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
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
3
Q
What are the only inhibitory hormones produced by the hypothalamus?
A
Somatostatin and dopamine
4
Q
Which two hormones are released by the posterior pituitary gland?
A
Vasopressin and oxytocin
5
Q
What are the functions of oxytocin?
A
Produces milk ejection in females and uterine myometrial contractions
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
7
Q
What is the most common cause of pituitary disease?
A
Benign pituitary adenomas
8
Q
What are the three major pathologies caused by secretory pituitary adenomas?
A
- Growth hormone excess causes acromegaly in adults and gigantism in children
- Prolactin excess
- Excess ACTH secretion causes Cushing’s Disease
9
Q
What are the symptoms of prolactin excess?
A
Galactorrhoea, amenorrhoea, erectile dysfunction
May be clinically silent
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
11
Q
Adenomas are the most common pituitary lesion. Give examples of some rarer ones.
A
Craniopharyngiomas, sarcoidosis, cystic lesions
12
Q
Describe the clinical presentation of gondaotrophin deficiency
A
Loss of libido, amenorrhoea, erectile dysfunction
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
14
Q
What are the symptoms of hyperprolactinaemia?
A
Galactorrhoea (spontaneous milk ejection unrelated to child birth or breast feeding), erectile dysfunction or amenorrhoea
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
16
Q
Long-standing hypopituartism can give what classical appearance of the skin?
A
Hairless and pale (alabaster skin)
17
Q
What is Sheehan’s Syndrome?
A
Pituitary infarct following severe post-partum haemorrhage
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.
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
20
Q
Outline the emergency treatment of pituitary apoplexy
A
- ABCDE approach
- Hydrocortisone 100mg bolus IV followed by 2-4mg/hr continuous IV infusion
21
Q
What important investigations should be performed in the case of hyperprolactinaemia?
A
Serum prolactin
Exclude macroprolactinaemia
Thyroid function tests
MRI of pituitary
22
Q
How is hyperprolactinaemia treated?
A
Dopamine agonists e.g. cabergoline
Bromocriptine is preferred if pregnancy is planned
23
Q
What approach is taken for surgery of the pituitary?
A
Trans-sphenoidal
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
25
Outline five signs of acromegaly
Any of the following:
Prominent supraorbital ridge, interdental separation, visual field defects, spade-like hands, carpal tunnel syndrome, hypertension, heart failure, oedema, proximal myopathy
26
What investigations are indicated in the case of acromegaly?
Plasma GH
Serum IGF-1
Glucose tolerance (diagnostic)
MRI scan of pituitary
27
How is acromegaly treated?
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
28
What is the difference between Cushing's Disease and Cushing's Syndrome?
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.
29
What thyroid hormone is predominantly secreted from the thyroid gland?
T4
30
Which of the thyroid hormones is more biologically active?
T3
31
Where does the majority of circulating T3 come from?
Peripheral conversion of T4 into T3
32
Over 99% of T3/T4 is bound to plasma proteins in the circulation. The most abundant of these proteins is called what?
Thyroxine-binding globulin
33
With regards to relative concentrations of both TSH, T3 and T4. What is the hormonal profile of a patient with thyrotoxicosis?
Decreased TSH
| Increased T3 and T4
34
With regards to relative concentrations of both TSH, T3 and T4. What is the hormonal profile of a patient with primary hypothyroidism?
Increased TSH
| Decreased/normal T3/T4
35
With regards to relative concentrations of both TSH, T3 and T4. What is the hormonal profile of a patient with TSH deficiency?
Low TSH, T3 and T4
36
With regards to relative concentrations of both TSH, T3 and T4. What is the hormonal profile of a patient with T3 toxicosis?
Low TSH
Normal T4
High T3
37
Thyroid function tests are indicated in what patient groups?
- 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
38
Outline five different aetiologies of hypothyroidism
```
Autoimmune (Hashimoto's)
Post-partum
Iatrogenic
Drug induced
Iodine deficiency
Congenital
```
39
What antibodies are associated with Hashimoto's Thyroiditis?
Serum antibodies against:
- Thyroglobulin
- Thyroid peroxidase enzyme (thyroid macrosomal antibodies)
- TSH receptor sites
40
Outline the potential disease progression in post-partum thyroiditis
Can cause either hypo- or hyperthyroidism or both sequentially.
Has the potential to progress to permanent disease
41
Give some examples of drugs that can cause drug induced hypothyroidism (4)
Hint - CALI
Carbimazole, amiodarone, lithium, interferon
42
What does the term 'myxoedema' refer to?
Accumulation of mucopolysaccharide in subcutaneous tissues.
43
Outline some symptoms of hypothyroidism
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
44
Outline some signs of hypothyroidism
Mental slowness, ataxia, poverty of movement, bradycardia, cold peripheries, carpal tunnel syndrome, hypertension, hypothermia, proximal myopathy
45
What investigations are considered in a suspected case of hypothyroidism?
```
Serum TSH (high with clinical picture confirms diagnosis)
Thyroid antibodies
Other features:
- Normocytic normochromic anaemia
- Hyperlipidaemia
- Hyponatraemia
- Increase creatine kinase if myopathy
```
46
How is hypothyroidism managed?
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
47
How is subclinical hypothyroidism managed?
Usually a consistently slightly increased TSH and normal T3/4 is indicative or early chronic autoimmune thyroiditis and therefore treatment with levothyroxine is recommended.
48
What is the typical presentation of myoedema coma?
Confusion, coma with hypothermia, hypoventilation, hypoglycaemia and hyponatraemia
49
How is myxoedema coma investigated in the acute presentation?
Serum TSH, T4 and cortisol
Full blood count, U/Es, blood glucose and blood cultures
ECG monitoring for cardiac arrhythmias
50
How is myxoedema coma managed in the acute presentation?
T3 orally or IV (2.5-5 micrograms every 8 hours)
Oxygen
Gradual rewarming
Hydrocortisone (100mg IV)
Glucose infusion
Supportive management of comatose patient
51
What three intrinsic disorders account for the majority of cases of hyperthyroidism?
Graves' disease
Toxic adenoma
Toxic multinodular goitre
52
What is the most common cause of hyperthyroidism?
Graves' disease
53
What is the pathophysiology of Graves' disease?
IgG antibodies binding to the TSH receptor and stimulating thyroid hormone production
54
What is de Quervain's thyroiditis?
Transient hyperthyroidism caused by acute inflammation of the gland, most likely as a result of a viral infection
55
What are the accompanying features of de Quervain's thyroiditis?
Fever, malaise, pain in neck
56
How is de Quervain's thyroiditis treated?
Aspirin
Reserving prednisolone for those severely affected
57
What signs/symptoms are only seen in Graves' disease?
Opthalmopathy, pretibial myxoedema and thyroid acropachy
58
What is pretibial myxoedema?
Rasied, purple-red symmetrical skin lesions over the anterolateral aspects of the shins
59
What is thyroid acropachy?
Clubbing, swollen fingers and periosteal bone formation
60
How may hyperthyroidism present in the elderly?
Think subtle cardiac signs and misleading symptoms
Atrial fibrillation/heart failure
or
Apathetic thyrotoxicosis
61
What is apathetic thyrotoxicosis?
When a patient presents with signs of hypothyroidism but their hormone profile shows the opposite.
62
What are the relevant investigations for hyperthyroidism?
```
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
63
List some common symptoms of hyperthyroidism
```
Weight loss
Irritability
Malaise
Itching
Sweating
Palpitations
Breathlessness
Thirst
Loss of libido
Goitre
```
64
List some common signs of hyperthyroidism
```
Tremor
Hyperkinesis
Psychosis
Tachycardia
Warm peripheries
Lid lag and "stare"
Goitre and bruit
```
65
How is hyperthyroidism managed?
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
66
What is the most severe complication of carbimazole?
Agranulocytosis
67
What is the main contraindication of radioactive iodine treatment?
Pregnancy or breastfeeding
68
What is thyroid crisis (storm)? What causes it?
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
69
How is thyroid crisis managed? (4)
- 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
What eye conditions can be seen in any form hyperthyroidism?
Lid lag and lid retraction.
71
What is the mechanism behind lid lag and retraction in hyperthyroidism?
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
What eye conditions are only seen in Grave's disease?
Opthalmoplegia (paralysis of eye movement) and proptosis (bulging of orbit)
73
What social risk factor is most strongly associated with eye Graves' orbitopathy?
Smoking
74
How is Grave's orbitopathy treated?
Thyroid dysfunction should be corrected
Smoking stopped
In severe cases, high-dose steroids, decompressive surgery or orbit radiation may be indicated
75
Goitre with associated lymphadenopathy is indicative of what?
Thyroid malignancy
76
What is the investigation of choice for exploration of a goitre?
Fine needle aspiration (FNA) for cytology
77
Name the five cell types for thyroid malignancy and indicate which is the most common
```
Papillary (most common)
Follicular
Anaplastic (most aggressive)
Lymphoma
Medullary cell
```
78
What are the treatments for the various thyroid malignancies?
Papillary and follicular - total thyroidectomy and neck dissection followed by ablative radioiodine
Anaplastic and lymphoma - external radiation (largely palliative)
79
Describe the release of leutinising releasing hormone (LHRH) in males
Released episodically both during and after puberty from the hypothalamus
80
What is the function of leutinising hormone releasing hormone (LHRH)?
Stimulates the release of leutinising hormone and follicle stimulating hormone from the anterior pituitary gland
81
What is the function of leutinising hormone in males?
Stimulates Leydig cells in the testes to release testosterone
82
What is the function of follicle stimulating hormone in males?
Stimulates the maturity of sperm and inhibin A and B to inhibit FSH (negative feedback loop)
83
Distinguish the difference between primary and secondary hypogonadism
Primary - disease of the testes
| Secondary - disease of the pituitary/hypothalamus
84
How does hypogonadism present in the pre-pubertal male?
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
What is the most common congenital abnormality resulting in primary hypogonadism in males?
Kleinfelter's Syndrome (47XXY)
86
What is the mechanism behind hypogonadism in Kleinfelter's Syndrome? What is the overall clinical presentation?
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
What is Kallman's Syndrome?
Congenital deficiency of gonadotrophin-releasing hormone
Anosimia, cleft palate and renal abnormalities are also found
88
What investigations are indicated in male hypogonadism?
Serum testosterone confrims diagnosis
Increased FSH/LH indicates primary disease (testicular)
Low FSH/LH may indicate secondary disease (pituitary/hypothalamic)
89
What is the main treatment of hypogonadism in males?
Supplementary androgens (testosterone)
90
What is the definition of erectile dysfunction?
Failure to initiate or maintain and erection to ejaculation
91
What division of the autonomic nervous system controls erections in males?
Parasympathetic
92
What is the first choice therapy for erectile dysfunction?
Phosphodiesterase-5 inhibitors (e.g. sildenafil)
93
What is the cause of gynaecomastia?
Imbalance between the ratio of oestrogen to androgen
94
What is the most common pathologies associated with gynaecomastia? (2)
Liver pathology or drugs (spironolactone or digoxin in particular)
95
What is the function of leutinising hormone in females?
It stimulates ovarian androgen production
96
What is the function of follicle stimulating hormone in females?
It stimulates follicular development and aromatase activity
97
What is the function of the armoatase enzyme?
Converts ovarian andorgens into oestrogens
98
What is the definition of the menopause?
Cessation of periods.
Natrually occuring process that usually happens aged 45-50.
May occur surgically (e.g. as a result of radiotherapy)
99
List some symptoms of the menopause
```
Hot flushes
Vaginal dryness
Breast atrophy
Depression
Loss of libido
Weight gain
Loss of bone density
```
100
Hormone replacement therapy increases the risk of what conditions? (4)
Breast cancer
Coronary heart disease
Stroke
Venous thromboembolism
101
Why is progesterone also prescribed to menopausal women who have not had a hysterectomy?
Oestrogen on its own increases the risk of endometrial cancer. Progesterone is protective of this.
102
What is amenorrhoea?
Absence of menstruation
103
What is the definition of primary amenorrhoea?
Failure to start menstruation before the age of 16
104
What is the definition of secondary amenorrhoea?
The absence of menstruation for three months in a woman who previously had menstrual cycles in the absence of pregnancy/post-menopausal
105
What is the definition of oligomenorrhorea?
Fewer than nine meneses per year
106
Other than the primary symptoms of amenorrhoea/oligomenorrhoea - what other features may be consistent with oestrogen deficiency?
Atrophy of the breasts and vagina, loss of pubic hair and osteoperosis
107
What is the most common cause of ameorrhorea/oligomenorrhoea in clinical practice?
Polycystic Ovarian Syndrome (PCOS)
108
List some other pathological causes for amenorrhoea
```
Weight loss
Hypopituartism
Hyperprolactinaemia
PCOS
Thyroid dysfunction
Adrenal tumours
```
109
What investigations would be relevant in the case of amenorrhoea?
Basal levels of FSH, LH, oestrogen and prolactin - to distinguish between gonadal or hypothalamic-pituitary cause
Imaging - ovarian ultrasound or biopsy, pituitary MRI
110
What are some clinical features of polycystic ovarian syndrome?
- Polycystic ovaries
- Androgen excess (causing hirsutism)
- Hyperinsulinaemia (causing type 2 diabetes mellitus)
- Hyperlipidaemia (causing hypertension and CVS disease)
- Menstrual irregularity
111
What diagnostic criteria is causes polycystic ovarian syndrome?
Rotterdam criteria
112
What investigations are indicated on the suspicion of polycystic ovarian syndrome?
- 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
What is the management of polycystic ovarian syndromes?
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
Roughly outline the two layers of the adrenal gland and what they secrete
Outer cortex - secreting androgens, cortisol and aldosterone
Inner medulla - secretes catecholamines
115
Outline the glucocorticoid hormone cascade
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
What are some of the functions of cortisol?
- Increases protein catabolism
- Increases fat and glycogen deposition
- Increases sodium retention
- Increase potassium loss
- Increased susceptibility to infection
- Anti-insulin effects
117
What is Addison's Disease?
Primary hypoadrenalism caused by auto-immune destruction of the entire adrenal cortex
118
What is the presentation of Addison's Disease?
- Insidious onset of lethargy, depression, anorexia and weight-loss
- Postural hypotension
- Hyperpigmentation (buccal mucosa, skin creases, scars)
119
Hypoadrenalism can also present in the emergency setting; called Addisonian Crisis. How does it present?
Vomiting, abdominal pain, profound wekaness, hypoglycaemia and hypovolaemic shock
120
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.
1. Plasma ACTH level:
High ACTH with low cortisol = primary disease and Low ACTH and low cortisol = secondary/tertiary disease
2. Short ACTH stimulation test - demonstrates failure of exogenous ACTH to increase cortisol in primary disease.
3. Dictated by the results of the previous tests
121
How is Addison's Disease managed?
Lifelong steroid replacement with hydrocortisone/fludrocortisone
122
What electrolyte distrubances may be present in Addison's disease?
Hyponatraemia, hyperkalaemia and raised urea
Occasionally hypoglycaemia and hypercalcaemia
123
How is Addisonian Crisis managed in the acute setting?
Hydrocortisone 100mg IV
0.9% saline 1L over 1hr
(50ml of 50% dextrose if hypoglycaemic)
124
What is the definition of Cushing's syndrome?
Persistently and inappropriately raised serum glucocorticoid levels
125
What is the most common cause of Cushing's syndrome?
Occur secondary to use of exogenous steroids for conditions e.g. asthma
126
What is Cushing's disease?
Cushing's disease specifically refers to excess glucocorticoids resulting from ACTH productions from a pituitary tumour (usually adenoma)
127
What is the clinical presentation of Cushing's disease? List five.
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
Outline the investigations of Cushing's Syndrome
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
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?
Powerful vasoconstriction
Increases aldosterone production
130
What is the function of aldosterone?
Sodium retention and potassium loss which both contribute to increased blood pressure
131
What is primary hyperaldosteronism?
Increase mineralocorticoid secretion from the adrenal cortex (glomerulosa layer).
132
What are the two potential causes of primary hyperaldosteronism?
1. Adrenal adenoma (Conn's syndrome)
| 2. Bilateral adrenal hyperplasia
133
What are the clinical features of the hyperaldosteronism?
Hypertension and hypokalaemia
134
How is hyperaldosteronism treated?
Surgery to remove adrenal tumour if Conn's syndrome
Anti-aldosterone drugs for hypertension e.g. spironolactone
135
What is phaeochromocytoma?
A catecholamine secreting tumour.
136
What are the symptoms associated with phaeochromocytoma?
Episodic headaches, palpitations, sweating, anxiety, nausea and weight-loss
137
What are the signs associated with phaeochromocytoma?
Intermittent hypertension, tachycardia and pallor
Potentially hyperglycaemia
138
What investigations are indicated in the case of phaeochromocytoma?
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
What inheritance pattern does Multiple Endocrine Neoplasia demonstrate?
Autosomal dominant
140
What mutation results in Type 1 Multiple Endocrine Neoplasia?
Menin gene on chromosome 11
141
What mutation results in Type 2 Multiple Endocrine Neoplasia?
Ret proto-oncogene on chromosome 10
142
How is Multiple Endocrine Neoplasia screened for in at-risk family members?
Serum calcium - due to high penetrance (95%) of parathyroid involvement
143
What is the principle determinant of ADH secretion?
Plasma osmolality
144
What is the function of the ADH?
Act on collecting tubules of the kidneys to increase water reabsorption
145
At high concentrations, what other function does ADH serve?
Increase blood pressure
146
With reference to plasma osmolality values, when is ADH secreted maximally and minimally?
Maximum secretion at plasma osmolality 295mOsm/kg
Minimum secretion at plasma osmolality below 280mOsm/kg
147
What are the two types of diabetes insipidus (DI)?
1. Cranial DI- impaired ADH secretion from the posterior pituitary
2. Nephrogenic DI - renal resistance to ADH action
148
What is the presentation fo diabetes insipidus?
- Polyuria of dilute urine (in excess of 3L per day)
Nocturia
- Compensatory polydipsia (thirst)
149
What is the difference between primary and compensatory polydipsia?
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
What can cause cranial diabetes insipidus?
Disease of the hypothalamus e.g. primary or secondary tumours, trauma, infiltrative disease e.g. tuberculosis or sarcoidosis
151
What can cause nephrogenic diabetes insipidus?
- Hypokalaemia (loss of renal medullary concentration gradient)
- Hypercalcaemia
- Renal tubular acidosis
- Drugs e.g. lithium
152
How is diabetes insipidus measured?
- 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
How is diabetes insipidus treated?
Difficult to improve established cranial diabetes insipidus.
Desmopressin and thiazide diuretics can improve ADH sensitivity
154
What is SIADH?
Syndrome of Inappropriate Anti-Diuretic Hormone
155
What is the pathophysiology of SIADH?
Continued ADH secretion in spite of plasma hypotonicity and a normal/increased plasma volume
156
Give three examples of causes of SIADH?
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
What hormone regulates the concentration of calcium?
Parathyroid hormone
158
What is the action of increased parathyroid hormone?
Increases calcium
159
How is calcium transported around the body?
40% is free and ionised in the plasma (physiologically relevant)
The rest is bound to albumin
160
What is the most common cause of severe hypercalcaemia?
Hypercalcaemia (>3.5mmol/L) is usually caused by malignancy
161
What is the difference between primary and secondary hyperparathyroidism?
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
What is the presentation of hypercalcaemia?
Remember: Stones, bones abdominal groans and psychic moans
Malaise, depression, bone pain, abdominal pain, nausea, compensation, renal calculi, dehhydration, confusion
163
What investigations are indicated for suspected hypercalcaemia?
Fasting calcium and phosphate
| Serum PTH
164
How is acute severe hypercalcaemia treated?
Rehydrate with IV 0.9% saline 4-6L over 24 hours
165
What is the most common cause of hypocalcaemia?
Chronic kidney disease leading to inadequate production of vitamin D and phosphate retention
166
What are the clinical features of hypocalcaemia?
```
Circumoral paraesthesia
Paraesthesia in the extremities
Cramps
Tetany
Convulsions
Death
```
167
What two signs may be elicited in the patient with hypocalcaemia?
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
How is hypocalcaemia managed acutely?
10ml of 10% calcium gluconate diluted in 50-100ml 5% glucose administered IV over 10 mins
169
Hyperphosphataemia most commonly occurs in which chronic condition?
Chronic Kidney Disease
170
How is hyperphosphataemia treated?
Gut phosphate binders and dialysis
171
What three mechanisms can cause hypophosphataemia?
1. Redistribution
2. Increased renal excretion
3. Decreased intake/ absorption
172
What is the clinical presentation of hypophosphataemia?
- Muscle weakness (diaphragmatic weakness leading to respiratory failure)
- Impaired myocardial contractility (leading to cardiac failure)
- Encephalopathy (confusion, hallucinations, convulsions)
