

The most common cause of diabetes in the developed world

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78
Q

What are the other types of diabetes mellitus?

A
  1. Prediabetes: used for patients who don’t yet meet the criteria for a formal diagnosis of T2DM to be made but are likely to develop the condition over the next few years (require monitoring and advice)
  2. Gestational: raised glucose levels during pregnancy (important to detect)
  3. MODY: Maturity onset diabetes of the young, group of inherited genetic disorders affecting the production of insulin, results in younger patients developing symptoms similar to those with T2DM
  4. Latent autoimmune diabetes of adults (LADA): a small group of patients who develop autoimmune diabetes later in life
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79
Q

What are typical presenting symptoms of Type 1 DM?

A
  1. Weight loss
  2. Polyuria
  3. Polydipsia
  4. DKA:
    a. Abdominal pain
    b. Vomiting
    c. Reduced consciousness
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80
Q

What are the presenting symptoms of Type 2 DM?

A
  1. Often picked up incidentally on routine blood tests
  2. Polydipsia
  3. Polyuria
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81
Q

What are the investigations for Type 1 DM?

A
  1. Urine: dip for glucose (and ketones)
  2. Fasting glucose and random glucose
  3. C-peptide levels are typically low in patients with T1DM
  4. Antibody testing: e.g. Antibodies to glutamic acid decarboxylase (anti-GAD), Islet cell antibodies, Insulin antibodies
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82
Q

What is the diagnostic criteria for Type 1 DM if the patient is symptomatic?

A
  1. Fasting glucose greater than or equal to 7.0 mmol/l
  2. Random glucose greater than or equal to 11.1 mmol/l (or after 75g oral glucose tolerance test)
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83
Q

What is the diagnostic criteria for Type 1 DM if the patient is asymptomatic?

A

Must be demonstrated on two separate occassions:
1. Fasting glucose greater than or equal to 7.0 mmol/l
2. Random glucose greater than or equal to 11.1 mmol/l (or after 75g oral glucose tolerance test)

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84
Q

What additional tests should be performed in adults with suspected Type 1 DM but atypical features?

A

Atypical features e.g. age 50 years or above, BMI of 25 kg/m² or above, slow evolution of hyperglycaemia or long prodrome: measurement of C‑peptide and/or diabetes‑specific autoantibody titres

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85
Q

What are the investigations for Type 2 DM?

A

Diagnosis can be made from either a plasma glucose or a HbA1c sample

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86
Q

What is the diagnostic criteria for Type 2 DM if the patient is symptomatic?

A
  1. Fasting glucose greater than or equal to 7.0 mmol/l
  2. Random glucose greater than or equal to 11.1 mmol/l (or after 75g oral glucose tolerance test)
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87
Q

What is the diagnostic criteria for Type 2 DM if the patient is asymptomatic?

A

Demonstrated on two separate occasions:
1. Fasting glucose greater than or equal to 7.0 mmol/l
2. Random glucose greater than or equal to 11.1 mmol/l (or after 75g oral glucose tolerance test)

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88
Q

What is the HbA1c criteria for Type 2 DM?

A

Greater than or equal to 48 mmol/mol (6.5%) is diagnostic of diabetes mellitus

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89
Q

What is important to consider when using HbA1c in the diagnosis of Type 2 DM?

A
  1. A HbAlc value of less than 48 mmol/mol (6.5%) does not exclude diabetes
  2. In patients without symptoms, the test must be repeated to confirm the diagnosis
  3. It should be remembered that misleading HbA1c results can be caused by increased red cell turnover e.g.:
    a. haemoglobinopathies
    b. haemolytic anaemia
    c. untreated iron deficiency anaemia
    d. CKD
    e. HIV
    f. Children
    g. People taking medication that may cause hyperglycaemia (e.g. corticosteroids)
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90
Q

What is the HbA1c criteria for prediabetes?

A

42-47 mmol/mol
(Or fasting glucose 6.1 -6.9 mmol/l)

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91
Q

What is the difference between impaired fasting glucose and impaired glucose tolerance?

A
  1. Impaired fasting glucose = a fasting glucose greater than or equal to 6.1 but less than 7.0 mmol/l implies
  2. Impaired glucose tolerance = fasting plasma glucose less than 7.0 mmol/l and OGTT 2-hour value greater than or equal to 7.8 mmol/l but less than 11.1 mmol/l
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92
Q

What are the major differences in Type 1 and Type 2 DM?

A

Type 1:
1. Typically presents < 20 years
2. Presents more acutely (hours-days)
3. Recent weight loss is typical
4. Features of DKA
Type 2:
1. Typically presents > 40 years (can present in younger, obese patients)
2. Presents more slowly (weeks to months)
3. Obesity is a strong RF
4. Milder symptoms e.g. polyuria, polydipsia
5. Ketonuria is rare

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93
Q

What is the management of Type 1 DM?

A
  1. Patients always require insulin to control the blood sugar levels
  2. This is because there is an absolute deficiency of insulin with no pancreatic tissue left to stimulate with drugs
  3. Different types of insulin are available according to their duration of action: short, immediate and long acting
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94
Q

How is insulin given in patients with Type 1 DM?

A

Subcutaneous: direct replacement for endogenous insulin

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95
Q

What are the main side effects of insulin?

A
  1. Hypoglycaemia
  2. Weight gain
  3. Lipodystrophy
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96
Q

What is the management of Type 2 DM?

A
  1. Majority of patients are controlled using oral medication (after lifestyle advice)
  2. First-line drug for the vast majority of patients is Metformin
  3. Second-line drugs include sulfonylureas, gliptins and pioglitazone
  4. If oral medication is not controlling the blood glucose to a sufficient degree then insulin is used
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97
Q

What is Metformin in the management of Type 2 DM?

A
  1. Oral medication
  2. Increases insulin sensitivity and decreases hepatic gluconeogenesis
  3. First line medication
  4. Not to be used in patients with an eGFR < 30ml/min
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98
Q

What are the side effects of Metformin?

A
  1. Gastrointestinal upset: should be slowly titrated up to minimise this
  2. Lactic acidosis
    *If standard-release metformin is not tolerated then modified-release metformin should be trialled
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99
Q

What are the second line medications for Type 2 DM?

A

1st: Metformin + SGLT-2 inhibitor (first line for patients with CVD/HF)
Then: Metformin + gliptin/ sulphonylurea
(only add a second drug if HbA1c > 58mmol/mol)

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100
Q

What is DPP-4 inhibitors?

A
  1. Oral medication, end in -gliptin
  2. Increases incretin levels which inhibit glucagon secretion
  3. Generally well tolerated, increased risk of pancreatitis
  4. Good for patients with CKD
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101
Q

What are sulfonylureas?

A
  1. Oral medication
  2. Stimulate pancreatic beta cells to secrete insulin
  3. E.g. gliclazide and glimepiride
  4. SE: Hypoglycaemia, weight gain, hyponatraemia
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102
Q

What are SGLT-2 inhibitors (-gliflozins)?

A
  1. Oral medication
  2. Inhibits reabsorption of glucose in the kidney
  3. Typically results in weight loss
  4. SE: UTI
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103
Q

What is the third line medical management of Type 2 DM?

A

Triple therapy: Metformin + sulfonylurea + gliptin/ SGLT-2 inhibitors

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104
Q

What can be added before triple therapy in some patients in the management of Type 2 DM?

A

Insulin

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105
Q

What is the fourth line management if triple therapy is not effective/ tolerated and BMI > 35 in Type 2 DM?

A

Metformin + sulfonylurea + GLP-1

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106
Q

What are GLP-1 agonists?

A
  1. SC medication in Type 2 DM
  2. Incretin mimetic which inhibits glucagon secretion
  3. Typically results in weight loss
  4. SEs: Nausea and vomiting, pancreatitis
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107
Q

When is SGLT-2 monotherapy used in the management of Type 2 DM?

A

If Metformin in contraindicated and there is a risk of CVD/ HF

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108
Q

How often should HbA1c be checked in the management of Type 2 DM?

A
  1. Individual targets should be agreed with patients to encourage motivation
  2. HbA1c should be checked every 3-6 months until stable, then 6 monthly
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109
Q

What are the HbA1c targets for the different management options of Type 2 DM?

A
  1. Lifestyle alone: 48 mmol/mol (6.5%)
  2. Lifestyle and metformin: 48 mmol/mol (6.5%)
  3. Lifestyle and any drug that could lead to hypoglycaemia e.g. sulfonylurea: 53 mmol/mol (7.0%)
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110
Q

What is the HbA1c target for patients already on treatment (on one drug)?

A

53 mmol/mol (7.0%)

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111
Q

What lifestyle advice should be given to all patients with Type 2 DM?

A
  1. Ecourage high fibre, low glycaemic index sources of carbohydrates
  2. Control the intake of foods containing saturated fats and trans fatty acids
  3. Discourage the use of foods marketed specifically at people with diabetes
  4. Initial target weight loss in an overweight person is 5-10%
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112
Q

What advice should be given to patients with Type 2 DM regarding sick days?

A

If they become unwell:
1. Increase frequency of blood glucose monitoring to four hourly or more frequently
2. Encourage fluid intake aiming for at least 3 litres in 24hrs
3. If struggling to eat they may need sugary drinks to maintain carbohydrate intake
4. It is useful to educate patients so that they have a box of ‘sick day supplies’ that they can access if they become unwell
5. Access to a mobile phone has been shown to reduce progression of ketosis to diabetic ketoacidosis
6. If a patient is taking oral hypoglycaemic medication, they should be advised to continue taking their medication even if they are not eating much

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113
Q

Which medication should be stopped for Type 2 DM patients if they become ill?

A

Insulin, due to risk of DKA

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114
Q

What medications should be stopped for Type 2 DM patients if they become dehydrated?

A

Metformin due to potential impact on renal function

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115
Q

What are the features of hypoglycaemia in patients with DM?

A

Depends on the blood glucose level

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116
Q

What are the features of hypogylcaemia when blood glucose concentrations are <3.3 mmol/L?

A

Autonomic symptoms due to the release of glucagon and adrenaline:
1. Sweating
2. Shaking
3. Hunger
4. Anxiety
5. Nausea

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117
Q

What are the features of hypoglycaemia when blood glucose concentrations are below <2.8 mmol/L?

A

Neuroglycopenic symptoms due to inadequate glucose supply to the brain:
1. Weakness
2. Vision changes
3. Confusion
4. Dizziness

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118
Q

What are the more severe but rarer symptoms of hypoglycaemia?

A

Convulsions and coma

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119
Q

What is the management of hypoglycaemia in the community?

A
  1. Initially, oral glucose 10-20g should be given in liquid, gel or tablet form
  2. Alternatively, a propriety quick-acting carbohydrate may be given: GlucoGel or Dextrogel.
  3. A ‘HypoKit’ may be prescribed which contains a syringe and vial of glucagon for IM or SC injection at home
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120
Q

What is the management of hypoglycaemia in a hospital setting?

A
  1. If the patient is alert, a quick-acting carbohydrate may be given e.g. GlucoGel
  2. If the patient is unconscious or unable to swallow, SC or IM glucagon may be given
  3. Alternatively, intravenous 20% glucose solution may be given through a large vein
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121
Q

What is the DVLA guidance for patient with DM?

A
  1. There has not been any severe hypoglycaemic event in the previous 12 months
  2. The driver has full hypoglycaemic awareness
  3. The driver must show adequate control of the condition by regular blood glucose monitoring (memory function monitors), at least twice daily and at times relevant to driving
  4. The driver must demonstrate an understanding of the risks of hypoglycaemia
  5. There are no other debarring complications of diabetes
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122
Q

What is the management of hypertension and DM?

A

ACE inhibitors are first line with a blood pressure target of < 140/90 mmHg for type 2 diabetics

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123
Q

What is Hyperosmolar hyperglycaemic state?

A
  1. Due to insulin deficiency, as is diabetic ketoacidosis, but patients are usually old and may be presenting for the first time
  2. History is longer (e.g. 1 week)
  3. There is marked dehydration, high Na + , high glucose (>35 mmol/ L), high osmolality (>340 mosmol/kg), BUT no acidosis and no ketones
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124
Q

How are the complications for DM divided?

A
  1. Microvascular:
    a. Neuropathy
    b. Nephropathy
    c. Retinopathy
  2. Macrovascular:
    a. Ischaemic heart disease
    b. Stroke
    c. Peripheral vascular disease
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125
Q

What is diabetic neuropathy?

A
  1. Diabetes typically leads to sensory loss and not motor loss
  2. Sensory loss typically results in a ‘glove and stocking’ distribution, with the lower legs affected first due to the length of the sensory neurons supplying this area
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126
Q

What is the management of diabetic neuropathy?

A
  1. First-line treatment: amitriptyline, duloxetine, gabapentin or pregabalin
  2. If the first-line drug treatment does not work try one of the other 3 drugs
  3. Tramadol may be used as ‘rescue therapy’ for exacerbations of neuropathic pain
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127
Q

What are the different types of gastrointestinal autonomic neuropathy?

A
  1. Gastroparesis:
    a. Symptoms include erratic blood glucose control, bloating and vomiting
    b. Management: metoclopramide, domperidone or erythromycin (prokinetic agents)
  2. Chronic diarrhoea: often at night
  3. GORD: decreased lower esophageal sphincter (LES) pressure
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128
Q

What is diabetic foot disease?

A

An important complication of diabetes mellitus which should be screen for on a regular basis

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129
Q

What are the two main factors contributing to diabetic foot?

A
  1. Neuropathy: resulting in loss of protective sensation (e.g. not noticing a stone in the shoe), Charcot’s arthropathy, dry skin
  2. Peripheral arterial disease: diabetes is a risk factor for both macro and microvascular ischaemia
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130
Q

What are the common presentations of diabetic foot?

A
  1. Neuropathy: loss of sensation
  2. Ischaemia: absent foot pulses, reduced ankle-brachial pressure index (ABPI), intermittent claudication
  3. Complications: calluses, ulceration, Charcot’s arthropathy, cellulitis, osteomyelitis, gangrene
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131
Q

What is the screening programme for diabetic foot disease?

A

All diabetic patients on at least an annual basis:
1. Screening for ischaemia: done by palpating for both the dorsalis pedis pulse and posterial tibial artery pulse
2. Screening for neuropathy: a 10 g monofilament is used on various parts of the sole of the foot

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132
Q

How are patients with diabetic foot disease risk stratified?

A
  1. Low risk: no risk factors except a callus alone
  2. Moderate risk: deformity or neuropathy or non-critical limb ischaemia
  3. High risk: (should be followed up regularly)
    a. previous ulceration or
    b. previous amputation or
    c. on renal replacement therapy or
    d. neuropathy and non-critical limb ischaemia together or
    e. neuropathy in combination with callus and/or deformity or
    f. non-critical limb ischaemia in combination with callus and/or deformity
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133
Q

What is diabetic nephropathy?

A

Common complication of diabetes mellitus, all patient should be screened annually:
1. Using urinary albumin:creatinine ratio (ACR)
2. Should be an early morning specimen
3. ACR > 2.5 = microalbuminuria

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134
Q

What is the management of diabetic nephropathy?

A
  1. Dietary protein restriction
  2. Tight glycaemic control
  3. BP control: aim for < 130/80 mmHg
  4. ACE inhibitor or angiotensin-II receptor antagonist (not both) should be started if urinary ACR of 3 mg/mmol or more
  5. Control dyslipidaemia with statins
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135
Q

What is diabetic ketoacidosis (DKA)?

A

A serious complication or first presentation of type 1 diabetes mellitus (rarely type 2)

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136
Q

What is the pathophysiology of DKA?

A
  1. Uncontrolled lipolysis which results in the excess production of free fatty acids
  2. These are ultimately converted to ketone bodies
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137
Q

What is type 1 diabetes mellitus?

A
  1. Autoimmune disorder
  2. Insulin producing beta-cells in the in the Islet of Langerhans in the pancreas are destroyed
  3. Results in an absolute deficiency of insulin resulting in raised glucose levels
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138
Q

What are the features of DKA?

A
  1. Abdominal pain
  2. Of type 1: polyuria, polydipsia, dehydration
  3. Kussmaul breathing: deep hyperventilation
  4. Acetone-smelling breathing
  5. Low GCS
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139
Q

What are the precipitating factors for DKA?

A
  1. Infection
  2. Missed insulin doses
  3. Myocardial infarction
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140
Q

What are the investigations for DKA?

A
  1. A to E approach
  2. Key investigations include VBG (pH, glucose) bloods for ketones, U&Es
  3. Urine dip
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141
Q

What is the diagnostic criteria for DKA?

A
  1. Glucose > 11 mmol/L or known DM
  2. pH < 7.3
  3. Bicarbonate < 15 mmol/L
  4. Presence of ketones:
    a. Ketones > 3mmol/L
    b. Urine ketones ++ on dipstick
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142
Q

What are the management principles of DKA?

A

MEDICAL EMERGENCY: A to E approach
1. Fluid resuscitation
2. Insulin
3. Correction of electrolyte disturbance
4. Long-term management e.g. insulin

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143
Q

What is the fluid replacement management in DKA?

A
  1. Most patients with DKA will be deplete of 5-8 L
  2. Isotonic saline is used initially (0.9% sodium chloride)
  3. Bolus of 500ml over 10-15 minutes
  4. Then replacement fluids: 100 ml/kg/day for the first 10kg, 50 ml/kg/day for the next 10kg, 20 ml/kg/day for weight over 20kg
  5. Plus maintenance fluids
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144
Q

What is the greatest risk in fluid resuscitation in children in the management of DKA?

A

Cerebral oedema:
1. Children and young adults are particularly vulnerable
2. Slower infusion rates may be indicated
3. Presents with headache, irritability, visual disturbance, focal neurology
4. If suspicion: CT head and senior review

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145
Q

What is the insulin management of DKA?

A
  1. Start an IV infusion at 0.1unit/kg/hour
  2. Once the blood glucose has been bought down to < 14mmol/L, continue the IV insulin and add 10% dextrose
  3. Infusion of 10% dextrose should be started at 125 mls/hr in addition to the 0.9% sodium chloride regime
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146
Q

How are electrolyte disturbances corrected in the management of DKA?

A
  1. Serum potassium levels fall after the administration of insulin
  2. Therefore may need to add potassium to the fluids
  3. Of the rate of potassium infusion is > 20 mmol/hour then cardiac monitoring may be required
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147
Q

What is DKA resolution?

A
  1. pH > 7.3
  2. Blood ketones < 0.6 mmol/L
  3. Bicarbonate > 15 mmol/L
    If the patient is eating and drinking at this point = switch to S/C insulin
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148
Q

What must happen before a patient is discharged for an admission of DKA?

A

The patient must be reviewed by a diabetes specialist nurse

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149
Q

How quickly should ketonaemia and acidosis resolve in the management of DKA?

A
  1. Should resolve within 24 hours
  2. If not, requires senior review from endocrinologist
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150
Q

What are the complications of a DKA?

A

Can be from DKA or the management of it:
1. Gastric stasis
2. VTE
3. Arrhythmias secondary to hyperkalaemia
4. Incorrect fluid therapy: cerebral oedema, hypokalaemia, hypoglycaemia
5. ARDS
6. AKI

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151
Q

What is the prognosis of DKA?

A

Although a serious condition, mortality has decreased significantly due to improved understanding of pathophysiology and close monitoring of electrolytes

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152
Q

What is Dyslipidaemia?

A

Classified as serum Total cholesterol, LDL-C, triglycerides, apolipoprotein B, or lipoprotein(a) concentrations above the 90th percentile for the general population

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153
Q

What is the aetiology of Dyslipidaemia?

A
  1. Primary causes: due to single or multiple gene mutations, resulting in a disturbance of LDL and triglyceride production or clearance (most commonly seen in children and young adults)
  2. Secondary causes: caused by lifestyle factors or disorders that interfere with blood lipid levels over time such as obesity, CKD
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154
Q

What is the epidemiology of Dyslipidaemia?

A
  1. Common, particularly in developing countries
  2. Strong correlation between body mass index and coronary heart disease
  3. Primary causes are common in children and young adults whereas secondary is seen more in adults
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155
Q

What are the presenting symptoms of Dyslipidaemia?

A
  1. Excess body weight
  2. PMH Diabetes Mellitus Type 2 or cardiovascular disease
  3. Consumption of saturated fats
  4. FH of early onset of coronary heart disease or Dyslipidaemia
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156
Q

What are the signs of Dyslipidaemia on physical examination?

A
  1. Xanthelasmas: Yellow plaques that occur most commonly near the inner canthus of the eyelid
  2. Tendinous xanthomas: Slowly enlarging subcutaneous nodules (on tendons or ligaments)
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157
Q

What are the appropriate investigations for Dyslipidaemia?

A

Lipid profile:
1. Total cholesterol (TC) >5.18 mmol/L (>200 mg/dL)
2. LDL-cholesterol >2.59 mmol/L (>100 mg/dL)
3. triglycerides >1.7 mmol/L (>150 mg/dL)
4. Fasting (12h) triglycerides: ≥2.3 mmol/L (200 mg/dL)
Can also offer TFTs

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158
Q

What is the management of dyslipidaemia divided into?

A

Primary prevention: 20mg atorvastatin
1. 10-year cardiovascular risk > 10%
2. Type 1 DM
3. CKD, eGFR < 60ml/min
Secondary prevention: 80mg atorvastatin
1. Known ischaemic heart disease
2. Cerebrovascular disease
3. Peripheral arterial disease

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159
Q

What are the management principles of dyslipidaemia?

A

Combination of lifestyle changes to diet and exercise, medications, and dietary supplements
1. Lifestyle changes: dietary reduction in total and saturated fat, weight loss in overweight patients, aerobic exercise
2. Drug therapy: Statins inhibit 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, a key enzyme in cholesterol synthesis, which leads to up-regulation of LDL receptors and increased LDL clearance

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160
Q

What are the complications of dyslipidaemia?

A

Due to atherosclerosis:
1. Ischaemic heart disease
2. Peripheral vascular disease
3. Acute coronary syndrome
4. Stroke
5. Erectile dysfunction (endothelial dysfunction)

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161
Q

What is the prognosis of dyslipidaemia?

A

The rate of adverse outcomes has been significantly reduced with the use of statins

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162
Q

What is Graves’ Disease?

A
  1. An autoimmune thyroid condition associated with hyperthyroidism caused by TSH (thyroid-stimulating hormone) receptor antibodies
  2. The most common cause of thyrotoxicosis
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163
Q

What is the epidemiology of Grave’s disease?

A

Typically seen in women aged 30-50 years

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164
Q

What is the aetiology of Graves’ Disease?

A

Autoantibodies:
1. TSH receptor stimulating antibodies (90%)
2. Anti-thyroid peroxidase antibodies (75%)
These lead to stimulation of the thyroid and overproduction of thyroxine

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165
Q

What are the features specific to Grave’s disease?

A
  1. Eye signs (30% of patients)
    a. exophthalmos
    b. ophthalmoplegia
  2. Pretibial myxoedema
  3. Thyroid acropachy, a triad of:
    a. digital clubbing
    b. soft tissue swelling of the hands and feet
    c. periosteal new bone formation
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166
Q

What are the signs of Grave’s disease on examination?

A
  1. Diffuse, smooth enlarged goitre
  2. Exophthalmos - bulging of the eye anteriorly
  3. Signs of thyrotoxicosis
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167
Q

How can the features of thyrotoxicosis be dividided?

A
  1. General: WL, manic, heat intolerance
  2. Cardiac: palpitations, high-output HF
  3. Skin: increased sweating, pretibial myxoedema, thyroid acropachy: clubbing
  4. GI: diarrhoea
  5. Oligomenorrhoea
  6. Neuro: anxiety, tremor
168
Q

What is pretibial myxoedema?

A

Erythematous, oedematous lesions above the lateral malleoli

169
Q

What are the investigations for Grave’s disease?

A
  1. Thyroid function tests: High T3/4, low TSH
  2. Autoantibodies:
    a. TSH receptor stimulating antibodies (90%)
    b. anti-thyroid peroxidase antibodies (75%)
  3. Thyroid scintigraphy: diffuse, homogenous, increased uptake of radioactive iodine
170
Q

What is the general management of Grave’s disease?

A
  1. Initial treatment
  2. Anti-thyroid drugs: carbimazole
  3. Radioiodine treatment
  4. Surgery
171
Q

What is the initial treatment of Grave’s disease?

A

Propranolol: used to help block the adrenergic effects

172
Q

What is the anti-thyroid drug management of Grave’s disease?

A
  1. Carbimazole is started at 40mg and reduced gradually to maintain euthyroidism
  2. Typically continued for 12-18 months
  3. An alternative regime is termed ‘block-and-replace’:
    a. carbimazole is started at 40mg
    b. thyroxine is added when the patient is euthyroid
    c. treatment typically lasts for 6-9 months
173
Q

What is the benefit of a anti-thyroid drug titration regime over a ‘block and replace’ regime?

A

Patients following atitration regime have been shown to suffer fewer side-effects than those on a block-and-replace regime

174
Q

What is the main complication of Carbimazole?

A

Agranulocytosis

175
Q

What is the radioiodine management of Grave’s disease and when is it indicated?

A
  1. Often used in patients who relapse following ATD therapy or are resistant to primary ATD treatment
  2. The proportion of patients who become hypothyroid depends on the dose given, but as a rule the majority of patient will require thyroxine supplementation after 5 years
176
Q

What are the contraindications of radioiodine management of Grave’s disease?

A
  1. Pregnancy (should be avoided for 4-6 months following treatment)
  2. Age < 16 years
  3. Thyroid eye disease is a relative contraindication, as it may worsen the condition (e.g. exophthalmos, ophthalmoplegia, optic disc swelling, conjunctival oedema)
177
Q

What is the management of thyroid eye disease?

A

Alongside management of Grave’s with Carbimazole:
1. Topical lubricants may be needed to help prevent corneal inflammation caused by exposure
2. Steroids
3. Surgery

178
Q

What is Hyperparathyroidism?

A

Disorders of calcium metabolism, where the parathyroid hormone levels are elevated by different pathologies

179
Q

What is the overview of the three different types of hyperparathyroidism?

A
  1. Primary: high PTH and high calcium, most likely due to a solitary adenoma
  2. Secondary:
    high PTH, low calcium, low Vitamin D, parathyroid gland hyperplasia as a result of low calcium due to CKD
  3. Tertiary: high PTH, high/ normal calcium, occurs as a result of ongoing hyperplasia of the parathyroid glands after correction of underlying renal disorder
180
Q

What is primary hyperparathyroidism?

A

Excess secretion of PTH resulting in hypercalcaemia, most commonly (85%) caused by a solitary adenoma of the parathyroid gland

181
Q

What is the main symptom of primary hyperparathyroidism?

A

80% of patients are asymptomatic (diagnosed on routine bloods)

182
Q

What are the symptomatic features of primary hyperparathyroidism?

A

‘bones, stones, abdominal groans and psychic moans’:
1. Polydipsia, polyuria
2. Depression
3. Anorexia, nausea
4. Constipation
5. Peptic ulceration
6. Pancreatitis
7. Bone pain/fracture
8. Renal stones
9. Hypertension

183
Q

What is associated with primary hyperparathyroidism?

A

Hypertension and multiple endocrine neoplasia: MEN I and II

184
Q

What are the investigations for primary hyperparathyroidism?

A
  1. Bloods:
    a. High calcium, low phosphate
    b. PTH may be raised or (inappropriately, given the raised calcium) normal
  2. Technetium-MIBI subtraction scan
  3. X-ray findings:
    a. pepperpot skull
    b. osteitis fibrosa cystica
185
Q

What is the management for primary hyperparathyroidism?

A
  1. Definitive: total parathyroidectomy
  2. Conservative: may be offered if the calcium level is less than 0.25 mmol/L above the upper limit of normal AND the patient is > 50 years AND there is no evidence of end-organ damage
  3. Patients not suitable for surgery: cinacalcet, a calcimimetic, ‘mimics’ the action of calcium on tissues by allosteric activation of the calcium-sensing receptor
186
Q

What are the indications for a total parathyroidectomy in primary hyperparathyroidism?

A
  1. Elevated serum Calcium > 1mg/dL above normal
  2. Hypercalciuria > 400mg/day
  3. Creatinine clearance < 30% compared with normal
  4. Episode of life threatening hypercalcaemia
  5. Nephrolithiasis: kidney stones
  6. Age < 50 years
  7. Neuromuscular symptoms
  8. Reduction in bone mineral density of the femoral neck, lumbar spine, or distal radius (T score lower than -2.5)
187
Q

What is secondary hyperparathyroidism?

A

Parathyroid gland hyperplasia occurs as a result of low calcium, almost always in a setting of chronic renal failure

188
Q

What are the features of secondary hyperparathyroidism?

A
  1. May have few symptoms
  2. Eventually may develop bone disease, osteitis fibrosa cystica and soft tissue calcifications
189
Q

What are the blood results of secondary hyperparathyroidism?

A
  1. PTH = Elevated
  2. Calcium = Low or normal
  3. Phosphate = Elevated
  4. Vitamin D levels = Low
190
Q

What is the management of secondary hyperparathyroidism?

A
  1. Usually managed with medical therapy
  2. Indications for surgery in secondary (renal) hyperparathyroidism:
    a. Bone pain
    b. Persistent pruritus
    c. Soft tissue calcifications
191
Q

What is tertiary hyperparathyroidism?

A
  1. Occurs as a result of ongoing hyperplasia of the parathyroid glands after correction of underlying renal disorder
  2. Hyperplasia of all 4 glands is usually the cause
192
Q

What are the features and blood findings of tertiary hyperparathyroidism?

A
  1. Metastatic calcification
  2. Bone pain and / or fracture
  3. Nephrolithiasis: kidney stones
  4. Pancreatitis
    Bloods:
    a. Calcium = Normal or high
    b. PTH = Elevated
    c. Phosphate levels = decreased/ normal
    d. Vitamin D = normal or decreased
    e. Alkaline phosphatase = elevated
193
Q

What is the management of tertiary hyperparathyroidism?

A
  1. Alow 12 months to elapse following renal transplant as many cases will resolve
  2. The presence of an autonomously functioning parathyroid gland may require surgery
  3. If the culprit gland can be identified then it should be excised - otherwise total parathyroidectomy and re-implantation of part of the gland may be required
194
Q

What is the management of acute hypercalcaemia?

A
  1. IV fluids (often 4–6 in the first 24 h)
  2. Conservative management:
    a. Avoid factors that can exacerbate hypercalcaemia including thiazide diuretics
    b. Maintain adequate hydration (at least 6–8 glasses of water per day), moderate calcium and vitamin D intake
195
Q

What is Female Hypogonadism?

A

Characterized by impairment of ovarian function

196
Q

What are the causes of primary female hypogonadism?

A
  1. Gonadal dysgensis: Chromosomal abnormalities (e.g. Turner’s syndrome), FMR1 gene pre-mutation carriers
  2. Gonadal damage: Autoimmune, iatrogenic (chemotherapy, radiation, surgery)
197
Q

What are the causes of secondary female hypogonadism?

A
  1. Functional: Stress, weight loss, excessive exercise, eating disorders (anorexia nervosa, bulimia)
  2. Pituitary/hypothalamic tumours and infiltrative lesions: Pituitary adenomas, craniopharyngiomas, haemochromatosis
  3. Hyperprolactinaemia: Prolactinomas or tumours causing pituitary stalk compression
  4. Congenital GnRH deficiency: Kallmann’s syndrome, idiopathic
198
Q

What is the epidemiology of Female Hypogonadism?

A
  1. Secondary hypogonadism is a more common cause of anovulation and amenorrhoea than primary hypogonadism
  2. Turner’s syndrome occurs in up to 1.5% of conceptions,
199
Q

What are the presenting symptoms of Female Hypogonadism?

A

Symptoms of oestrogen deficiency:
1. Night sweats
2. Hot flush
3. Vaginal dryness and dyspareunia (painful intercourse)
4. Reduced libido
5. Infertility
Symptoms of the underlying cause e.g. prolactinomas

200
Q

What are the signs of female hypogonadism divided into?

A

Divided into pre-pubertal hypogonadism or post pubertal hypogonadism

201
Q

What are the signs of pre-pubertal female hypogonadism?

A
  1. Delayed puberty:
    a. primary amenorrhoea
    b. absent breast development
    c. no secondary sexual characteristics
  2. Eunuchoid proportions (e.g. long legs, increased arm span for height)
202
Q

What are the signs of post-pubertal female hypogonadism?

A
  1. Regression of secondary sexual characteristics (loss of secondary sexual hair, breast atrophy)
  2. Perioral and periorbital fine facial wrinkles
  3. Signs of the underlying cause/associated conditions:
    a. Hypothalamic/pituitary disease: Visual field defects (bitemporal hemianopia)
    b. Kallmann’s syndrome: Anosmia
    c. Turner’s syndrome: Short stature, low posterior hairline, high arched palate, widely spaced nipples, wide carrying angle, short fourth and fifth metacarpals, congenital lymphoedema
  4. Patients with autoimmune primary ovarian failure, signs of Addison’s
203
Q

What are the appropriate investigations in Female Hypogonadism?

A
  1. Serum oestradiol: LOW
  2. Serum FSH and LH:
    a. HIGH in primary hypogonadism (due to -ve feedback inhibition by ovarian oestradiol and inhibin).
    b. LOW or inappropriately normal FSH/LH in secondary hypogonadism
  3. Investigating aetiology:
    a. Primary: Genetic testing/ Karyotype
    b. Secondary: Pituitary function tests (9 a.m. cortisol, TFTs, prolactin), pituitary MRI
204
Q

What is Male Hypogonadism?

A

A syndrome of reduced testosterone production, sperm production or both

205
Q

What are the causes of primary male hypogonadism?

A
  1. Gonadal dysgensis: Klinefelter’s syndrome (XXY), undescended testes (cryptorchidism)
  2. Gonadal damage: Infection (e.g. mumps), torsion, trauma, autoimmune, iatrogenic (chemotherapy, surgery, radiation)
  3. Rare causes: Defects in enzymes involved in testosterone synthesis, myotonic dystrophy
206
Q

What are the causes of secondary male hypogonadism?

A
  1. Pituitary/hypothalamic lesions
  2. GnRH deficiency: Kallmann’s syndrome (associated with anosmia)
  3. Idiopathic 4. Hyperprolactinaemia
  4. Systemic/chronic diseases
  5. Rare causes: Genetic mutations, e.g. Prader–Willi syndrome: loss of a critical region on chromosome 15 causing obesity and short
    stature, small hands, almond-shaped eyes, learning difficulty/postnatal hypotonia
207
Q

What is the epidemiology of Male Hypogonadism?

A
  1. The prevalence of hypogonadism increases with age
  2. Primary hypogonadism accounts for 30–40% of cases of male infertility; secondary hypogonadism accounts for 1–2%
  3. Most common cause of primary hypogonadism is Klinefelter’s syndrome
208
Q

What are the presenting symptoms of Male Hypogonadism?

A
  1. Delayed puberty (if the onset is before puberty)
  2. Reduced libido, impotence, infertility
  3. Symptoms of the underlying cause: Klinefelter’s syndrome: intellectual dysfunction and
    behavioural abnormalities which cause difficulty in social interactions
209
Q

What are the signs of pre-pubertal male hypogonadism on physical examination?

A

Signs of delayed puberty:
1. High-pitched voice
2. Lack of pubic/axillary/facial hair
3. Small or undescended testes, small phallus
4. Gynaecomastia
5. Eunuchoid proportions (due to delayed fusion of the epiphyses and continued growth of long bones)
Features of the underlying cause e.g. cryptorchidism, anosmia in Kallmann’s syndrome

210
Q

What are the signs of post pubertal male hypogonadism on examination?

A
  1. Lack of Pubic/axillary/facial hair
  2. Soft and small testes
  3. Gynaecomastia
  4. Fine perioral wrinkles
  5. Features of the underlying cause e.g. visual field defects due to a pituitary tumour, signs of systemic/chronic illness
211
Q

What are the appropriate investigations for Male Hypogonadism?

A
  1. Serum total testosterone:
    Check between 6 a.m. and 8 a.m. ideally
    -less than 10.4 nanomol/L (<300 nanograms/dL) = as hypogonadism
    Results:
    a. Primary: LOW Testosterone, HIGH LH and FSH (due to -ve negative feedback)
    b. Secondary: LOW Testosterone, LOW or inappropriately normal LH and FSH levels
  2. Secondary causes: Pituitary function tests, pituitary MRI
212
Q

What is androgen insensitivity syndrome?

A
  1. An X-linked recessive condition due to end-organ resistance to testosterone causing genotypically male children (46XY) to have a female phenotype
  2. Complete androgen insensitivity syndrome is the new term for testicular feminisation syndrome
213
Q

What are the features of androgen insensitivity syndrome?

A
  1. ‘primary amenorrhoea’
  2. Undescended testes causing groin swellings
  3. Breast development may occur as a result of conversion of testosterone to oestradiol
214
Q

How is androgen insensitivity syndrome diagnosed?

A

buccal smear or chromosomal analysis to reveal 46XY genotype

215
Q

What is the management of androgen insensitivity syndrome?

A
  1. Counselling - raise child as female
  2. Bilateral orchidectomy (increased risk of testicular cancer due to undescended testes)
  3. Oestrogen therapy
216
Q

What is hypopituitarism?

A

The inadequate production of one or more of the hormones secreted by the pituitary gland

217
Q

What is the most common cause of hypopituitarism?

A

Compression of the pituitary gland by non-secretory pituitary macroadenoma

218
Q

What are the other causes of hypopituitarism?

A
  1. Pituitary apoplexy
  2. Sheehan’s syndrome: postpartum pituitary necrosis secondary to a postpartum haemorrhage
  3. Hypothalamic tumours e.g. craniopharyngioma
  4. Trauma
  5. Iatrogenic irradiation
  6. Infiltrative e.g. hemochromatosis, sarcoidosis
219
Q

What are the anterior pituitary hormones?

A

GH
FSH/LH
Prolactin
ACTH
TSH

220
Q

What are the posterior pituitary hormones?

A

Vasopressin (ADH)
Oxytocin

221
Q

What is the epidemiology of hypopituitarism?

A

Relatively rare

222
Q

What do the features of hypopituitarism depend on?

A

Which hormones are deficient

223
Q

What are the features of low ACTH?

A
  1. Tiredness
  2. Postural hypotension
224
Q

What are the features of low FSH/LH?

A
  1. Amenorrhoea
  2. Infertility
  3. Loss of libido
225
Q

What are the features of low TSH?

A
  1. Feeling cold
  2. Constipation
226
Q

What are the features of low prolactin?

A

Problems with lactation

227
Q

What are the features of hypopituitarism depending on the underlying cause?

A
  1. Pituriary macroadenoma → bitemporal hemianopia
  2. Pituitary apoplexy → sudden, severe headache
228
Q

What are the investigations for hypopituitarism?

A
  1. Pituitary function tests: 9am hormone profile testing
  2. Imaging: MRI or CT to show pituitary masses, vascular lesions
  3. Visual field testing
229
Q

What is the management of hypopituitarism?

A
  1. Treatment of any underlying cause (e.g. surgical removal of pituitary macroadenoma)
  2. Replacement of deficient hormones
230
Q

What are the hormones replacement therapy in the management of hypopituitarism?

A
  1. Hydrocortisone: 20 mg in morning, 10 mg in evening (double oral dose for febrile illnesses, IM hydrocortisone at times of surgery). Should be provided with Medicalert bracelet and steroid card!
  2. Levothyroxine: 100 mg daily (always taken after hydrocortisone to avoid Addisonian crisis)
  3. Sex hormones: Testosterone/ Oestrogen and progestogerone
  4. Growth hormone: SC 1.2 unit/day in adults, children require specialist supervision
231
Q

What is the hormone replacement if hypopituitarism results in deficiency of the posterior pituitary hormones?

A

Effectively lead to cranial DI: Desmopressin (vasopressin analogue) 10–20 mg/day intranasally

232
Q

What are the complications of Hypopituitarism?

A
  1. Adrenal crisis
  2. Hypoglycaemia
  3. Myxoedema coma: severe hypothyroidism leading to decreased mental status, hypothermia, and slowing of function in multiple organs- it is a medical emergency with a high mortality rate
  4. Infertility
  5. Osteoporosis; dwarfism (children)
233
Q

What are the complications of an non-secretory adrenal mass leading to hypopituitarism?

A
  1. Optic chiasm compression
  2. Hydrocephalus (third ventricular compression)
  3. Temporal lobe epilepsy
234
Q

What is the prognosis of Hypopituitarism?

A

Good with lifelong hormone replacement

235
Q

What is Hypothyroidism?

A

The clinical syndrome resulting from insufficient secretion of thyroid hormones

236
Q

What does primary hypothyroidism mean?

A

Reduced thyroid hormone production (high TSH, low T3/T4)

237
Q

What are the causes of primary hypothyroidism?

A
  1. Acquired:
    a. Autoimmune (Hashimoto’s) thyroiditis (cellular and antibody-mediated)
    b. Iatrogenic (post-surgery, radioiodine, Lithium, medication for hyperthyroidism e.g. carbimazole)
    c. Severe iodine deficiency or iodine excess (Wolff–Chaikoff effect)
    d. Thyroiditis
  2. Congenital:
    a. Thyroid dysgenesis
    b. Inherited defects in thyroid hormone biosynthesis
238
Q

What does secondary hypothyroidism mean?

A

Pituitary or hypothalamic disease resulting in reduced TSH, therefore low T3/T4

239
Q

What are the causes of secondary hypothyroidism?

A

Uncommon, <5% of cases:
Pituitary or hypothalamic tumours resulting in low TSH, pituitary failure

240
Q

What is the epidemiology of hypothyroidism?

A

Affects around 1-2% of women in the UK and is around 5-10 times more common in females than males

241
Q

What is the most common cause of hypothyroidism?

A

Hashimoto’s thyroiditis:
1. Autoimmune disease
2. Associated with T1DM, Addison’s or pernicious anaemia
3. May cause transient thyrotoxicosis in the acute phase
4. 5-10 times more common in women

242
Q

How can the features of hypothyroidism be divided?

A

Into system e.g. general, skin, GI
Overall:
1. Cold intolerance
2. Lethargy
3. Weight gain
4. Constipation
5. Dry skin
6. Hair loss

243
Q

What are the general features of hypothyroidism?

A
  1. Weight gain
  2. Lethargy
  3. Cold intolerance
244
Q

What are the skin features of hypothyroidism?

A
  1. Dry (anhydrosis), cold, yellowish skin
  2. Non-pitting oedema (e.g. hands, face)
  3. Dry, coarse scalp hair, loss of lateral aspect of eyebrows
245
Q

What is the main GI feature of hypothyroidism?

A

Constipation

246
Q

What is the main gynaecological feature of hypothyroidism?

A

Menorrhagia

247
Q

What are the neurological features of hypothyroidism?

A
  1. Decreased deep tendon reflexes
  2. Carpal tunnel syndrome
248
Q

What are the signs of hypothyroidism on physical examination?

A
  1. Hands: Bradycardia, cold hands
  2. Head/Neck/Skin:
    a. Pale puffy face
    b. Oedema
    c. Hair loss
    d. Dry skin
    e. Vitiligo
  3. Chest: Pericardial or pleural effusions
  4. Abdomen: Ascites
  5. Neurological: Slow relaxation of reflexes, signs of carpal tunnel syndrome
249
Q

What are the main investigations for hypothyroidism?

A

Thyroid function tests:
1. Primary: Low T4/T3 and High TSH (due to negative feedback)
2. Secondary: Low T3/T4 and Low or inappropriately normal TSH

250
Q

What other investigations can be ordered for hypothyroidism?

A

General bloods: including anti-thyroid peroxidase (TPO) for Hashimoto’s
Imaging: MRI/ CT head to identify pituitary/ hypothalamic tumours

251
Q

What is the management of hypothyroidism?

A

Levothyroxine replacement therapy:
1. Star on a dose of 50-100mcg od
2. Following a change in thyroxine dose TFTs should be checked after 8-12 weeks
3. The therapeutic goal is ‘normalisation’ of TSH levels, aim for a value 0.5-2.5 mU/

252
Q

Which hypothyroid patients should be started on a 25mcg dose of levothyroxine?

A

Patients with cardiac disease, severe hypothyroidism or patients over 50 years (this can then be slowly titrated up)

253
Q

What should happen to patients with established hypothyroidism if they become pregnant?

A

Should have their dose increased ‘by at least 25-50 micrograms levothyroxine’ due to the increased demands of pregnancy - the TSH should be monitored carefully, aiming for a low-normal value

254
Q

What are the side effects of Levothyroxine?

A
  1. Hyperthyroidism: due to over treatment
  2. Reduced bone mineral density
  3. Worsening of angina
  4. Atrial fibrillation
255
Q

What are the interactions of levothyroxine?

A

Iron, calcium carbonate:
Absorption of levothyroxine reduced, give at least 4 hours apart

256
Q

What are the features of Myxoedema coma in hypothyroidism?

A

Severe hypothyroidism usually seen in the elderly:
1. Hypothermia
2. Hypoventilation
3. Hyponatraemia
4. Heart failure
5. Confusion
6. Coma

257
Q

What is the management of Myxoedema coma in hypothyroidism?

A
  1. Oxygen
  2. Rewarming
  3. Rehydration
  4. IV T4/T3
  5. IV hydrocortisone (in case hypothyroidism is secondary to hypopituitarism)
  6. Treat the underlying disorder e.g. infection
258
Q

What are the complications of hypothyroidism?

A
  1. Myxoedema coma
  2. Mxoedema madness: psychosis with delusions and hallucinations or dementia in severe hypothyroidism (may be seen in the elderly after starting levothyroxine treatment)
259
Q

What is the prognosis of Myxoedema coma?

A

80% mortality rate

260
Q

What is the prognosis of hypothyroidism?

A

Good, lifelong levothyroxine therapy is required

261
Q

What is subclinical hypothyroidism?

A

Incidental finding of high TSH but normal T3/4, often no obvious symptoms

262
Q

What is the significance of subclinical hypothyroidism?

A
  1. Risk of progressing to overt hypothyroidism is 2-5% per year (higher in men)
  2. Risk increased by the presence of thyroid autoantibodies
263
Q

What is the management of subclinical hypothyroidism?

A
  1. Not all patients require treatment
  2. Depends on TSH and free thryoxine level
264
Q

What is the management of subclinical hypothyroidism if the TSH is > 10mU/L?

A

Consider offering levothyroxine if the TSH level is > 10 mU/L on 2 separate occasions 3 months apart

265
Q

What is the management of subclinical hypothyroidism if the TSH is between 5.5 - 10mU/L?

A
  1. If < 65 years: consider offering a 6-month trial of levothyroxine if: the TSH level is 5.5 - 10mU/L on 2 separate occasions 3 months apart PLUS
    there are symptoms of hypothyroidism
  2. In older people (especially those > 80 years) follow a ‘watch and wait’ strategy is often used
  3. In asymptomatic people, observe and repeat thyroid function in 6 months
266
Q

What is the menopause?

A
  1. The permanent cessation of menstruation due to reduced levels of female hormones, principally oestrogen
  2. Caused by the loss of follicular activity
  3. Clinical diagnosis: when a woman has not had a period for 12 months
267
Q

What is the climacteric in regards to the menopause?

A

The period prior to the menopause where women may experience symptoms, as ovarian function starts to fail

268
Q

How can the symptoms of the menopause be divided?

A
  1. Changes in periods
  2. Vasomotor symptoms
  3. Urogenital changes
  4. Psychological changes
  5. Longer term complications
269
Q

What are the changes in periods in the menopause?

A
  1. Change in length of menstrual cycles
  2. Dysfunctional uterine bleeding may occur
270
Q

What are the vasomotor symptoms in the menopause?

A

Affect up to 80% of women: Usually occur daily and may continue for up to 5 years:
1. Hot flushes
2. Night sweats

271
Q

What are the urogenital symptoms in the menopause?

A

Affects up to 35% of women:
1. Vaginal dryness and atrophy
2. Urinary frequency

272
Q

What are the psychological symptoms in the menopause?

A
  1. Anxiety and depression may be seen - around 10% of women
  2. Short term memory impairment
273
Q

What are the longer term complications of the menopause?

A
  1. Osteoporosis
  2. Increased risk of ischaemic heart disease
274
Q

What is the management of the menopause?

A

Three categories:
1. Lifestyle modifications
2. Hormone replacement therapy (HRT)
3. Non-hormone replacement therapy

275
Q

What are the lifestyle modifications in the management of the menopause?

A
  1. Hot flushes: regular exercise, weight loss and reduce stress
  2. Sleep disturbance: avoiding late evening exercise and maintaining good sleep hygiene
  3. Mood: sleep, regular exercise and relaxation
  4. Cognitive symptoms: regular exercise and good sleep hygiene
276
Q

What is the management of the menopause with HRT?

A

Hormone replacement therapy:
1. If the woman has a uterus then it is important not to give unopposed oestrogens as this will increase her risk of endometrial cancer: therefore oral or transdermal combined HRT is given
2. If the woman does not have a uterus then oestrogen alone can be given either orally or in a transdermal patch

277
Q

What are the contraindications of HRT?

A
  1. Current or past breast cancer
  2. Any oestrogen-sensitive cancer
  3. Undiagnosed vaginal bleeding
  4. Untreated endometrial hyperplasia
278
Q

What are the risks of HRT?

A
  1. VTE: a slight increase in risk with all forms of oral HRT, but NO increased risk with transdermal HRT
  2. Stroke: slightly increased risk with oral oestrogen
  3. Coronary heart disease: combined HRT may be associated with a slight increase in risk
  4. Breast cancer: there is an increased risk with all combined HRT although the risk of dying from breast cancer is not raised
  5. Ovarian cancer: increased risk with all HRT
279
Q

What are the non-hormonal treatments of the menopause?

A
  1. Vasomotor symptoms: fluoxetine, citalopram or venlafaxine
  2. Vaginal dryness: vaginal lubricant or moisturiser
  3. Psychological symptoms: self-help groups, CBT or antidepressants
  4. Urogenital symptoms:
    a. if suffering from urogenital atrophy vaginal oestrogen can be prescribed (even on HRT)
    b. vaginal dryness can be treated with moisturisers and lubricants (can be offered alongside vaginal oestrogens if required)
280
Q

What is Multiple Endocrine Neoplasia (MEN)?

A

Hereditary tumours of variable neoplastic patterns and characterised by the development of multiple endocrine tumours

281
Q

What is the aetiology of Multiple Endocrine Neoplasia (MEN)?

A

Tnherited as an autosomal dominant disorder:
MEN type 1: 3Ps
MEN type 2a: 2Ps
MEN type 2b: 1P

282
Q

What are the 3P’s of MEN type 1?

A
  1. Parathyroid (95%): hyperparathyroidism due to parathyroid hyperplasia
  2. Pituitary (70%)
  3. Pancreas (50%): e.g. insulinoma, gastrinoma (leading to recurrent peptic ulceration)
283
Q

What are the 2P’s of MEN type 2a?

A
  1. Parathyroid (60%)
  2. Phaeochromocytoma
    Important: Medullary thyroid cancer (70%)
284
Q

What is the 1P of MEN type 2b?

A

Phaeochromocytoma
(may have Marfanoid body habitus, neuromas, Medullary thyroid cancer)

285
Q

What is the most common presentation of MEN type 1?

A

Hypercalaemia (from hyperparathyroidism from parathyroid hyperplasia)

286
Q

What is the epidemiology of MEN?

A

Relatively rare
In MEN type 1: at least 90% of patients develop primary hyperparathyroidism

287
Q

What are the presenting symptoms and signs of MEN type 1 on physical examination?

A
  1. Facial lesions (angiofibromas)
  2. Irregular menses/ infertility/ erectile dysfunction
  3. Visual changes
  4. Clinical features of acromegaly
  5. Clinical features of thyrotoxicosis
  6. Heat intolerance
288
Q

What are the presenting symptoms and signs of MEN type 2 on physical examination?

A
  1. Episodic triad of sweating, palpitations and headaches
  2. Palpable thyroid nodule (medullary thyroid cancer)
  3. Unexplained flushing
  4. GI bleeding
  5. Hepatomegaly: if there are liver metastases
289
Q

What are the investigations for MEN?

A

Type 1:
1. Fasting serum gastrin: raised
2. Serum chromogranin A: raised
3. Serum prolactin: raised
4. Insulin-like Growth Factor 1 (IGF-1): raised
5. Pituitary MRI: adenoma
Type 2:
1. Serum calcitonin: raised (medullary thyroid cancer)
2. Plasma metanephrines: elevated levels suggest phaeochromocytoma
3. 24h urine metanephrines and catecholamines

290
Q

What is obesity?

A

Can be defined as a chronic adverse condition due to an excess amount of body fat

291
Q

What is the aetiology of obesity?

A

Caused by calorie intake, over time, is greater than the calorie expenditure
Other factors:
1. Genetic predisposition
2. Behavioural dynamics (portion sizes)
3. Hormonal disturbances

292
Q

What are the presenting symptoms/signs of Obesity?

A
  1. Calculate BMI: (weight/height2)
  2. Waist circumference
  3. Co-morbidities such as type 2 diabetes, cardiovascular disease, hypertension, hyperlipidaemia
293
Q

What are the appropriate investigations for Obesity?

A

Usually a clinical diagnosis, can consider:
1. ECG: Routine screen for signs of heart disease if suspected
2. TFTs: Routine screen if hypothyroidism is suspected
3. Abdominal ultrasound: Routine screen for fatty liver, steatohepatitis

294
Q

How is obesity classified?

A

Underweight: < 18.49
Normal: 18.5 - 25
Overweight: 25 - 30
Obese class 1: 30 - 35
Obese class 2: 35 - 40
Obese class 3: > 40

295
Q

What is the management approach to obesity?

A
  1. Conservative: diet, exercise
  2. Medical:
    a. Orlistat
    b. Liraglutide
  3. Surgical
296
Q

What is Orlistat in the medical management of obesity?

A
  1. A pancreatic lipase inhibitor 2. Adverse effects: faecal urgency/incontinence and flatulence
  2. A lower dose version is now available without prescription (‘Alli’)
  3. It should only be prescribed as part of an overall plan for managing obesity in adults who have:
    a. BMI of 28 kg/m^2 or more with associated risk factors, or
    b. BMI of 30 kg/m^2 or more
    continued weight loss e.g. 5% at 3 months
  4. Orlistat is normally used for < 1 year
297
Q

What is Lireglutide in the medical management of obesity?

A
  1. A glucagon-like peptide-1 (GLP-1) mimetic that is used in the management of T2DM
  2. Given as a once daily SC injection
  3. For use in a person with:
    a. BMI of at least 35 kg/m²
    b. prediabetic hyperglycaemia (e.g. HbA1c 42 - 47 mmol/mol)
298
Q

What are the different types of bariatric surgery for the management of obesity?

A
  1. Primarily restrictive operations:
    a. laparoscopic-adjustable gastric banding (LAGB)
    b. Sleeve gastrectomy
    c. Intragastric balloon
  2. Primary malabsorptive operations: biliopancreatic diversion with duodenal switch
  3. Mixed
299
Q

What is Oestomalacia?

A

Softening of the bones secondary to low vitamin D levels that in turn lead to decreased bone mineral content (rickets in children)

300
Q

What is the main cause of osteomalacia?

A

Vitamin D deficiency:
1. Malabsorption
2. Lack of sunlight
3. Diet

301
Q

What are the other causes of osteomalacia?

A
  1. Chronic kidney disease
  2. Drug induced e.g. anti-convulsants
  3. Inherited: hypophosphatemic rickets
  4. Liver disease: e.g. cirrhosis
  5. Coeliac disease
302
Q

What are the features of osteomalacia?

A
  1. Bone pain
  2. Bone/muscle tenderness
  3. Fractures: especially femoral neck
  4. Proximal myopathy: may lead to a waddling gait
303
Q

What are the investigations for osteomalacia?

A
  1. Bloods:
    a. Low vitamin D levels
    b. Low calcium, phosphate (in around 30%)
    c. Raised alkaline phosphatase (in 95-100% of patients)
  2. X-ray: translucent bands (Looser’s zones or pseudofractures)
304
Q

What is the management of osteomalacia?

A
  1. Vitamin D supplementation: a loading dose is often needed initially
  2. Calcium supplementation if dietary calcium is inadequate
305
Q

What are the signs of rickets on examination?

A
  1. Bossing of frontal and parietal bones- unusually prominent forehead
  2. Swelling of costochondral junctions (upper ribs) (rickety rosary)
  3. Bow legs in early childhood, knock knees in later childhood
  4. Short stature
306
Q

What are the complications of osteomalacia?

A
  1. Bone deformities
  2. Hypocalcaemia may cause epileptic seizures
  3. Cardiac arrhythmias
  4. Hypocalcaemic tetany: spasms of the hands and feet, cramps, spasm of the larynx and overactive neurological reflexes
  5. Depression
307
Q

What are the signs of hypocalcaemia on examination?

A
  1. Trousseau’s sign: Inflation of the sphygmomanometer cuff to above the systolic pressure for >3 min causes tetanic spasm of wrist and fingers.
  2. Chvostek’s sign: Tapping over the facial nerve causes twitching of the ipsilateral facial muscles
308
Q

What is the prognosis of osteomalacia?

A
  1. Symptoms and radiological appearances improve with vitamin D supplementation
  2. Bone deformities in children tend to be permanent
309
Q

What is osteoporosis?

A

A complex skeletal disease characterised by low/reduced bone density and micro-architectural defects in bone tissue, resulting in:
1. Increased bone fragility
2. Susceptibility to fracture

310
Q

What is reduced bone density defined as?

A

<2.5 standard deviations below peak bone mass achieved by healthy adults

311
Q

What are the two most significant risk factors for osteoporosis?

A

Advancing age and female sex

312
Q

What is the epidemiology of osteoporosis?

A

The prevalence of osteoporosis increases from 2% at 50 years to more than 25% at 80 years in women

313
Q

What are some of the other risk factors and secondary causes of osteoporosis?

A
  1. History of glucocorticoid use
  2. Rheumatoid arthritis
  3. Alcohol excess
  4. History of parental hip fracture (FH)
  5. Low BMI
  6. Current smoking
  7. CKD
  8. GI disease: IBD, coeliac disease
  9. Endocrine: hyperthyroidism, hypogonadism, DM
314
Q

What are the presenting symptoms of osteoporosis?

A

Often asymptomatic until characteristic fractures occur:
1. Femoral neck fractures (commonly after minimal trauma)
2. Vertebral factures (loss of height or stooped posture or acute back pain after lifting)
3. Colles’ fracture of the distal radius after fall onto outstretched hand

315
Q

What are the signs of osteoporosis on physical examination?

A

Often no signs until complications develop:
1. Tenderness on percussion (over vertebral fractures)
2. Thoracic kyphosis-roundback (if multiple vertebral fractures)
3. Severe pain with leg shortened and externally rotated (in a femoral neck fracture)

316
Q

What is the FRAX screening tool?

A

A screening tool in osteoporosis to assess the 10-year risk of a patient developing a fragility fracture

317
Q

What are the investigations for osteoporosis?

A

If a patient is diagnosed with osteoporosis or has a fragility fracture further investigations may be warranted:
1. History and physical examination
2. Blood cell count, ESR, CRP, serum calcium
3. LFTs: albumin, creatinine, phosphate, alkaline phosphatase and liver transaminases
4. TFTs
5. Bone densitometry (DXA)

318
Q

What are the DEXA scan findings for osteoporosis?

A

T-score: based on bone mass of young reference population
> -1.0 = normal
-1.0 to -2.5 = osteopaenia
< -2.5 = osteoporosis

319
Q

What T score is defined as osteoporotic?

A

< -2.5

320
Q

What is the management for osteoporosis?

A
  1. Vitamin D and calcium supplementation should be offered to all women
  2. Bisphosphonates: Alendronate is first-line
  3. If cannot tolerate alendronate (upper GI problems): should be offered risedronate or etidronate
321
Q

What are the management guidelines regarding the use of bisphosphonates for oestoporosis?

A
  1. Alendronate is first line
  2. The T-score criteria for risedronate or etidronate are less than the others implying that these are the second line drugs
  3. If alendronate, risedronate or etidronate cannot be taken then strontium ranelate or raloxifene may be given based on quite strict T-scores (e.g. a 60-year-old woman would need a T-score < -3.5)
  4. The strictest criteria are for denosumab
322
Q

What is Paget’s disease of the bone?

A

Disease of increased but uncontrolled bone turnover

323
Q

What is the aetiology of Paget’s disease?

A

Thought to be primarily a disorder of osteoclasts, with excessive osteoclastic resorption followed by increased osteoblastic activity

324
Q

What is the epidemiology of Paget’s disease?

A

Common (UK prevalence 5%) but symptomatic in only 1 in 20 patients

325
Q

What are the predisposing factors for Paget’s disease?

A
  1. Increasing age
  2. Male sex
  3. Northern latitude
  4. Family history
326
Q

What are the common affected sites in Paget’s disease?

A

The skull, spine/pelvis, and long bones of the lower extremities

327
Q

What are the features of Paget’s disease?

A

Only 5% of people are symptomatic:
1. Stereotypical presentation: older male with bone pain and an isolated raised ALP
2. Bone pain (e.g. pelvis, lumbar spine, femur)

328
Q

What are the features of untreated Paget’s disease?

A

Bowing of tibia and bossing of skull

329
Q

What are the investigations for Paget’s disease?

A
  1. Bloods:
    a. raised ALP
    b. Normal calcium and phosphate (hypercalcaemia may occasionally occur with prolonged immobilisation)
  2. Other arkers of bone turnover include:
    a. procollagen type I N-terminal propeptide (PINP)
    b. serum C-telopeptide (CTx)
  3. X-rays:
    a. Osteolysis in early disease → mixed lytic/sclerotic lesions later
    b. Skull x-ray: thickened vault, osteoporosis circumscripta
  4. Bone scintigraphy: increased uptake is seen focally at the sites of active bone lesions
330
Q

What is the indication for management of Paget’s disease?

A
  1. Bone pain
  2. Skull or long bone deformity
  3. Fracture
  4. Periarticular Paget’s
331
Q

What is the mainstay of management of Paget’s disease?

A

Bisphosphonate: either oral risedronate or IV zoledronate

332
Q

What are the complications of Paget’s disease?

A
  1. Deafness: cranial nerve, vestibulocochlear entrapment
  2. Bone sarcoma: 1% if affected for > 10 years
  3. Fractures
  4. Skull thickening
  5. High-output cardiac failure
333
Q

What is a Phaeochromocytoma?

A

A rare catecholamine secreting tumour

334
Q

What are Phaeochromocytomas associated with ?

A

About 10% are familial and may be associated with MEN type II, neurofibromatosis and von Hippel-Lindau syndrome

335
Q

What is the aetiology of Phaeochromocytomas?

A
  1. Usually arises from chromaffin cells of the adrenal medulla
  2. Bilateral in 10%
  3. Malignant in 10%
  4. Extra-adrenal in 10% (most common site = organ of Zuckerkandl, adjacent to the bifurcation of the aorta)
336
Q

What is the epidemiology of Phaeochromocytomas?

A

Rare condition

337
Q

What are the features of Phaeochromocytomas?

A

Typically episodic:
1. Hypertension (around 90% of cases, may be sustained)
2. Headaches
3. Palpitations
4. Sweating
5. Anxiety

338
Q

What is the investigation of choice for Phaeochromocytomas?

A

24 hr urinary collection of metanephrines (sensitivity 97%) - this has replaced collection of catecholamines

339
Q

What is the management of Phaeochromocytomas?

A
  1. Stabilisation with medical:
    a. alpha-blocker (e.g. phenoxybenzamine), given first
    b. Then given a beta-blocker (e.g. propranolol)
  2. Surgical = definitive
340
Q

What is a non-functioning Pituitary tumour?

A

Pituitary adenomas that do not cause a characteristic hormone hypersecretion syndrome

341
Q

What is the aetiology of non-functioning Pituitary tumours?

A
  1. Exact aetiology is unknown
  2. FH of multiple endocrine neoplasia type1 (MEN1) and Familial pituitary adenomas
342
Q

What is the epidemiology of non-functioning Pituitary tumours?

A
  1. Pituitary adenomas are the third most common intracranial neoplasms
  2. Account for about 10% of all intracranial tumours in adults
343
Q

What are the different types of pituitary adenomas?

A
  1. Prolactinomas
  2. Non-secreting adenomas
  3. GH secreting adenomas
  4. ACTH secreting adenomas
344
Q

What do non-functioning pituitary tumours present with and why?

A
  1. Depletion of hormones
  2. This is due to compression of the normal functioning pituitary gland
  3. Therefore, present with generalised hypopituitarism
345
Q

What are the symptoms of non-functioning pituitary tumours?

A

Generalised hypopituitarism:
1. Headaches
2. Decreased visual acuity- bitemporal hemianopia
3. Adrenal insufficiency: Nausea and vomiting, weakness, anorexia
4. Hypogonadism: Gynaecomastia, erectile dysfunction, amenorrhoea, infertility
5. Hypothyroidism:, Weight gain, cold intolerance, fatigue
6. GH deficiency: Similar to above plus increased central adiposity and reduced muscle mass

346
Q

What are the appropriate investigations for non-functioning pituitary tumours?

A
  1. Pituitary blood profile:
    a. GH, FSH/LH, TSH, ACTH
    b. Prolactin levels: exclude prolactinomas
  2. Pituitary MRI with gadolinium contrast
  3. Formal visual field testing
347
Q

What are the differential diagnoses for non-functioning pituitary tumours?

A
  1. Pituitary hyperplasia (if secreting hormone (s))
  2. Craniopharyngioma
  3. Meningioma
  4. Brain metastases
  5. Lymphoma
  6. Hypophysitis (inflammation of pituitary)
  7. Vascular malformation (e.g. aneurysm)
348
Q

What is the management of non-functioning pituitary tumours?

A

May include a combination of:
1. Surgery (e.g. transsphenoidal transnasal hypophysectomy): if progression in size
2. Radiotherapy

349
Q

What is polycystic ovary syndrome (PCOS)?

A

A complex condition of ovarian dysfunction characterised by:
1.Oligomenorrhoea/amenorrhoea
2. Hyper-androgenism (clinical symptoms or biochemical)

350
Q

What is PCOS associated with?

A

Obesity, insulin resistance and an increased risk of developing type 2 diabetes

351
Q

What is the aetiology of PCOS?

A

Not fully understood: combination of environmental factors (related to diet and development of obesity) and
genetic determinants

352
Q

What are the risk factors for PCOS?

A
  1. FHx of PCOS
  2. Premature adrenarche
  3. Weaker risk factors: obesity, low birth weight
353
Q

What is the epidemiology for PCOS?

A

PCOS is the most common cause of infertility in women, thought to affect between 5-20% of women of reproductive age

354
Q

What are the features of PCOS?

A
  1. Subfertility and infertility
  2. Menstrual disturbances: oligomenorrhoea and amenorrhoea
  3. Hirsutism, acne (due to hyperandrogenism)
  4. Obesity
  5. Acanthosis nigricans (due to insulin resistance)
355
Q

What are the investigations for PCOS?

A
  1. Pelvic ultrasound: multiple cysts on the ovaries
  2. Baseline investigatons: FSH, LH, prolactin, TSH, testosterone, sex hormone-binding globulin (SHBG):
    a. raised LH:FSH ratio is a ‘classical’ feature but is no longer thought to be useful in diagnosis
    b. Prolactin may be normal or mildly elevated
    c. Testosterone may be normal or mildly elevated - however, if markedly raised consider other causes
    d. SHBG is normal to low in women with PCOS
  3. Check for impaired glucose tolerance
356
Q

What is the Rotterdam criteria for PCOS?

A

If 2 of the following 3 are present:
1. Infrequent or no ovulation (menstruation)
2. Clinical and/or biochemical signs of hyperandrogenism (e.g. hirsutism, acne, or elevated levels of total or free testosterone)
3. Polycystic ovaries on ultrasound scan:
a. defined as the presence of ≥ 12 follicles in one or both ovaries and/or increased ovarian volume > 10 cm³
b. Follicles measuring 2-9 mm in diameter

357
Q

What is the general management for PCOS?

A
  1. Weight reduction if appropriate
  2. If a women requires contraception then a combined oral contraceptive (COC) pill may help regulate her cycle and induce a monthly bleed
358
Q

What is the management for the features of hyperandrogenism in PCOS?

A
  1. A COC pill may be used help manage hirsutism
    a. Third generation COC which has fewer androgenic effects or co-cyprindiol which has an anti-androgen action
    b. An increased risk of VTE with these
  2. If doesn’t respond to COC then topical eflornithine may be tried
  3. Spironolactone, flutamide and finasteride may be used under specialist supervision
359
Q

What is the management of subfertility/ infertility in PCOS?

A
  1. Weight reduction if appropriate
  2. Should be supervised by a specialist.
  3. Options include metformin, clomifene or a combination to stimulate ovulation
  4. Some evidence showed clomifene was the most effective treatment- but potential risk of multiple pregnancies with anti-oestrogen therapies such as clomifene
  5. Metformin is also used, either combined with clomifene or alone, particularly in patients who are obese
  6. Gonadotrophins
360
Q

What is the role of anti-oestrogens therapies in the management of PCOS?

A
  1. Work by occupying hypothalamic oestrogen receptors without activating them
  2. This interferes with the binding of oestradiol and thus prevents negative feedback inhibition of FSH secretion
361
Q

What is primary hyperaldosteronism?

A

Characterized by autonomous aldosterone overproduction from the adrenal gland with subsequent suppression of plasma renin activity

362
Q

What is the aetiology of primary hyperaldosteronism?

A
  1. Bilateral idiopathic adrenal hyperplasia: 60-70%
  2. Adrenal adenoma, also known as Conn’s syndrome: 20-30%
  3. Unilateral hyperplasia
  4. Familial hyperaldosteronism
  5. Adrenal carcinoma
363
Q

What is the pathophysiology of primary hyperaldosteronism?

A

Excess aldosterone results in:
1. Increased Na+ and water retention causing hypertension
2. Increased renal K+ loss and hypokalaemia
3. Suppression of renin because of NaCl retention

364
Q

What is the epidemiology of primary hyperaldosteronism?

A
  1. The prevalence in hypertensive patients is 1–2%
  2. Aldosterone producing adenoma (Conns) occurs more commonly in women and in younger patients (<50 years)
  3. Bilateral adrenal hyperplasia occurs more commonly in men and usually presents at an older age
365
Q

What are the two main features of primary hyperaldosteronism?

A
  1. Hypertension:
    increasingly recognised but still underdiagnosed cause of hypertension
  2. Hypokalaemia
    e.g. muscle weakness, is more common with adrenal adenomas
  3. Can also present with metabolic alkalosis
366
Q

Who should be screened for primary hyperaldosteronism?

A

Patients with:
1. Hypertension with hypokalemia
2. Treatment-resistant hypertension

367
Q

What is the first line investigation for primary hyperaldosteronism?

A

Plasma aldosterone/renin ratio:
1. Should show high aldosterone levels alongside low renin levels
2. This because of negative feedback due to sodium retention from aldosterone

368
Q

What are the next investigations following plasma aldosterone/ renin ratio in primary hyperaldosteronism?

A
  1. High-resolution CT abdomen to differentiate between unilateral and bilateral sources of aldosterone excess
  2. If the CT is normal: adrenal venous sampling (AVS) can be used to distinguish between unilateral adenoma and bilateral hyperplasia
369
Q

What is the management of primary hyperaldosteronism?

A
  1. For adrenal adenoma: surgery (laparoscopic adrenalectomy)
  2. For bilateral adrenocortical hyperplasia: aldosterone antagonist e.g. spironolactone
370
Q

What are the complications of primary hyperaldosteronism?

A

Complications of hypertension:
1. Heart failure
2. Coronary artery disease and MI
3. Cerebrovascular accident
4. Peripheral vascular disease
5. Thomboembolism
6. Retinopathy
7. Renal failure

371
Q

What is the prognosis for primary hyperaldosteronism?

A

Surgery may either cure hypertension (in about 50-60%) or make it more amenable to anti-hypertensive therapy in those who are not cured (usually the elderly or those with long-standing hypertension)

372
Q

What is a Prolactinoma?

A
  1. A type of pituitary adenoma
  2. A benign tumour expressing and secreting prolactin
373
Q

What is the aetiology of Prolactinoma?

A
  1. The majority of prolactinomas occur sporadically
  2. A small percentage of patients may have multiple endocrine neoplasia syndrome type 1 (MEN-1) or familial isolated pituitary adenoma (FIPA)
374
Q

What is the epidemiology of Prolactinomas?

A
  1. Prolactinomas are the most common type of pituitary adenoma, constituting about 40% of these tumours
  2. More frequent in women, mainly during the child-bearing years, with a peak incidence between 20-30s
  3. Women and men of 10:1 but once over 50, frequency of prolactinomas is similar in men and women
375
Q

How can pituitary adenomas be classified?

A
  1. Size (a microadenoma is <1cm and a macroadenoma is >1cm)
  2. Hormonal status: a secretory/functioning adenoma produces and excess of a particular hormone and a non-secretory/functioning adenoma does not produce a hormone to excess
376
Q

What are the features of Prolactinomas?

A

Women:
1. Amenorrhoea
2. Infertility
3. Galactorrhoea
4. Osteoporosis
Men:
1. Impotence
2. Loss of libido
3. Galactorrhoea

377
Q

What are the features of macroadenoma prolactinomas?

A
  1. Headache
  2. Visual disturbances: classically, a bitemporal hemianopia (lateral visual fields) or upper temporal quadrantanopia
  3. Symptoms and signs of hypopituitarism
378
Q

What is the diagnostic investigation for Prolactinomas?

A

Pituitary MRI (plus pituitary hormone profile, specifically Prolactin)

379
Q

What is the management of Prolactinomas?

A
  1. Medical:
    a. Majority of cases
    b. Dopamine agonists (e.g. cabergoline, bromocriptine) which inhibit the release of prolactin from the pituitary gland
    c. Result in prolactin normalisation, tumour shrinkage or disappearance, and rapid visual improvement
  2. Surgery:
    a. Performed for patients who cannot tolerate or fail to respond to medical therapy
    b. A trans-sphenoidal approach is generally preferred
380
Q

What are the complications of Prolactinomas?

A
  1. Visual field impairment
  2. Cabergoline associated (at high doses) valvular disease
  3. Pituitary apoplexy: due to acute haemorrhage into or ischaemic infarction of a large pituitary prolactinoma
  4. From Trans-sphenoidal surgery: anterior pituitary failure/ diabetes insipidus
381
Q

What is Syndrome of inappropriate ADH (SIADH)?

A

Characterised by continued secretion of ADH, despite the absence of normal stimuli for secretion (i.e. increased serum osmolality or low blood volume)

382
Q

What is SIADH characertised by?

A

Hyponatraemia secondary to the dilutional effects of excessive water retention

383
Q

What are the different causes of SIADH?

A
  1. Malignancy:
    a. Small cell lung cancer
    b. Pancreas, prostate
  2. Neurological:
    a. Stroke
    b. Subarachnoid haemorrhage
    c. Subdural haemorrhage
    d. Meningitis/encephalitis/abscess
  3. Infections:
    a. TB
    b. Pneumonia
  4. Drugs:
  5. sulfonylureas*
  6. SSRIs, tricyclics
  7. carbamazepine
  8. Other causes:
    a. positive end-expiratory pressure (PEEP)
    b. porphyrias
384
Q

What is the epidemiology of Syndrome of inappropriate ADH (SIADH)?

A

Hyponatraemia is the most common electrolyte imbalance seen in hospitals
<50% of all severe hyponatraemia are due to SIADH

385
Q

What are the presenting symptoms of Syndrome of inappropriate ADH (SIADH)?

A
  1. Mild hyponatraemia (Na+ : 125–135 mmol/L) may be asymptomatic
  2. Headache
  3. Nausea/vomiting
  4. Muscle cramp/weakness
  5. Irritability
  6. Confusion, drowsiness
  7. Convulsions
  8. Coma
  9. Symptoms of the underlying cause
386
Q

What are the signs of Syndrome of inappropriate ADH (SIADH) on physical examination?

A

Mild hyponatraemia: No signs
Severe hyponatraemia:
Reduced reflexes, extensor plantar reflexes (Babinski reflex)

387
Q

What are the appropriate investigations for Syndrome of inappropriate ADH (SIADH)?

A

Diagnosis of exclusion:
1. Bloods:
a. Serum sodium: low, <135 mmol/L
b. Serum osmolality:low, <280 mmol/kg (hypotonic)
2. Urine:
1. Urine osmolality: elevated, >100 mmol/kg H2O
-2. Urine sodium: elevated, >40 mmol/L
The presence of the above and absence of hypovolaemia/hypotension, oedema, renal failure, adrenal insufficiency and hypothyroidism are required for a diagnosis of SIADH

388
Q

What is the management of SIADH?

A
  1. Correction must be done slowly to avoid precipitating central pontine myelinolysis
  2. Fluid restriction
  3. Demeclocycline: reduces the responsiveness of the collecting tubule cells to ADH
  4. ADH (vasopressin) receptor antagonists have been developed
389
Q

What is central pontine myelinolysis?

A

Rapid rise in sodium concentration is accompanied by the movement of small molecules and pulls water from brain cells
Presents with: quadreparesis, respiratory arrest, fits

390
Q

What are the complications of Syndrome of inappropriate ADH (SIADH)?

A

Convulsions, coma, death

391
Q

What is the prognosis of Syndrome of inappropriate ADH (SIADH)?

A
  1. If the underlying cause is found and treated successfully, SIADH typically resolves
  2. High morbidity and mortality with [Na+] <110 mmol/L
  3. Up to 50% mortality with central pontine myelinolysis
392
Q

What is thyroid cancer?

A

The most common endocrinological malignancy and 4 types account for more than 98% of thyroid malignancies:
1. Papillary
2. Follicular
3. Anaplastic
4. Medullary

393
Q

What is the aetiology of thyroid cancer?

A

Genetic alterations are thought to underlie thyroid cancers (Family history is a strong RF)

394
Q

What are the presenting symptoms of thyroid cancer?

A
  1. Neck lump
  2. Hoarseness
  3. Dyspnoea
  4. Dysphagia
395
Q

What are the signs of thyroid cancer on physical examination?

A
  1. Palpable thyroid nodule (most common in early adulthood)
  2. Tracheal deviation: enlarged goitre
  3. Cervical lymphadenopathy suggestive of neck metastasis
396
Q

What is papillary thyroid carcinoma?

A
  1. 70% of cases
  2. Often young females
  3. Excellent prognosis
  4. Usually contain a mixture of papillary and colloidal filled follicles
  5. Lymph node metastasis predominate
397
Q

What is follicular thyroid adenoma/ carcinoma?

A
  1. 20% of cases
  2. Usually present as a solitary thyroid nodule
  3. Malignancy can only be excluded on formal histological assessment
398
Q

What is medullary thyroid carcinoma?

A
  1. 5% of cases
  2. Part of MEN-2
  3. Cancer of parafollicular (C) cells, secrete calcitonin
399
Q

What is anaplastic thyroid carcinoma?

A
  1. 1% of cases
  2. Most common in elderly females
  3. Local invasion is a common feature
  4. Not responsive to treatment, can cause pressure symptoms
  5. Treatment is by resection where possible, palliation may be achieved through isthmusectomy and radiotherapy
400
Q

What are the investigations for thyroid cancer?

A
  1. TFTs: TSH often normal
  2. Ultrasound neck: micro-calcifications, a more-tall-than-wide shape, hypervascularity, marked hypoechogenicity, or irregular margins
  3. Fine needle biopsy: cytology of malignant features (variations in appearance), anapaestic (poorly differentiated)
  4. Laryngoscopy: paralysed vocal cord is highly suggestive of malignancy
401
Q

What is the management of papillary and follicular thyroid cancer?

A
  1. Total thyroidectomy
  2. Followed by radioiodine (I-131) to kill residual cells
  3. Yearly thyroglobulin levels to detect early recurrent disease
402
Q

What are Thyroid nodule(s)?

A

Solid or fluid-filled lumps that form within the thyroid (majority are not serious. and do not cause symptoms)

403
Q

What are different types of thyroid nodule(s)?

A

Benign:
1. Multinodular goitre
2. Thyroid adenoma
3. Hashimoto’s thyroiditis
4. Cysts (colloid, simple, or hemorrhagic)
Malignant:
1. Papillary carcinoma (most common malignant cause)
2. Follicular carcinoma
3. Medullary carcinoma
4. Anaplastic carcinoma
5. Lymphoma: rare, Hashimoto’s thyroiditis

404
Q

What are the features of Thyroid nodule(s)?

A
  1. Most thyroid nodules don’t cause signs or symptoms
  2. Neck lump
  3. Cause dyspnoea or dysphagia (suggestive of malignancy)
  4. Can cause hypo or hyperthyroidism features
405
Q

What are the appropriate investigations for Thyroid nodule(s)?

A
  1. Bloods: Thyroid function test, FBC
  2. First line: ultrasonography: to determine if the nodule has features suspicious of malignancy
406
Q

What is Thyroiditis?

A
  1. An autoimmune-mediated lymphocytic inflammation of the thyroid gland resulting in a destructive thyroiditis with release of thyroid hormone and transient thyrotoxicosis (hyperthyroidism)
  2. This is frequently followed by a hypothyroid phase and full recovery
407
Q

What are the different types of Thyroiditis?

A
  1. Hashimoto’s thyroiditis (chronic autoimmune thyroiditis): most common cause of hypothyroidism
  2. Postpartum thyroiditis
  3. Subacute thyroiditis (also known as De Quervain’s thyroiditis): following viral infection and typically presents with hyperthyroidism
408
Q

What are the presenting symptoms of Thyroiditis?

A

Features of hyperthyroidism:
1. Heat intolerance
2. Nervousness
3. Palpitations
4. Weight loss
5. Excessive fatigue

409
Q

What are the three stages of postpartum thyroiditis?

A
  1. Thyrotoxicosis
  2. Hypothyroidism
  3. Normal thyroid function (but high recurrence rate in future pregnancies)
410
Q

What are found in 90% of patients with postpartum thyroiditis?

A

Thyroid peroxidase antibodies

411
Q

What is the management of postpartum thyroiditis?

A
  1. Thyrotoxic phase:
    a. Propranolol is typically used for symptom control
    b. Not usually treated with anti-thyroid drugs as the thyroid is not overactive
  2. Hypothyroid phase:
    usually treated with thyroxine
412
Q

What are the four stages of Subacute (De Quervain’s) thyroiditis?

A
  1. Phase 1 (lasts 3-6 weeks): hyperthyroidism, painful goitre, raised ESR
  2. Phase 2 (1-3 weeks): euthyroid
  3. Phase 3 (weeks - months): hypothyroidism
  4. Phase 4: thyroid structure and function goes back to normal
413
Q

What is the investigation of choice for Subacute (De Quervain’s) thyroiditis?

A

Thyroid scintigraphy: globally reduced uptake of iodine-131

414
Q

What is the management of Subacute (De Quervain’s) thyroiditis?

A
  1. Usually self-limiting - most patients do not require treatment
  2. Thyroid pain may respond to aspirin or other NSAIDs
  3. In more severe cases steroids are used, particularly if hypothyroidism develops (phase 3)
415
Q

What are the complications of Thyroiditis?

A
  1. Arrhythmias: AF
  2. Exacerbation of co-morbidities particularly ismchaemic heart disease and congestive heart failure (lower risk)
  3. More likely to develop permanent hypothyroidism
  4. Can also develop Graves’ disease, recurrent hyperthyroidism
416
Q

What is the prognosis of Thyroiditis?

A

Most patients recover normal thyroid function, but:
1. 6% remain permanently hypothyroid
2. 1/3 have persistent goitre or thyroid peroxidase (TPO) antibodies
3. Recurrent episodes are common postnatally (69%) but may also occur in up to 11% of patients with sporadic disease

!Final Year (26 decks)

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