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4th year everything > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What functions of the body are regulated by the hypothalamus?

A

Appetite, thirst, thermal regulation and sleep/waking, circadian rhythm, the menstrual cycle, stress and mood

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2
Q

What eight hormones does the hypothalamus produce?

A 
Growth-hormone releasing hormone
Gonadotropin releasing hormone
Somatostatin
Dopamine
Thyrotrophin releasing hormone
Corticotropic releasing hormone
Vasopressin
Oxytocin
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3
Q

What are the only inhibitory hormones produced by the hypothalamus?

A

Somatostatin and dopamine

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4
Q

Which two hormones are released by the posterior pituitary gland?

A

Vasopressin and oxytocin

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5
Q

What are the functions of oxytocin?

A

Produces milk ejection in females and uterine myometrial contractions

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6
Q

What hormones are released by the anterior pituitary gland?

A 
Leutinising hormone
Follicle stimulating hormone
Growth hormone
Prolactin
Thyroid stimulating hormone
Adreno-corticotrophic hormone
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7
Q

What is the most common cause of pituitary disease?

A

Benign pituitary adenomas

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8
Q

What are the three major pathologies caused by secretory pituitary adenomas?

A
  1. Growth hormone excess causes acromegaly in adults and gigantism in children
  2. Prolactin excess
  3. Excess ACTH secretion causes Cushing’s Disease
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9
Q

What are the symptoms of prolactin excess?

A

Galactorrhoea, amenorrhoea, erectile dysfunction

May be clinically silent

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10
Q

What local structures may be affected by either pressure or infiltration of a pituitary lesion? What are the associated pathologies of each?

A

Optic chiasm - bitemporal hemianopia
Cavernous sinus - CN III, IV and VI lesions
Bony structures and menignes - causing headaches
Hypothalamic centres - obesity, altered appetite, thirst, precocious puberty in children
Ventricles - hydrocephalus

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11
Q

Adenomas are the most common pituitary lesion. Give examples of some rarer ones.

A

Craniopharyngiomas, sarcoidosis, cystic lesions

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12
Q

Describe the clinical presentation of gondaotrophin deficiency

A

Loss of libido, amenorrhoea, erectile dysfunction

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13
Q

In hypopituartism, rather than prolactin deficiency, hyperprolactinaemia occurs. Why is this?

A

Early loss of the inhibitory effect of dopamine on prolactin leads to hyperprolactinaemia in hypopituartism

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14
Q

What are the symptoms of hyperprolactinaemia?

A

Galactorrhoea (spontaneous milk ejection unrelated to child birth or breast feeding), erectile dysfunction or amenorrhoea

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15
Q

Describe the clinical presentation of growth hormone deficiency.

Consider presentations in both children and adults

A

Short stature in children

Often clinically silent in adults

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16
Q

Long-standing hypopituartism can give what classical appearance of the skin?

A

Hairless and pale (alabaster skin)

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17
Q

What is Sheehan’s Syndrome?

A

Pituitary infarct following severe post-partum haemorrhage

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18
Q

What is pituitary apoplexy? Describe it clinical picture

A

Rapid enlargement of a pituitary tumour due to severe infarct or haemorrhage.

Clinical picture includes severe headache and sudden severe visual loss. Ocular palsies, fever, neck stiffness and photophobia may also be present.

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19
Q

Outline the emergency investigations of pituitary apoplexy

A 
Investigations:
Serum cortisol, IGF-1, GH, Prolactin, T3/T4, LH, FSH, testosterone or oestrodiol 
FBC, U/Es, LFTs
Assessment of visual acuity
Urgent MRI to confirm
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20
Q

Outline the emergency treatment of pituitary apoplexy

A
  • ABCDE approach

- Hydrocortisone 100mg bolus IV followed by 2-4mg/hr continuous IV infusion

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21
Q

What important investigations should be performed in the case of hyperprolactinaemia?

A

Serum prolactin
Exclude macroprolactinaemia
Thyroid function tests
MRI of pituitary

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22
Q

How is hyperprolactinaemia treated?

A

Dopamine agonists e.g. cabergoline

Bromocriptine is preferred if pregnancy is planned

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23
Q

What approach is taken for surgery of the pituitary?

A

Trans-sphenoidal

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24
Q

Outline five symptoms of acromegaly

A

Any of the following:

Change in facial appearance, headaches, deep voice, goitre, tiredness, weight gain, breathlessness, excessive sweating, muscle/joint pain, amenorrhoea, galactorrhoea, impotence

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25
Q

Outline five signs of acromegaly

A

Any of the following:

Prominent supraorbital ridge, interdental separation, visual field defects, spade-like hands, carpal tunnel syndrome, hypertension, heart failure, oedema, proximal myopathy

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26
Q

What investigations are indicated in the case of acromegaly?

A

Plasma GH
Serum IGF-1
Glucose tolerance (diagnostic)
MRI scan of pituitary

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27
Q

How is acromegaly treated?

A

Transphenoidal surgical ressection

Medical therapy (on the failure or unsuitability of surgery):

  • Somatostatin analogues (first line) e.g. octreotide, lanreotide
  • Dopamine agonists e.g. cabergoline
  • Pegvisomant (GH-receptor antagonsit) - last resort
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28
Q

What is the difference between Cushing’s Disease and Cushing’s Syndrome?

A

Cushing’s disease refers to a specific pathology; primary hypercortisolism caused by a pituitary adenoma

Cushing’s Syndrome is the term used to describe the clincial state of increased free circulating glucocorticoids, most commonly caused by therapeutic administration.

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29
Q

What thyroid hormone is predominantly secreted from the thyroid gland?

A

T4

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30
Q

Which of the thyroid hormones is more biologically active?

A

T3

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31
Q

Where does the majority of circulating T3 come from?

A

Peripheral conversion of T4 into T3

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32
Q

Over 99% of T3/T4 is bound to plasma proteins in the circulation. The most abundant of these proteins is called what?

A

Thyroxine-binding globulin

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33
Q

With regards to relative concentrations of both TSH, T3 and T4. What is the hormonal profile of a patient with thyrotoxicosis?

A

Decreased TSH

Increased T3 and T4

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34
Q

With regards to relative concentrations of both TSH, T3 and T4. What is the hormonal profile of a patient with primary hypothyroidism?

A

Increased TSH

Decreased/normal T3/T4

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35
Q

With regards to relative concentrations of both TSH, T3 and T4. What is the hormonal profile of a patient with TSH deficiency?

A

Low TSH, T3 and T4

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36
Q

With regards to relative concentrations of both TSH, T3 and T4. What is the hormonal profile of a patient with T3 toxicosis?

A

Low TSH
Normal T4
High T3

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37
Q

Thyroid function tests are indicated in what patient groups?

A
  • Those with signs/symptoms suggestive of thyroid disease
  • Those receiving treatment for thyroid disease
  • Those being treated with drugs that can cause thyroid dysfunction e.g. amiodarone
  • Post-irradiation
  • Post-surgery - subtotal thyroidectomy
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38
Q

Outline five different aetiologies of hypothyroidism

A 
Autoimmune (Hashimoto's) 
Post-partum
Iatrogenic 
Drug induced
Iodine deficiency 
Congenital
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39
Q

What antibodies are associated with Hashimoto’s Thyroiditis?

A

Serum antibodies against:

  • Thyroglobulin
  • Thyroid peroxidase enzyme (thyroid macrosomal antibodies)
  • TSH receptor sites
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40
Q

Outline the potential disease progression in post-partum thyroiditis

A

Can cause either hypo- or hyperthyroidism or both sequentially.

Has the potential to progress to permanent disease

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41
Q

Give some examples of drugs that can cause drug induced hypothyroidism (4)

Hint - CALI

A

Carbimazole, amiodarone, lithium, interferon

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42
Q

What does the term ‘myxoedema’ refer to?

A

Accumulation of mucopolysaccharide in subcutaneous tissues.

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43
Q

Outline some symptoms of hypothyroidism

A

Tiredness, Malaise, Weight gain, Cold intolerance
Goitre, dry and brittle hair, course and dry skin
Depression, Psychosis, Coma, Poor memory
Athralgia, myalgia, muscle weakness, low libido, puffy eyes, anorexia

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44
Q

Outline some signs of hypothyroidism

A

Mental slowness, ataxia, poverty of movement, bradycardia, cold peripheries, carpal tunnel syndrome, hypertension, hypothermia, proximal myopathy

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45
Q

What investigations are considered in a suspected case of hypothyroidism?

A 
Serum TSH (high with clinical picture confirms diagnosis)
Thyroid antibodies 
Other features:
- Normocytic normochromic anaemia
- Hyperlipidaemia
- Hyponatraemia 
- Increase creatine kinase if myopathy
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46
Q

How is hypothyroidism managed?

A

Lifelong levothyroxine (daily dose of 1. micrograms/kg)

Average 100/150 micrograms

Efficacy is assessed with thyroid function tests at 6 weeks post-commencement followed by annual checkups

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47
Q

How is subclinical hypothyroidism managed?

A

Usually a consistently slightly increased TSH and normal T3/4 is indicative or early chronic autoimmune thyroiditis and therefore treatment with levothyroxine is recommended.

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48
Q

What is the typical presentation of myoedema coma?

A

Confusion, coma with hypothermia, hypoventilation, hypoglycaemia and hyponatraemia

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49
Q

How is myxoedema coma investigated in the acute presentation?

A

Serum TSH, T4 and cortisol
Full blood count, U/Es, blood glucose and blood cultures
ECG monitoring for cardiac arrhythmias

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50
Q

How is myxoedema coma managed in the acute presentation?

A

T3 orally or IV (2.5-5 micrograms every 8 hours)
Oxygen
Gradual rewarming
Hydrocortisone (100mg IV)
Glucose infusion
Supportive management of comatose patient

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51
Q

What three intrinsic disorders account for the majority of cases of hyperthyroidism?

A

Graves’ disease
Toxic adenoma
Toxic multinodular goitre

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52
Q

What is the most common cause of hyperthyroidism?

A

Graves’ disease

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53
Q

What is the pathophysiology of Graves’ disease?

A

IgG antibodies binding to the TSH receptor and stimulating thyroid hormone production

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54
Q

What is de Quervain’s thyroiditis?

A

Transient hyperthyroidism caused by acute inflammation of the gland, most likely as a result of a viral infection

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55
Q

What are the accompanying features of de Quervain’s thyroiditis?

A

Fever, malaise, pain in neck

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56
Q

How is de Quervain’s thyroiditis treated?

A

Aspirin

Reserving prednisolone for those severely affected

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57
Q

What signs/symptoms are only seen in Graves’ disease?

A

Opthalmopathy, pretibial myxoedema and thyroid acropachy

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58
Q

What is pretibial myxoedema?

A

Rasied, purple-red symmetrical skin lesions over the anterolateral aspects of the shins

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59
Q

What is thyroid acropachy?

A

Clubbing, swollen fingers and periosteal bone formation

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60
Q

How may hyperthyroidism present in the elderly?

Think subtle cardiac signs and misleading symptoms

A

Atrial fibrillation/heart failure

or

Apathetic thyrotoxicosis

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61
Q

What is apathetic thyrotoxicosis?

A

When a patient presents with signs of hypothyroidism but their hormone profile shows the opposite.

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62
Q

What are the relevant investigations for hyperthyroidism?

A 
Serum TSH (suppressed) 
Serum T3/T4 (elevated)

TSH antibodies are highly sensitive/specific for Graves’
Thyroid ultrasound can help identify multi-nodular goitre from toxic adenoma

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63
Q

List some common symptoms of hyperthyroidism

A 
Weight loss
Irritability
Malaise
Itching
Sweating
Palpitations 
Breathlessness
Thirst
Loss of libido
Goitre
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64
Q

List some common signs of hyperthyroidism

A 
Tremor
Hyperkinesis
Psychosis 
Tachycardia
Warm peripheries
Lid lag and "stare" 
Goitre and bruit
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65
Q

How is hyperthyroidism managed?

A

Anti-thyroid drugs (carbimazole) prescribed in conjunction with a beta-blocker (typically propranolol) for rapid symptomatic control

Interventions such as radioactive iodine and surgery is also considered if medical therapy fails or relapses

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66
Q

What is the most severe complication of carbimazole?

A

Agranulocytosis

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67
Q

What is the main contraindication of radioactive iodine treatment?

A

Pregnancy or breastfeeding

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68
Q

What is thyroid crisis (storm)? What causes it?

A

A rare- life threatening condition in which there is rapid deterioration of thyrotoxicosis with hyperpyrexia, tachycardia, extreme restlessness which eventually progresses to delerium, coma and death.

It is usually precipitated by infection, stress or surgery

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69
Q

How is thyroid crisis managed? (4)

A
  • Large doses of anti-thyroid drugs
  • Propranolol
  • Potassium iodide (actuely blocks release of thyroid hormones)
  • Hydrocortisone (to stop conversion of T4 to T3 peripherally)
70
Q

What eye conditions can be seen in any form hyperthyroidism?

A

Lid lag and lid retraction.

71
Q

What is the mechanism behind lid lag and retraction in hyperthyroidism?

A

Lid lag - delay in moving the upper eyelid and the eyes move down
Lid retraction - white of sclera visable above cornea

Increased sensitivity of the levator palpabrae superioris to catecholamines

72
Q

What eye conditions are only seen in Grave’s disease?

A

Opthalmoplegia (paralysis of eye movement) and proptosis (bulging of orbit)

73
Q

What social risk factor is most strongly associated with eye Graves’ orbitopathy?

A

Smoking

74
Q

How is Grave’s orbitopathy treated?

A

Thyroid dysfunction should be corrected
Smoking stopped
In severe cases, high-dose steroids, decompressive surgery or orbit radiation may be indicated

75
Q

Goitre with associated lymphadenopathy is indicative of what?

A

Thyroid malignancy

76
Q

What is the investigation of choice for exploration of a goitre?

A

Fine needle aspiration (FNA) for cytology

77
Q

Name the five cell types for thyroid malignancy and indicate which is the most common

A 
Papillary (most common)
Follicular 
Anaplastic (most aggressive)
Lymphoma 
Medullary cell
78
Q

What are the treatments for the various thyroid malignancies?

A

Papillary and follicular - total thyroidectomy and neck dissection followed by ablative radioiodine

Anaplastic and lymphoma - external radiation (largely palliative)

79
Q

Describe the release of leutinising releasing hormone (LHRH) in males

A

Released episodically both during and after puberty from the hypothalamus

80
Q

What is the function of leutinising hormone releasing hormone (LHRH)?

A

Stimulates the release of leutinising hormone and follicle stimulating hormone from the anterior pituitary gland

81
Q

What is the function of leutinising hormone in males?

A

Stimulates Leydig cells in the testes to release testosterone

82
Q

What is the function of follicle stimulating hormone in males?

A

Stimulates the maturity of sperm and inhibin A and B to inhibit FSH (negative feedback loop)

83
Q

Distinguish the difference between primary and secondary hypogonadism

A

Primary - disease of the testes

Secondary - disease of the pituitary/hypothalamus

84
Q

How does hypogonadism present in the pre-pubertal male?

A

Delayed puberty and eunuchoid body proportions (long legs relative to upper body and long arms relative to height due to delayed fusion of epiphyses)

85
Q

What is the most common congenital abnormality resulting in primary hypogonadism in males?

A

Kleinfelter’s Syndrome (47XXY)

86
Q

What is the mechanism behind hypogonadism in Kleinfelter’s Syndrome? What is the overall clinical presentation?

A

Accelerated atrophy of testicular germ cells causes sterility and firm, small testes.

Clinical presentation includes the eunuchoid body proportions, subfertility, gynaecomastia and learning difficulties.

87
Q

What is Kallman’s Syndrome?

A

Congenital deficiency of gonadotrophin-releasing hormone

Anosimia, cleft palate and renal abnormalities are also found

88
Q

What investigations are indicated in male hypogonadism?

A

Serum testosterone confrims diagnosis
Increased FSH/LH indicates primary disease (testicular)
Low FSH/LH may indicate secondary disease (pituitary/hypothalamic)

89
Q

What is the main treatment of hypogonadism in males?

A

Supplementary androgens (testosterone)

90
Q

What is the definition of erectile dysfunction?

A

Failure to initiate or maintain and erection to ejaculation

91
Q

What division of the autonomic nervous system controls erections in males?

A

Parasympathetic

92
Q

What is the first choice therapy for erectile dysfunction?

A

Phosphodiesterase-5 inhibitors (e.g. sildenafil)

93
Q

What is the cause of gynaecomastia?

A

Imbalance between the ratio of oestrogen to androgen

94
Q

What is the most common pathologies associated with gynaecomastia? (2)

A

Liver pathology or drugs (spironolactone or digoxin in particular)

95
Q

What is the function of leutinising hormone in females?

A

It stimulates ovarian androgen production

96
Q

What is the function of follicle stimulating hormone in females?

A

It stimulates follicular development and aromatase activity

97
Q

What is the function of the armoatase enzyme?

A

Converts ovarian andorgens into oestrogens

98
Q

What is the definition of the menopause?

A

Cessation of periods.

Natrually occuring process that usually happens aged 45-50.

May occur surgically (e.g. as a result of radiotherapy)

99
Q

List some symptoms of the menopause

A 
Hot flushes
Vaginal dryness
Breast atrophy
Depression
Loss of libido
Weight gain
Loss of bone density
100
Q

Hormone replacement therapy increases the risk of what conditions? (4)

A

Breast cancer
Coronary heart disease
Stroke
Venous thromboembolism

101
Q

Why is progesterone also prescribed to menopausal women who have not had a hysterectomy?

A

Oestrogen on its own increases the risk of endometrial cancer. Progesterone is protective of this.

102
Q

What is amenorrhoea?

A

Absence of menstruation

103
Q

What is the definition of primary amenorrhoea?

A

Failure to start menstruation before the age of 16

104
Q

What is the definition of secondary amenorrhoea?

A

The absence of menstruation for three months in a woman who previously had menstrual cycles in the absence of pregnancy/post-menopausal

105
Q

What is the definition of oligomenorrhorea?

A

Fewer than nine meneses per year

106
Q

Other than the primary symptoms of amenorrhoea/oligomenorrhoea - what other features may be consistent with oestrogen deficiency?

A

Atrophy of the breasts and vagina, loss of pubic hair and osteoperosis

107
Q

What is the most common cause of ameorrhorea/oligomenorrhoea in clinical practice?

A

Polycystic Ovarian Syndrome (PCOS)

108
Q

List some other pathological causes for amenorrhoea

A 
Weight loss
Hypopituartism 
Hyperprolactinaemia 
PCOS
Thyroid dysfunction
Adrenal tumours
109
Q

What investigations would be relevant in the case of amenorrhoea?

A

Basal levels of FSH, LH, oestrogen and prolactin - to distinguish between gonadal or hypothalamic-pituitary cause

Imaging - ovarian ultrasound or biopsy, pituitary MRI

110
Q

What are some clinical features of polycystic ovarian syndrome?

A
  • Polycystic ovaries
  • Androgen excess (causing hirsutism)
  • Hyperinsulinaemia (causing type 2 diabetes mellitus)
  • Hyperlipidaemia (causing hypertension and CVS disease)
  • Menstrual irregularity
111
Q

What diagnostic criteria is causes polycystic ovarian syndrome?

A

Rotterdam criteria

112
Q

What investigations are indicated on the suspicion of polycystic ovarian syndrome?

A
  • Sex hormones - raised free androgen index
  • Serum prolactin - may be slightly increased
  • Serum 17-hydroxyprogesterone - elevated in the case of non-congenital adrenal hyperplasia
  • Trans-vaginal ultrasound - visualises the ovaries
113
Q

What is the management of polycystic ovarian syndromes?

A

Local therapy for hirsutism - eflornithine cream

Systemic therapy:

  • Oestrogens e.g. OCP
  • Anti-androgens
  • Finasteride (5-alpha reductase inhibitor) inhibits testosterone formation in the skin

Treatment of menstrual disturbance and infertility

114
Q

Roughly outline the two layers of the adrenal gland and what they secrete

A

Outer cortex - secreting androgens, cortisol and aldosterone
Inner medulla - secretes catecholamines

115
Q

Outline the glucocorticoid hormone cascade

A
  1. Corticotrophin releasing hormone from the hypothalamus
  2. Stimulates adrenocorticotrophic hormone from the anterior pituitary
  3. Stimulates cortisol from the adrenal cortex (negatively feedback messenger to hypothalamus)
116
Q

What are some of the functions of cortisol?

A
  • Increases protein catabolism
  • Increases fat and glycogen deposition
  • Increases sodium retention
  • Increase potassium loss
  • Increased susceptibility to infection
  • Anti-insulin effects
117
Q

What is Addison’s Disease?

A

Primary hypoadrenalism caused by auto-immune destruction of the entire adrenal cortex

118
Q

What is the presentation of Addison’s Disease?

A
  • Insidious onset of lethargy, depression, anorexia and weight-loss
  • Postural hypotension
  • Hyperpigmentation (buccal mucosa, skin creases, scars)
119
Q

Hypoadrenalism can also present in the emergency setting; called Addisonian Crisis. How does it present?

A

Vomiting, abdominal pain, profound wekaness, hypoglycaemia and hypovolaemic shock

120
Q

Investigation of hypoadrenalism are three-fold:

  1. To confirm pathologically low cortisol
  2. To determine if it’s ACTH dependent or independent
  3. To determine specific cause

Outline each of those three tests.

A
  1. Plasma ACTH level:

High ACTH with low cortisol = primary disease and Low ACTH and low cortisol = secondary/tertiary disease

  1. Short ACTH stimulation test - demonstrates failure of exogenous ACTH to increase cortisol in primary disease.
  2. Dictated by the results of the previous tests
121
Q

How is Addison’s Disease managed?

A

Lifelong steroid replacement with hydrocortisone/fludrocortisone

122
Q

What electrolyte distrubances may be present in Addison’s disease?

A

Hyponatraemia, hyperkalaemia and raised urea

Occasionally hypoglycaemia and hypercalcaemia

123
Q

How is Addisonian Crisis managed in the acute setting?

A

Hydrocortisone 100mg IV
0.9% saline 1L over 1hr
(50ml of 50% dextrose if hypoglycaemic)

124
Q

What is the definition of Cushing’s syndrome?

A

Persistently and inappropriately raised serum glucocorticoid levels

125
Q

What is the most common cause of Cushing’s syndrome?

A

Occur secondary to use of exogenous steroids for conditions e.g. asthma

126
Q

What is Cushing’s disease?

A

Cushing’s disease specifically refers to excess glucocorticoids resulting from ACTH productions from a pituitary tumour (usually adenoma)

127
Q

What is the clinical presentation of Cushing’s disease? List five.

A

Central obesity, buffalo hump (fat deposition on the dorsal neck), plethoric complexion with moon face

Thin skin, easy bruising, purple striae

Proximal myopathy, hypertension, hypokalaemia, impaired glucose tolerance

128
Q

Outline the investigations of Cushing’s Syndrome

A

Confirm raised cortisol:
- 24hr urinary free cortisol (positive if >700nm/24hr) - 48hr low-dose dexamethasone suppression test

Establish cause -

  • Plasma ACTH levels (low in non-ACTH dependent disease)
  • High-dose dexamethasone test (unsuppressable in adrenal disease)
  • Adrenal CT
  • Pituitary MRI
129
Q

The purpose of the renin-angiotension-aldosterone system (RAAS) controls blood pressure by either varying the stimulation of angiotensin II. What are the effects of angiotensin II?

A

Powerful vasoconstriction

Increases aldosterone production

130
Q

What is the function of aldosterone?

A

Sodium retention and potassium loss which both contribute to increased blood pressure

131
Q

What is primary hyperaldosteronism?

A

Increase mineralocorticoid secretion from the adrenal cortex (glomerulosa layer).

132
Q

What are the two potential causes of primary hyperaldosteronism?

A
  1. Adrenal adenoma (Conn’s syndrome)

2. Bilateral adrenal hyperplasia

133
Q

What are the clinical features of the hyperaldosteronism?

A

Hypertension and hypokalaemia

134
Q

How is hyperaldosteronism treated?

A

Surgery to remove adrenal tumour if Conn’s syndrome

Anti-aldosterone drugs for hypertension e.g. spironolactone

135
Q

What is phaeochromocytoma?

A

A catecholamine secreting tumour.

136
Q

What are the symptoms associated with phaeochromocytoma?

A

Episodic headaches, palpitations, sweating, anxiety, nausea and weight-loss

137
Q

What are the signs associated with phaeochromocytoma?

A

Intermittent hypertension, tachycardia and pallor

Potentially hyperglycaemia

138
Q

What investigations are indicated in the case of phaeochromocytoma?

A

24hr collection of urinary catecholamines
CT/MRI to localise tumour
Scitinigraphy (mIBG) - selectively taken up by androgenic cells and useful in the location of extra-adrenal tumours

139
Q

What inheritance pattern does Multiple Endocrine Neoplasia demonstrate?

A

Autosomal dominant

140
Q

What mutation results in Type 1 Multiple Endocrine Neoplasia?

A

Menin gene on chromosome 11

141
Q

What mutation results in Type 2 Multiple Endocrine Neoplasia?

A

Ret proto-oncogene on chromosome 10

142
Q

How is Multiple Endocrine Neoplasia screened for in at-risk family members?

A

Serum calcium - due to high penetrance (95%) of parathyroid involvement

143
Q

What is the principle determinant of ADH secretion?

A

Plasma osmolality

144
Q

What is the function of the ADH?

A

Act on collecting tubules of the kidneys to increase water reabsorption

145
Q

At high concentrations, what other function does ADH serve?

A

Increase blood pressure

146
Q

With reference to plasma osmolality values, when is ADH secreted maximally and minimally?

A

Maximum secretion at plasma osmolality 295mOsm/kg

Minimum secretion at plasma osmolality below 280mOsm/kg

147
Q

What are the two types of diabetes insipidus (DI)?

A
  1. Cranial DI- impaired ADH secretion from the posterior pituitary
  2. Nephrogenic DI - renal resistance to ADH action
148
Q

What is the presentation fo diabetes insipidus?

A
  • Polyuria of dilute urine (in excess of 3L per day)
    Nocturia
  • Compensatory polydipsia (thirst)
149
Q

What is the difference between primary and compensatory polydipsia?

A
  1. Primary polydipsia - psychiatric disorder characterised by excessive water intake
  2. Compensatory - in response to a systemic need for increased water intake e.g. diabetes insipidus
150
Q

What can cause cranial diabetes insipidus?

A

Disease of the hypothalamus e.g. primary or secondary tumours, trauma, infiltrative disease e.g. tuberculosis or sarcoidosis

151
Q

What can cause nephrogenic diabetes insipidus?

A
  • Hypokalaemia (loss of renal medullary concentration gradient)
  • Hypercalcaemia
  • Renal tubular acidosis
  • Drugs e.g. lithium
152
Q

How is diabetes insipidus measured?

A
  • Urine volume (to confirm polyuria)
  • Plasma osmolality: urine osmolality should be high due to dilute very urine
  • Water deprivation test should lead to rapid drop in body weight (>3%)
153
Q

How is diabetes insipidus treated?

A

Difficult to improve established cranial diabetes insipidus.

Desmopressin and thiazide diuretics can improve ADH sensitivity

154
Q

What is SIADH?

A

Syndrome of Inappropriate Anti-Diuretic Hormone

155
Q

What is the pathophysiology of SIADH?

A

Continued ADH secretion in spite of plasma hypotonicity and a normal/increased plasma volume

156
Q

Give three examples of causes of SIADH?

A

Any three of the following:

Cancer - most commonly small cell lung cancer (ectopic ADH production)
Brain - meningitis, head injury
Metabolic - alcohol withdrawal
Drugs - opiates

157
Q

What hormone regulates the concentration of calcium?

A

Parathyroid hormone

158
Q

What is the action of increased parathyroid hormone?

A

Increases calcium

159
Q

How is calcium transported around the body?

A

40% is free and ionised in the plasma (physiologically relevant)

The rest is bound to albumin

160
Q

What is the most common cause of severe hypercalcaemia?

A

Hypercalcaemia (>3.5mmol/L) is usually caused by malignancy

161
Q

What is the difference between primary and secondary hyperparathyroidism?

A

Primary disease - usually caused by single parathyroid gland adenoma

Secondary disease - compensatory hypertrophy of all the glands in response to prolonged hypocalcaemia (e.g. chronic kidney disease or vitamin D deficiency)

162
Q

What is the presentation of hypercalcaemia?

Remember: Stones, bones abdominal groans and psychic moans

A

Malaise, depression, bone pain, abdominal pain, nausea, compensation, renal calculi, dehhydration, confusion

163
Q

What investigations are indicated for suspected hypercalcaemia?

A

Fasting calcium and phosphate

Serum PTH

164
Q

How is acute severe hypercalcaemia treated?

A

Rehydrate with IV 0.9% saline 4-6L over 24 hours

165
Q

What is the most common cause of hypocalcaemia?

A

Chronic kidney disease leading to inadequate production of vitamin D and phosphate retention

166
Q

What are the clinical features of hypocalcaemia?

A 
Circumoral paraesthesia 
Paraesthesia in the extremities
Cramps
Tetany 
Convulsions 
Death
167
Q

What two signs may be elicited in the patient with hypocalcaemia?

A

Chvostek’s sign - tapping over parotid gland causing ipsilateral facial muscle spasms

Trousseau’s sign - carpopedal spasm induced by inflation of blood pressure cuff

168
Q

How is hypocalcaemia managed acutely?

A

10ml of 10% calcium gluconate diluted in 50-100ml 5% glucose administered IV over 10 mins

169
Q

Hyperphosphataemia most commonly occurs in which chronic condition?

A

Chronic Kidney Disease

170
Q

How is hyperphosphataemia treated?

A

Gut phosphate binders and dialysis

171
Q

What three mechanisms can cause hypophosphataemia?

A
  1. Redistribution
  2. Increased renal excretion
  3. Decreased intake/ absorption
172
Q

What is the clinical presentation of hypophosphataemia?

A
  • Muscle weakness (diaphragmatic weakness leading to respiratory failure)
  • Impaired myocardial contractility (leading to cardiac failure)
  • Encephalopathy (confusion, hallucinations, convulsions)

4th year everything (43 decks)

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