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Flashcards in Endocrine Deck (270):
1

What is an endocrine hormone?

blood borne and acts at distant sites

2

What is a paracrine hormone?

acting on adjacent cells

3

What is an autocrine hormone?

feedback on the same cell that secreted the hormone

4

What is an endocrine gland?

secretes into the blood stream (thyroid, adrenal, beta cells of the pancreas)

5

What is an exocrine gland?

secretes through a duct (pancreas amylase and lipase)

6

Do fat soluble of water soluble hormones have a longer half life?

fat soluble

7

Are fat soluble of water soluble hormones protein bound or unbound?

fat - protein bound
water - unbound

8

Where do peptides store hormones?

in secretary granules

9

What are the different classes of hormones?

peptides, amines, idothyronines, cholesterol derivatives and steroids

10

Synthesis of T3 and T4?

thyroglobulin released into colloid and acts as a base for thyroid hormone sysnthesis, the incorporation of iodine forms idothyrosines, it is conjugated and then forms T3 and T4 and stored in colloid bound to thyroglobulinm TSH stimulates the movement of colloid unto secretory cell, T4 and T3 cleaved from thyroglobulin

11

How do adrenocortical and gonadal steroids work?

enter call and pass to nucleus by diffusing through plasma membrane, altered to an active metabolite and bind to a cytoplasmic receptor, receptor hormone complex binds to GRE, initiating transcription of gene to mRNA, and this directs protein synthesis

12

How is hormone secretion controlled?

continuous basal secretion, superadded rhythms (day night cycle), release inhibiting factors, releasing factors

13

What is synergism?

combined effects of two hormones amplified

14

What is permissiveness?

a hormone needed for another's full potential effect

15

Function of the thyroid hormone?

accelerates food metabolism, increases protein synthesis, stimulation of carbohydrate metabolism, enhances fat metabolism, increase in ventilation rate, increase in cardiac output and heart rate, brain development during foetal life and postnatal development, growth rate accelerated

16

Function of growth hormone?

stimulates production of IGF-1 to induce metabolic changes

decreases adipose, increase liver function and increase muscle, increase protein synthesis, increase lipolysis

17

What hormone stimulates GH?

GHRH (grehlin increased GH secretion)

18

What hormone inhibits GH?

somatostatin

19

What is acromegaly?

an overgrowth of all organ systems, bones, joints, soft tissues from excessive GH secretion after fusion of the epiphyseal plates

20

What is giantism?

an overgrowth of all organ systems, bones, joints, soft tissues from excessive GH secretion before fusion of the epiphyseal plates

21

What causes acromegaly?

benign pituitary GH producing adenoma or GHRH producing bronchial carcinoid

22

Symptoms of acromegaly?

ABCDEF
arthralgia, arthritis, bp raised, carpal tunnel syndrome, diabetes, enlarged organs, field defect

prognathism, interdental separation, macro glossia, spade like hands and feet, increased jaw and hand size, lower pitch of voice, headaches

23

Investigations for acromegaly?

monitor visual fields, raised glucose, serum phosphate, urinary calcium and serum triglycerides, MRI and CT, IGFBP-3 increased, ECG, ECHO, serum prolcatin, raised IGF-1

24

What is the diagnostic test for acromegaly?

glucose tolerance test

GH is inhibited by glucose so should be suppressed 2 hours after oral glucose load, if not

25

What is IGFBP-3?

the main binding protein for circulating IGF, and is increased in acromegaly due to increased IGF-1

26

Management of acromegaly?

control symptoms, normalise hormones levels and correc tumour compression

trans-sphenoidal surgery of endoscopic trans sphenoidal treatment in pituitary adenomas if non invasive macroadenoma

pegvisomant

somatostatin nalogues

dopamine agonists

radiotherapy/sterotactic radiotherapy

follow ups

27

How does pegvisomant treat acromegaly?

for those who don't respond to somatostatin, suppressed IGF-1 levels - does not affect tumour size

28

How does somatostatin analogues treat acromegaly?

inhibit GH secretion

29

side effect of long term dopamine agonists for acromegaly?

cardiac fibrosis - need regualr ECHO

30

Why is stereotactic radiotherapy better than radiotherapy in acromegaly?

more accurate for tumour location and irradiation and is less radiation to normal brin tissue

31

Complications of acromegaly?

hypertension, cardiac faiure, diabetes, obsturctive sleep apnoea, increased colonic polyp risk, post surgery hypopituitarism, DI, CSF rhinorrhoea, infection, hyperprolactinaemia, hormone deficiencies, gestational diabetes, gravid hypertension

32

Prognosis of acromegaly?

2-3x increased mortality, prediction of survival is based of the post treatment GH conc, untreated lead to death by CV disease or cancer

33

What are carcinoid tumours?

slow growing tumours that originate in cells of the diffuse neuroendocrine system (enterochromaffin cells)

34

Where do carcinoid tumours usually occur?

gastro entero pancreatic tumours, in the appendix, ileum, rectum, bronchi of lung

35

What condition is carcinoid tumours related to?

carcinoid syndrome

36

Symptoms of carcinoid tumours?

pain, weight loss, appendicitis, intussception, obstruction, RUQ pain, bradykinin, tachykinin, subsatnce P, VIP, gastrin, insuline, glucagon, ACTH, parathyroid and thyroid hormone secretion

37

What is carcinoid syndrome?

increased release of 5-hydroxytryptamine, prostagladins, kinins, substance P, somatostatin, corticotropin and neuron specific enolase into the peripheral circulation, secretion depends on tumour location and metastases

38

Presentation of carcinoid syndrome?

bronchoconstriction, paroxysmal flushing in upper body and post alcohol, coffee, food or drugs, diarrhea, abdo pain, palpitations, increased peptic ulcer risk, changes in mental state

39

What is the common size of a carcinoid syndrome?

1-2cm, the bigger the more likely for metastases

40

Investigations of carcinoid syndrome?

plasma chromogranin reflects tumour mass

24hr urinary 5-hydroxyindoleacetic acid, >25mg is diagnostic (but can be changed by other drugs and food)

pentagastrin test

gastric US and endoscopy, CT, MRI, laparotomy, scintigraphic imagaing with labelled somatostatin to find site

somatostatin SPECT

41

Complications of carcinoid tumours?

MEN1, appendicitus, intussception, bowel obstruction, metastatic spread

42

Management of carcinoid tumour and syndrome?

avoid precipitating factors, chemo e.g. doxorubicin, external beam radiotherapy, chemoembolisation, liver transplant, octreotide (somatostatin analogue) to block release of tumour mediators, loperamide for diarrhea, IFN-a, resect tumours, bebulking, radiofrequency ablation, PPI do prevent ulceration

43

What is carcinoid crisis?

when tumour outgrows its riction, altered mental state, hyperglyaemiablood supply or handled too much during surgery so that vasoactive mediators flow out, causing life threatening vasodilations, hypotension, tachycardia, bronchoconst

44

Treatment for carcinoid crisis?

octrotidem supportive measure, fluid balance managment

45

Prognosis of carcinoid crisis?

5-8years survival, 3 if metasatases, prognosis depends on site

46

What is hypothyroidism?

decreased thyroid hormone production, causing a slow down in body's functions

47

Symptoms of hypothyroidism?

bradycardia, reflexes relax slowly/mentally slowing, aches, ataxia, dry skin and hair, fatigues, drowsy, cold intolerance, ascities, round puffy face, defeated demeanour, irregular/heavy periods, hoarse voice, carpal tunnel syndrome, weight gain, constripation, fluid retention, infetility, loss of libido, memory loss, confusion, goitre

48

What are the complications of hypothyroidism in pregnancy?

pre eclampsia, anaemia, premature labour, low birth weight, still birth, serious blleding post birth, hypothryoid coma (myxoedema coma)

49

How common is hypothyroidism?

0.1-0.2% of pop., increased risk with age and in women

50

Causes of hypothyroidism?

AUTOIMMUNE - attack thyroid gland, block binding of TSH to receptor (hashimotos if a goitre is formed)

surgery, radioactive treatment iron deficiency, medicine side effects, thyroiditis, pituitary gland problem, congenital (thyroid aplasia/dysplasia)

51

Risk factors for autoimmune hypothyroidism?

FH, downs, turner syndrome, enlarged thyroid, Graves disease, thyroiditis post birth, autoimmune conditions

52

Diagnosis of hypothyroidism?`

raised TSH, low thyroxine, thyroid antibodies, anaemia, hyperlipidaemia, hyponatraemia, incresed serum creatinine kinase levels, associated myopathy

53

What is subclinical hypothyroidism?

raised TSH, normal thyroxine, but thyroid glands need extra stimulation to make the required thyroxine needed, this increases hypothyroidism risk

54

Treatment of hypothyroidism?

lifelong levothyroxine, start low dose (esppecially in elderly) and increase dose

check TSH once a year for adjustment, which is also needed in weight gain and pregnancy

55

Complications of levothryoxine?

angina pain worsens, hyperthyroidism

56

How dose levothyroxine treat hypothyroidism?

replaces thyroxine production and normalises serum TSH concentrations

57

What is myxoedema coma?

severe hypothyroidism with confusion, coma, hypothermia, cardiac failure, hypoventilation, hypoglycaemia and hyponatraemia, common in elderly

58

Treatment of myxoedema coma?

oral T3, o2, gradual rewarming, hydrocortisone, glucose in fusion, supportive managment, thyroid diet by changing iodine in food into thyroid hormones

59

What is borderline hypothyroidism?

slight increased serum TSH, normal T4, due to early phase chronic autoimmune thyroiditis so 2-4% will develop overt hypothyroidism, treat with levothyroxine

60

What is Hashimoto's disease?

autoimmune hypothyroidism with a goitre

61

Examples of thyroid diet foods?

protein, green leafy vegetables, fish, iodized salt, eggs, seaweed, avoid alcohol

62

Cause of Hashimoto's disease?

iodine, medications, infection, smoking, stress

goitre associated with HLA-DR5 causing lymphatic and plasma cell infiltration, formation of lymphoid molecules from follicular hyperplasia, and damage to follicular basement membrane

63

In who is Hashimoto's disease most common?

women aged 60-70

64

Symptoms of Hashimoto's disease?

rapidly enlarged thyroid gland, dyspnoea, dysphagia, mild neck pain and tenderness, increase in size, thyrotoxicosis, hyperlipidaemia, fatigue, forgetfullness, myxoedema, feeling cold, weight gain, depression, poor memory

65

Investigations of Hashimoto's disease?

low T3 and T4, high thyroid antibodies (anti-TPO and anti-Tg) and TSH, damaged thyroid cells, increase lymphocytes and plasma cells, thyroid parenchyma atrophy, follicular hyperplasia, lymphoid follicles, radioactive iodine uptake for hot or cold classification

66

Whats the difference between a hot and cold thyroid nodule?

cold has higher malignancy risk and needs a fine needle aspiration biopsy

67

Treatment of Hashimoto's disease?

levothyroxine sodium to restore clinically and biochemically euthyroid state, surgery if large goitre or cosmetic reasons

68

Complications of Hashimoto's disease?

over replacement can cuase bone loss and increased heart rate, hyperlipidaemia if untreatment, Hashimoto's encephalopathy, myxoedema coma

69

Prognosis of Hashimoto's disease?

good and most achieve normal thyroid levels

70

What is hyperthyroidism?

raised thyroid level from overactive thyroid gland

71

Causes of hyperthyroidism?

grave's disease (most common), thyroid nodules, De Quervains thyroiditis, postpartum thyroiditis

72

What is De Quervains thyroiditis?

acute inflammation of the gland from viral infection, presenting with fever, maliase, goitre and neck pain, treated with aspirin

73

Symptoms of hyperthyroidism?

restless, nervous, emotional, irritable, poor sleeping, hand tremor, losing weight, increased appetite, palpitations, sweating, heat intolerance, increased thirst, diarrhoea, sob, hair thinning, irregular and light periods, tiredness, muscle weakess, neck goitree, exophthalmos, graves dermopathy

74

Complications of hyperthyroidism?

atrial fibrillation, cardio myopathy angina, heart failure, pregnancy complications, osteoporiosis

75

How common is hyperthyroidism?

10x more common in women, 20-40years

76

What does hyperthyroidism show in investigations?

high T4, high T3 in graves, suppressed TSH, thyroid ultrasound, positive microsomal and thyroglobulin antibodies, isotope scan to classify thyroid nodules, fine needle aspiration to exclude malignancy

77

Treatment of hyperthyroidism?

anti thyroid medications e.g. carbimazole to reduce thyroxine production, high dose then reduce

radioactive iodine drink to destroy thyroid tissue

regular bloods for thyroxine level check

remove part of thyroid gland

treat eye problems: artificial tears, sunglasses, eye protectors during sleep, surgery, radiation treatment, steroid tablets, stop smoking

BBs for first few weeks of treatment and reduces symptoms of tremor, palpitations, sweating, angitation and anxiety

78

Side effect of carbimazole?

agranulocytosis with fever, sore throat and mouth ulcers (propylthiouracil is better if pregnant)

79

Precautions during radioactive iodine treatment?

do not get pregnant for 6 months after, no breastfeeding, limit close contact with babies, children, pregnant women and pets, sleep alone, stay more than an arms length away from other people, avoid going places in close proximity to people, take time off work

80

Symptoms of ophthalmic Grave's disease?

bilateral eye involvement, pressure and pain in one eye, a gritty sensation, reduced vision, photophobia, exophthalmos and opthalmoplegia, MRI shows enlarged muscle and oedema

81

What is exophthalmos and opthalmoplegia?

retro orbital inflammation, causing eye popping, worse in smokers

82

Treatment of ophthalmic Grave's disease?

correct thyroid dysfunction, hyperthryoidism, smoking cessation, artificial tears, high dose systemic steroids to reduce inflammation, surgery to partially sew eyelids together to protect cornea, corrective eye muscle surgery

83

Triggers of ophthalmic Grave's disease?

stress, infection, childbirth, hyperthyroid

84

Pathophysiology of ophthalmic Grave's disease?

IgG autoantibodies bind to and activate G protein coupled thyrotropin receptors cyasing smooth thyroid enlargement, increased hormone production and react with orbital autoantigen, leading to catecholamine sensitivity of the levator palpebrae superioris causing lid retraction and lid lag. T lymphocytes react with antigens and cause retro orbital inflammation. Swelling and oedema of the extraocular muscles leading to movement limitation and proptosis, increasing pressure on optic nerve, leading to atrophy

85

How common is thyroid cancer?

1% of all malignancies, incidence is increasing, most common malignancy of endocrine system

86

Symptoms of thyroid cancer?

lymph node metastases, increased thyroid nodule size which is hard and irregular, enlarged lymph node

87

What are different types of thyroid cancer?

papillary, follicular, medullary, thyroid lymphoma, Hurthle cell, anaplastic thyroid

88

What is the most common thyroid cancer and in who is it most common?

papillary - women aged 35-40

89

What is the spread and prognosis of papillary and follicular thyroid cancer like?

spreads locally to neck, compressing trachea and recurrent laryngeal nerve, metastases most often in lung and bone

90

What causes follicular thyroid cancer?

areas of low iodine

91

In who is follicular thyroid cancer most common?

women 30-30years

92

Where does medullary thyroid cancer arise from?

parafollicular cells due to their malignancy making them produce carcinoembryonic antigen and calcitonin

mainly autosomal dominant inherited

93

Who gets thyroid lymphomas?

women aged 50 with Hashimoto's

94

Symptoms of thyroid lymphoma?

dyspnoea, dysphagia, non Hodgkin's,

95

Treatment of hurthle cell carcinoma?

surgery, postoperative radioative iodine 131, levotyroxine, external radiotherapy

96

What kind of thyroid cancers are more aggressive ?

medullar and anaplastic

97

Where do anaplastic thyroid cancers arise from?

follicular cells - normally from a pre existing, well differentiated thyroid tumour which has undergone additional mutational events

98

Risk factors of thyroid cancer?

exposure to ionising radiation, history/family history of thyroid problems, mutation in RET proto oncogenes which causes MEN2 as well, MEN1/2, Cowden's syndrome, familial adenomatous polyposis, obesity

99

TNM staging?

1 - no lymph node spread or metastases, 45
3 - >4cm but contained in thyroid, or localised tumour with spread to lymphs
4a - spread to nearby structure, or localised with distant lymph node spread
4b - spread beyond nearby structures
4c - metastases

100

Presentation of thyroid cancer?

thyroid nodule, hard and fixed nodules suggest malignancy more, usually non tender on palpitation, firm cervical masses suggest regional node mestastases, vocal cord paralysis suggests recurrent laryngeal nerve involvement

101

Investigations of thyroid cancer?

TFTs, serum thyroglobin, serum calcitonin, thyroid US, fine needle aspiration cytology if >1cm or suspected malignancy (distinguishes between benign and malignant), radionuclide imaging with 123 iodine uptake studies, Gallium 67 Ga for thyroid lymphoma diagnosis, Ct and MRI for metastatic spread

102

Treatment of thyroid cancer?

total thyroidectomy, may need intraoperative nerve monitoring for the laryngeal nerves, radioiodine remnant ablation and therapy, adjuvant external beam radiotherapy, targeted multikinase inhibitor (sorafenib), surgery, iodine 131 for microscopic residuals, effective thyroid ablation with TSH stimulation so need extra administration

103

Complications of thyroid cancer?

laryngeal nerve palsy, hypoparathyroidism, nerve damage

104

What is Cushing's syndrome?

increased glucocorticoid in the body

105

How common is Cushing's syndrome?

5/1 million a year develop ot, main women 20-50

106

Functions of cortisol?

regulate BP, regulate immune system, balance insulin effect, help stress response, bone formation inhibition, decreases immune function, increase gluconeogenesis, lipolysis and proteolysis

107

Causes of Cushing's syndrome?

long term steroid medication e.g. prednisolone, pituitary adenoma (Cushing's disease) which increases ACTH, adrenal hyperplasia, ectopic ACTH production (lung cancers, MEN1), alcohol, depression

108

Cushing's syndrome symptoms?

obesity, PLETHORIC complexion, moon face, facial puffiness and REDNESS, diabtes, facial hair in women, hypertension, thin EASILY BRUISED skin, STRIAE, tiredness, ache and pains, mood swings, loss of libuido, irregular periods, osteoporosis, ankle oedema, excess thirst, increased susceptibility of infections (children tend to be obese and short), PROXIMAL MUSCLE WEAKNESS

109

Investigations for Cushing's syndrome?

48hr low dose dexamethasone suppression test, suppressed in normal individuals

high dose dexamethasone suppression test in suppressed in pituitary dependent Cushing's syndrome and normal suggests ectopic source of ACTH

24hr urine cortisol (normal

110

Treatment of Cushing's syndrome?

trans-sphenoidal surgery to remove adenoma

hydrocortisone for several months post surgery to normalise cortisol levels

remove both adrenal glands - but will lead to lifelong replacement therapy

external beam radio therapy

drugs to inhibit cortisol synthesis e.g. metyrapone, ketoconazole, etomidate

remove ectopic tumours

immunosuppressants with steroids

intubation and mifepristone to compete with cortisol at receptors

stop steroids

111

What is Conn's syndrome?

hyperaldosterone, excessive levels of aldosterone, causing increase in sodium retention in distal convoluted tubule, increasing water retention, volume expansion with hypertension and excretion of potassium, leading to hypokalaemia

112

What is the most common cause of secondary hypertenision?

primary hyperaldosterone

113

What is primary hyperaldosterone?

excessive aldosterone independent of the RAAS, can be an adrenal adenoma (Conn's), familial hyperaldosterone, adrenal carcinoma

114

What are the 2 forms of familial hyperaldosterone?

1 - glucocorticoid remediable aldosterone (GRA) - regulatory portion of the 11b-OH gene binds to the aldosterone synthase gene, meaning ACTH releases stimulates this abnormal chimera and excessive aldosterone production from the zona fasciculata not zona glomerulosa, autosomal dominant

2 - inherited aldosterone producing adenoma or inherited bilateral adrenal hyperplasia, increasing aldosterone production, can also be unilateral

115

What can type 1 familial hyperaldosteronism lead to?

causes early age hypertension, leading to haemorrhagic strokes, so need regular aneurysm sceening, and can become hypokalaemic

116

Symptoms of hyperaldosteronism?

hypertension, hypokalaemia, metabolic alkalosis, slight increased sodium, polyuria, polydipsia as can't concentrate urine, weakness from hypokaelaemia, headaches, lethargy

117

What can Conn's syndrome lead to?

periodic cramps and occasional lower limb paralysis, the adenomas are usually unilateral

118

What will investigations show in hyperaldosteronism?

hypokalaemia, hypernatraemia, renal impairment, raised aldosterone and low renin, arrhythmias from electrlyte imblance, CT/MRI show adenomas and hyperplasia, selective adrenal venous sampling to localise cause, genetic testing, salt loading,

119

When should tests for hyperaldosteronism be done?

when the patient is off diuretics for 4 weeks and off BBs and CCBs for 2 weeks as can lead to false positives and false negatives, should also stop steroids, potassium suppplements and laxatives

120

How should aldosterone and renin levels be measured?

lying and standing as they are affected by the upright position, aldosterone should increases after being upright for a few hours

121

How is the salt loading done for hyperaldosteronism diagnosis?

loading with salt for 2 weeks, then take samples to suppress aldosterone, failure to suppress confirms primary hyperaldosteronism, if renin is high this excludes primary hyperaldosteronism

122

DD for hyperaldosteronism?

congenital adrenal hyperplasia, renal artery stenosis, coarctation of aorta, fibromuscular dysplasia, renin secreting tumors, congestive cardiac failure, nephortic syndrome, Gitelmans syndrome, Bartter's syndrome

123

Treatment of Conn's?

aldosterone anatgonists e.g. spironolactone or eplerenone before adrenalectomy, could be long term hypertension though, CT quided acetic acid injections into small functioning adenomas

124

Treatment of BAH?

aldosterone antangonists e.g. amiloride, spironolactone, eplerenone

125

Treatment of GRA?

steroids to reduce aldosterone productioon drive, dexamethasone

spironolactone if hypertension persists after

126

Treatment of adreanl carcinoma?

surgery with post operative adrenolytic therapy with mitotane

127

What is secondary hyperaldosteronism?

excessive renin due to reduced renal perfusion, stimulating the normal adrenals to produce more aldosterone

128

Causes of secondary hyperaldosteronism?

diuretics, congestive cardiac failure, hepatic failure, nephrotic syndrome, renal artery stenosis, malignant hypertension

129

Complications of secondary hyperaldosteronism?

causes myocardial fibrosis, reducin cardiac function and can lead to long term hypertension

130

Treatment of secondary hyperaldosteronism?

lifelong antihypertensive therapy, aldosterone antagonists

131

side effects of spironolactone?

gynaecomastia, menstural problems and erectile dysfunction

132

Which aldosterone antagonists is best to prevent hypokalaemia?

amiloride as it is potassium sparing and counteracts hypokalaemia (but lacks mineralcorticoid inhibition and is only a week antihypertensive)

133

Which aldosterone antagonist is selctive?

eplerenone

134

What is Addison's disease?

lack of steroid hormone rlease form the adrenal glands

135

How common is Addison's disease?

8000 people in the UK, age 30-50 normally

136

What makes steroid hormones?

adrenal cortex

137

What controls steroid release?

ACTH from the pituitary gland which is stimulated by CRH from the hypothalamus

138

What makes adrenaline and noradrenaline?

adrenal medulla

139

Causes of adrenal insufficiency?

autoimmune (80%), TB, meningitis, HIV, cancer, adrenoleukodystrophy, congenital adrenal hyperplasia, critical illness, trauma to adrenal gland, radiotherapy, medicine e.g. ketoconazole

140

Symptoms of Addison's disease?

general weakness, easily fatigued, pigmentation on sun exposed areas and pressure points from excess ACTH, vitiligo, loss of body hair in women, postural hypotension, dizziness, loss of appetite, weight loss, food cravings, abdominal pains, diarrhea, constipation, cramps, muscle pain, decreased or irregular menstural cycle, depression, psychosis

141

What sudden symptoms occur in Addison's crisis of sudden low cortisol?

severe vomiting and diarrhea, pain andback and abdomen, dehydration, hypotension, collapse, severe illness

142

When would Addison's crisis occur?

triggered by other illnesses when more cortisol is needed of after a period of less severe symptoms

143

Tests for Addison's disease?

decreased sodium and glucose, increased postassium and calcium, morning cortisol levels, tetracosactide stimulation test, x-rays to find cause, ACTH levels are high or low depending on cause, 21-hydroxylase adrenal autoantibodies if autoimmune, plasma renin and aldosterone levels

144

How is a short tetracosactide stimulation test from ACTH used for Addison's disease diagnosis?

there is no cortisol rise in blood post injection in Addison's disease - Synacthen test

145

What does high ACTH and low cortisol in the morning suggest?

primary adrenal insufficiency

146

What does low ACTH and low cotrisol in the morning suggest?

secondary or tertiary adrenal insufficiency

147

Treatment of Addison's disease?

hydrocortisone for cortisol replacement, 2 or 3 doses a day to mimic cortisol changes in the day, dose based on weight, height, age, gender, activity levels, ill, surgery, trauma, shift work etc, reduce dose gradually

fludrocortisone regular BP and blood salt levels

need steroid card

148

Treatment of Addison's crisis?

hydrocortisone injections and fluids to increase BP, may need ICU

149

When are cortisol level highest?

in the morning

150

Complications of Addison's disease?

other autoimmune disease, adrenal crisis, osteoporosis

151

What is secondary adrenal insufficiency?

inadequate pituitary of hypothalamic stimulation of the adrenal glands, from hypothalamic-pituitary disease or long term steroid therapy

152

What is critical illness related corticosteroid insufficiency (CIRCI)?

patients who are critically ill and at increased risk of adrenal dysfunction e.g. in sepsis, severe pneumonia, ARDS, trauma, HIV infection

153

How do renin levels differ in primary and secondary adrena insufficiency?

renin high and aldosterone low in primary, and unaffected in secondary

154

How is secondary adrenal insufficiency diagnosed?

insulin tolerance test, hypoglycaemia is induced by an insulin infusion and cortisol response is monitored

test other hormones from the hypotahalmus/pituitary

screen for adrenoleukodystrophy (x linked condition) by measuring very long chain fatty acids in serum sample

CRH stimulation test

155

Management of secondary adrenal insufficiency?

hydrocortisonem fludrocortisone, regular examinations, educate, steroid card, emergency self injection kit,

156

Prognosis of adrenal insufficiency?

can be fatal in untreated, prognosis is based on the underlying cause

157

What diabetes insipidus?

hyposecretion of or insensitivity to the effects of ADH, leading to the inability to concentrate urine in the distal renal tubules, so increased passage of dilute urine, usually >3L/24hrs of low osmolality

158

Where is ADH made?

in the hypothalamus, transported as neurosecretory vesicles to posterior pituitary and released into the circulation

159

What is gestational diabetes insipidus?

results from degradation of ADH by a placental vasopressinase

160

What is dipsogenic diabetes insipidus?

primary polydipsia, caused by primary defect in osmoregulation of thirst, seen in TB meningitis, MS and neurosarcoidosis

161

What are the two types of diabetes insipidus?

cranial - decreased ADH secretion
nephrogenic - resistance to ADH in kidney

162

Causes of cranial diabetes insipidus?

idiopathic, tumours, head injury, TB, sarcoidosis, Wegeners granulomatosis, encephalitis, meningitis, cerebral abscess, haemorrhage, thrombosis, sickle cell disease, auto immune hypophysitis, hypophysectomy, post radiotherapy, Woldrams syndrome, mutations in ADH gene

163

Causes of nephrogenic diabetes insipidus?

idiopathic, hypokalaemia, hypercalcaemia, CKD, drugs, renal tubular acidosis, pregnancy, post obstructive uropaathy, X linked mutation in V2 ADH receptor gene, defect in AQP2 gene, sporadic

164

Symptoms of diabetes insipidus?

polyuria, >3L or urine a day, polydispsia, dehydration, chronic thirst, hypernatraemia, nocturia/bed wetting, failure to thrive in infants with irritability fever and feeding problems, chronic overdistention, urinary incontinenece, enlarged bladder

165

DD of diabetes insipidus?

psychogenic or primary polydipsia, DM, Cushings syndrome, hypercalcaemia, hyperkalaemia, diuretic abuse

166

Investigations in diabetes insipidus?

24 hour urine collection, water deprivation test, MRI to find cause, US, IV peylogram to assess obstruction, increased plasma osmolality, decreased urine osmolality, increased sodium, increased urine output

167

What is the water deprivation test for diabetes insipidus?

deprive patient of fluids for 8 hours, if patient has >600, it is primary polydipsia, then use desmopressin 2mg IM, if >600 it is cranial, if less it is nephrogenic

168

Management of cranial diabetes insipidus?

oral/nasal/parenteral desmopressin increased AQP-2 channels in distal convoluted tubule and collecting ducts, miss dose once a week to prevent overdosing, increase water intake

169

Management of nephrogenic diabetes insipidus?

treat cause, high dose desmopressin with thiazide diuretic, NSAIDs reduce urine volume and plasma sodium by inhibiting PG synthase which can inhibit ASH action, surgery, intermittent catheterisation to reduce urinary tract back pressure complications

170

Complications of nephrogenic diabetes insipidus treatment?

desmopressin can worsen MI

171

prognosis of diabetes insipidus?

rare death form dehydration, hypernatraemia, fever, CV etc

annual review of symptoms and 24 hour urinary measurement if lithium use

good prognosis

172

What is hyponatraemia?

excess of water in relation to serum sodium which is

173

What is SIADH?

syndrome of inappropriate ADH secretion from posterior pituitary/ectopic source despite low serum osmolarity

174

Who is most at risk of hyponatraemia?

infants and elderly as less likely to express their thirst and control their own fluid intake , infants with diarrhea and given tap water not fluids as treatment, or given watered down milk formula

175

Presentation of hyponatraemia?

mild - asymptomatic, anorexia, headache, nausea, vomiting, lethargy
moderate - personality change, muscle cramps, weakness, confusion, ataxia
severe - drowsiness, decreased consciousness, cognitive impairment, seizures, brainstem herniation, can be no symptoms due to cerebral adaption

signs of hypovalaemia - dry mucous membranes, tahycardia, diminished skin turgor
signs of hypervolaemia - pulmonary rales, s3 gallop, JV distention, peripheral oedema, ascites

176

Diagnostic features of SIADH?

hyponatraemia, plasma hypo-osmolality proportional to hyponataemia, inappropriately elevated urine osmolality (>100mOsmol/kg) commonly >plasma osmolarity, persistent urine Na>30mmol/L with normal salt intake, euvolaemia, normal thyroid and adrenal function , elevated ADH level and low blood uric acid levels

177

Causes of SIADH?

thiazide diuretics, SSRIs, ACE-I, PPIs, llop diuretics, opiates, idiopathic, hereditary, stress, endurance exercise, marathon runners, herpses zoster, trauma, tumours, infection, MS, GBS, SLE

178

What will investigations show in SIADH?

low sodium, and low or high serum hypo osmolality, absence of hypervolaemia, adrenal or thyroids dysfunction and use of diuretics, continued urine sodium level (if >20mmol/L, a renal cause should be looked for), serum TSH and thyroxine normal, imaging, will not respond to slaine, radom serum cortisol levels of ACTH stimulation test

179

Management of SIADH?

correct underlying cause

severe - hypertonic saline with furosemide to prevent circulatory overload and gradually correct hyponatraemia, not rapid as that can cause osmotic demyelination syndrome

hypovolaemic - IV saline replacement, may need desmopressin
normovolaemic - fluid restriction, demeclocycline blocks ADH and induces partial nephrogenic DI, vaptans (vasopressin receptor antagonists)
hypervolaemia - treat hypervalemia, usually HF, AKI, liver cirrhosis

180

Complications of vaptans?

used in hyponatraemia secondary to SIADH, can induce thirst, expensive, limited availability and can increase sodium levels too rapidly

181

Complications of hyponatraemia?

gait disturbance in elderly leading to falls, reduces bone mass, increased fractures, severe cerebral oedema with cerebral herniation and death if the fall in sodium is too quick, permanent neurological sequelae, seizures, respiratory arrest, pontine myelinolysis from too rapid a correction

182

Symptoms of pontine myelinolysis?

quadriplegia, pseudobulbar palasy, locked in syndrome (risk factors: females, hypokalaemia, alcoholism, liver transplant)

183

What is hypokalaemia?

mild = 3.1-3.5mmol/L
moderate = 2.3-3mmol/L
severe =

184

What are the classifications of hypokalaemia causes?

increased excretion via kidney, skin or Gi tract, trans-cellular shift, decreased intake (other include chronic alcoholism, chronic peritoneal dialysis and plasmapheresis)

185

Causes of hypokalaemia from increased loss in kidney, skin and GI?

kidney - diuretics, renal tubular acidosis, hypomagnesaemia, hyperalsosteronism, tubulointerstitial renal disease, liquorice, RAAS activation

GI - diarrhea, vomiting (causing increased Cl, increased aldosterone, inhibiting potassium reabsorption), intestinal fistula, villous adenoma, pyloric stenosis, laxative abuse

skin - burns, erythroderma, increased sweating or increased loss in sweat

186

Causes of hypokalaemia from transcellular shift

alkalosis, insuline and glucose administration, catecholamines and B2 sympathomimetics, toluene intoxication, CCB, hypothermia

187

Causes of hypokalaemia from decreased intake?

inadequate fluid replacement during nil by mouth, parenteral nutrition, malnutrition, anorexia, hypocaloric protein diets

188

Presentation of hypokalaemia?

asymptomatic then lassitudem general weakness and muscle pain and constipation, thread pulse, shallow respirations, confusion, alkalosis

if more severe: severe muscle weakness and paralysis, starts in lower extremities and ascends, resp failure, paraesthesia, tetany, hyporeflexia, arrhythmias, light headedness

189

What is the most common cause of hypokalaemia?

Gitelman's syndrome - with impaired renal tubular ion transport from mutation in Na/Cl transporter gene, presents with hypotension, alkalosis, salt wasting, hypomagnesaemia, hypocalciuria, hypermagnesuria, salt cravings, cramps, muscle weakness, aches, fatigue, general weakness, dizziness, nocturia and polydipsia

190

Investigations in hypokalaemia?

low sodium suggests thiazide use of marked volume depletion, serum bicarbonate is high on long term diuretics, serum glucose, chloride, low serum magnesium, spurious potassium, ECG, low urinary potassium, urinary sodium, urinary osmolality, serum digoxin, ABGs, urine calcium, 24 hour uruine matanhephrines, sodium and potassium, sweat chloride test, low dose dexamethasone suppression test, renal angiogram

191

What do ECGs show in hypokalaemia?

ST depression, prominent U wave, shallow T wave, slightly prolonged PR interval

premature ventricular contractions, torsades de pointes, ventricular tachycardia and ventricular fibrillation may occur

192

Treatment of hypokalaemia?

oral (IV if severe) potassium supplements/replacement (KCl), regular potassium monitoring, take potassium sparing diuretic if on diuretic, no potassium if oliguric or as fast stat bolus, normalize serum magnesium, never more IV potassium than 20mmol/hr unless ECG monitoring and hourly serum potassium measurement, treat underlying cause , potassium rich foods, avoid glucose solutions, ampoules of potassium mixed with saline to prevent hypoglycaemia

193

Complications of hypokalaemia?

cardiac arrhythmias, sudden cardiac death, muscle weakness, flaccid paaralysism rhadomylysis, abnormal renal function (DI, metabolic alkalosis), iatrogenic hyperkalaemia, digoxin toxicity, hepatic encephalopathy in cirrhosis

194

Prevention of hypokalaemia?

potassium supplements, loss dose diuretics in hypertension, potassium sparing diuretics, needs careful monitoring

195

What is hyperkalaemia?

mild = 5.5-5.9mmol/L
moderate = 6-6.6mmol/L
severe = >6.5mmol/L

196

How much of potassium is intracellular?

98%

197

Who is most at risk of hyperkalaemia?

young and elderly, hopsital, men

198

What is artefactual hyperkalaemia and what causes it?

lysis of RBC during vigorous phlebotomy or in vitro release from red cells in some blood disorders (leukaemia) or thrombocytoenia or contaminated with potassium EDTA anticoagulant in FBC bottles

199

What classifications of hyperkalaemia are there?

renal cause, increased circulation (endogenous or exogenous), shift from transcellular to extracellular space, psuedohyperkalaemia, dehydration, diabetics

200

What are renal causes of hyperkalaemia?

AKI, CKD as most potassium is excreted renally, renal tubular acidosis, Addison's, hypereninaemic hyperaldosteronism, drugs that interfere with poassium excretion

201

What can cause an increase of potassium in the circulation?

potassium supplementation, tumour lysis syndrome, trauma, burns, massive tissue damage, fresh water drowning which causes lysis or erythrocytes, releasing potassium suddenly

202

What causes a shift of potassium from intracellular to extracelullar?

acidosis (diabetic ketoacidosis), digoxin toxicity, beta blockade, theophylline, hyperkalaemic periodic paralysis, metabolic acidosis, tissue necrosis or lysis

203

What can give unexpectedly high results of potassium?

prolonged tourniquet time, clenched fist, difficulty collecting sample, test tube haemolysis, wrong anticoagulant, excessive cooling of a specimen, length of storage of specimen, marked leucocytosis, thrombocytosis, sample from a limb that is receiving IV fluids with potassium

204

Why can diabetic patients get hyperkalaemia?

they are on ACE-I and low in sodium and high in potassium, insulin pushes glucose and potassium into cells and glucagon impairs the intracellular shift of potassium

205

Symptoms of hyperkalaemia?

MURDER
muscle cramps and parakysis, urine abnormalities, respiratory distress, decreased cardiac contractility with bradycarida, ECG changes, reflexes depressed or absent

palipitations, chest pain, fast irregular pulse

206

What will and ECG show in hyperkalaemia?

peaked T waves, prolonged PR interval, widened QRS complex, reduced/loss p wave, AV dissociation, sine wave pattern, asystole

207

What will blood show in hyperkalaemia?

normocytic normochromic anaemia, thrombocytosis, leukocytosis

208

Management of hyperkalaemia?

ABCDE and early warning score and start escalating

determine severity, ECG, find cause and treat, reduce potassium diet

10ml 10% calcium gluconate to protect cardiac membrane and improve ECG, give 10ml every 10 minutes till ECG normalises

the use insulin glucose IV to shift potassium into cells, give nebulised salbutamol to reduce potassium

add bicarbonate is added until pH is normalised but there are many risks, then use calcium resonium with regular lactulose to remove potassium via GI tract

plan dialysis if necessary

209

Treatment of resistant hyperkalaemia?

further glucose and IV insuin/iv calcium, IV diuretics, sodium bicarbonate, haemodialysis

210

Prognosis of hyperkalaemia?

an independent risk factorr for death, most fatal cases are complicated by AKI

211

Prevention of hyperkalaemia?

reduced potassium retaining drugs, reduce potassium diet, potassium excreting diuretics

212

What is crush syndrome?

severe systemic manifestation of trauma and ischemia from prolonged severe crushing, increased permeability of the cell membrane and postassium, enzyme and myoglobin release from within cells, results in acute tubular necrosis and uraemia

213

Cause of crush syndrome?

continuous pressure on muscle tissue due to ischemic reperfusion causing muscle injury, common after earthquakes, during war, after explosions and industrial accidents. It is in 2-15% of all trauma patients.

214

Pathophysiology of crush syndrome?

the muscle injury causes potassium and other substance leakage into circulation causing renal tubular obstruction and renal damage (mainly from increased myoglobin levels as it is nephrotoxic), also causes intravascular volume depletion and renal hypoperfusion, causing renal dysfunction

215

How is crush syndrome characterised?

hypovolaemic shock from sequestrain of water in the injured muscle cells and hyperkalaemia

216

Complications of crush syndrome?

metabolic acidosis from release of cellular phosphate and sulphate by the injury muscle cells, AKI, DIC, compartment syndrome, peaked creatinine kinase levels, infection, hyperkalaemia

217

Symptoms of crush syndrome?

crushing injury into a large mass of skeletal muscle, sensory and motor disturbances in the compressed limbs which then become tense and swollen, body parts may be pulseless, myoglobinuria, haemoblobinuria, oliguria, hypovolaemic shock, nausea, confusion, vomiting, agitation, hypocalcaemia

218

Initial management of crush syndrome?

ABC, monitor vital signs, O2, assess limbs using the 5 ps to estimate ischemic injury, venous access, preserve body heat, arterial tourniquet if compression was more than 30 mins, saline infusion, hydration, catheter to monitor urine output, analgesics

219

What is rhabdomyolysis?

total creatine kinase levels 5-10x above normal, with other symptoms/risk factors

220

Investigations for crush syndrome?

bloods, electrolyte measurements, LFTs show hepatic dysfunction, ECG shows hyperkalaemia, x-ray, assess compartment pressures, urine dipstick for myoglobin, clotting studies to look for DIC

221

Further management in crush syndrome?

maintain urine output until myoglobinuria has ceased

forced mannitol alkaline diuresis for increased renal perfusion and reduce muscle injury to prevent against myoglobin damage and reduce risk of hyperkalaemia

urinary alkalinisation with sodium bicarbonate to prevent AKI

treat hyperkalaemia, renal dialysis, treat DIC and may need to amputate crushed limbs

222

Prevention of crush syndrome?

adequate rehydration and fluid support reduce AKI and improves prognosis, identify those who need urgent attention

223

What is hyperparathyroidism?

increased parathyroid hormone release leading to increased calcium levels in the blood

224

Effects of parathyroid hormone?

causes bone to release calcium, calcium absorption in the gut, reduces kidney calcium excretion, increases phosphate excretion

225

Effects of calcium?

combines with phosphate to make calcium phosphate to make bones and teeth hard and strong, helps to clot blood after injury, for muscle function (phosphate works alongside and is also used for energy production)

226

What is primary hyperparathyroidism and the causes?

enlarged and overactive parathyroid gland, increasing parathyroid hormone caused by parathyroid benign adenoma, parathyroid gland hyperplasia, parathyroid carcinoma and familial isolated hyperparathyroidism or multiple endocrine neoplasia (MEN)

227

What is secondary hyperparathyroidism and the causes?

caused by diseases that causes hypocalaemia so the parathyroid glands are continually being stimulated to increase calcium levels so it becomes enlarged caused by CKD, vit D deficiency (rickets/osteomalacia) and gut malabsorption

228

What is tertiary hyperparathyroidism and the causes?

caused by longstanding secondary hyperparathyroidism so the parathyroid glands are no longer sensitive to blood calcium levels, seen in CKD or after kidney transplant

229

Symptoms of primary and tertiary hyperparathyroidism?

tiredness, weak and fatigued muscles, nausea, vomiting, loss of appetite, constipation, abdominal pain, thirsty, depression

if extreme: confusion, loss of consciousness, heart rhythm disturbances, hypertension

no symptoms in seconday as low calcium - but can develop osteoporosis

230

Complications of hyperparathyroidism?

kidney stones, haematuria, corneal calcification, pancreatitis, peptic ulceration, kidney damage, osteoporosis

231

hyperparathyroidism investigations?

high calcium (low in 2) and parathyroid hormone, low blood phosphate (high in CKD), 24h urine calcium, DEXA for osteoporosis, x-rays show changes in bones from calcium release, kidney US for kidney stones, US/CT to show enlarged parathyroid gland, biopsy to exclude cancer

232

Treatment of primary hyperparathyroidism?

regular monitoring, stay hydrated, avoid diuretics, avoid vomiting and diarrhea, parathyroidectomy if severe (try and leave a little to have some hormone), bisphosphonate medication if severe but no surgery to improve bone density and correct calcium, cinacalcet reduces calcium and parathyroid hormone levels and increase phosphate levels, HRT if post menopause

233

Treatment of secondary hyperparathyroidism?

treat underlying cause, reduce phosphate in diet, calcium carbonate medication to bind to phosphate and prevent its absorption, vit d supplements, calcimimetic cinacalet to reduce parathyroid hormone release, parathyroidectomy

234

Treatment of tertiary hyperparathyroidism?

parathyroidectomy, put a small amount of one of the glands into forearms, so the body has some calcium control but it is then easier to get to if further surgery is needed

235

Complications of parathyroidectomy?

hypocalcaemia, hypoparathyroidism, never damage in neck, bleeding infecton, persistant hyperparathyroidism

236

Prognosis of hyperparathyroidism?

primary is good, but secondary and tertiary are worse as they are associated with CKD

237

How common is hypercalcaemia?

uncommon, 30/100,000, but is the most frequently encountered endocrine/electrolyte disorder in malignancy associated hospital patients

238

Presentation of hypercalcaemia?

3.5mmol/L - abdominal pain, vomiting, dehydration, lethargy, cardiac arrhythmias, shortened QT, coma, pancreatitis

239

Causes of hypercalcaemia?

hyperparathyroidism, malignancy of squamous cell lung, breast, renal cell, sarcoidosis, TB, thyrotoxicosis, phaeochromocytoma, primary adrenal insufficiency, thiazide diuretics, vit d and vit supplements, familial hypocalciuric hypercalcaemia, prolonged immbolisation, calcium alkali syndrome, AIDS

240

Investigations of hypercalcaemia?

x rays show bone abnormalities like demineralisation, bone cysts, pathological fractures, bony metastases, US/CT, 24 urine calcium, protein electrophoresis for myeloma, TSH to exclude hyperthyroidism

serum phosphate, serum alk pho, urine calcium, urine phophate and PTH depend on cause

241

What is the cause of hypercalcaemia if urine calcium, phosphate, PTH and serum alk phos are high but serum phosphate low?

hyperparathyroidism

242

What is the cause of hypercalcaemia if urine phosphate is high, serum phosphate low and alk phos, calcium and pTH are variable?

malignancy

243

What is the causes of hypercalcaemia if serum phosphate, urine phosphate and urine calcium are high but PTH and alk phos low?

vitmain D excess

244

Management of hypercalcaemia?

increase circulating volume with saline to increase urine output of calcium, loop diuretics for fluid overload, rehydrate, bisphosphonates e.g. oamidronate, salmon calcitonin, UV gallium if malignant cause, cinacalcet HCl reduces parathyroid levels, block RANK-L to prevent calcium release from bones,dialysis

245

What does a raised calcitonin level in hypercalcaemia suggest?

B cell lymphoma

246

What does a raised alk phos with hypercalcaemia suggest?

bony metastases, sarcoidosis, thyrotoxicosis

247

What is hypoparathyroidism?

characterised as hypocalcaemia, hyperphosphateaemia, low or inappropriately normal PTH

248

What 3 things are involved in calcium regulation?

calcitrol, PTH, 1,25-dihydroxyvitamin D3

249

What causes calcium absorption?

1,25 dihydroxyvitamin D3

250

What stimulated calcium release from bone?

1,25-dihydroxyvitamin D3 and PTH

251

What is transient hypoparathyroidism in the neonatal period?

when neonates reduce calcium levels in first 24-48 hours of age, but can develop hypocalcaemia at 72 hours

252

What causes hypocalcaemia in neonates?

mothers with diabetes, delay in PTH surge, maternal hyperparathyroidism, premature birth

253

Causes of hypoparathyroidism?

Di George's syndrome, defects in PTH gene, defects in calcium sensing receptor gene, pseudohypoparathyroidism, autoimmune polyglandular syndrome type 1 or 2, isolated hypoparathyroidism, HDR, HRD, neck surgery, radiotherapy, magnesium deficiency/excess

254

Presentation of hypoparathyroidism?

muscle pains, bone pain, abdominal pain, paraesthesiae of face fingers and toes, facial twitching, carpopedal spasm, convulsions, syncope, emotional lability, anxiety, depression, memory impairment, lethargy, headahces, brittle nails, dry gair and skin, painful menstruation, Chvostek's sign, Trousseaus sign, raised ICP, papilloedema, cataracts, dental abnormalities, enamel dysplasia, hyperreflexia

255

Typical blood result in hypoparathyroidism?

low serum calcium, high serum phosphate, low PTH, normal alkaline phosphatase

256

Typical blood results in pseudohypoparathyroidism?

low serum calcium and normal or high PTH

257

What is pseudohypoparathyroidism?

defects in PTH action - can be hypo or normocalcaemia and associated with somatic anomalies, short staurs, round face, short neck, shorteing of metacarpals and metatarsals

258

Treatment of hypoparathyroidism?

IV calcium, rich calcium diet with vit D and calcitrol, wear bracelet, recombinant PTH or post menopausal osteoporosis and prevent hypercalcuria, monitoring, parathyroid autotransplantation and allotransplantation

259

Complications of hypoparathyroidism?

laryngospasm, stridor, airway obsturction, neuromuscular irritability, muscle cramps, tetany, seizures, arrhythmias, death, calcium deposition in kidneys, stunted growth, malformed teeth, mental impairement, dental problems, hypercalcaemia, renal impairment, cataracts

260

How common is hypocalcaemia?

very common, in up to 88% of ICU patients

261

Symptoms of hypocalcaemia?

SPASMODIC
spasms (Trousseau's sign), paraesthesia, anxious, seizures, muscle cramps, orientation impaired, dermatitis, impetigo herptiformis, tetany, Chvostek's sign

prolonged QT, laryngospasm, bronchospasm, subcapsular cataract, papilloedema, abnomral teeth, ectopic calcification

262

What is Trousseau's sign?

occlude arterial circulation of the forearm using a blood pressure cuff inflated to the systolic blood pressure for 3 minutes

capopedal spasm involving flexion at the wrist, metacarpophalangeal joint, extension of the interphalangeal joints, adduction of the thumbs and fingers

263

Causes of hypocalcaemia?

CKD, pseudohypoparathyroidism, acute rhabdomyolysis, vit D deficiency, hypomagnesaemia, osteomalacia, acute pancreatitis, over hydration, respiratory alkalosis, hyperventilation, calcium chelators, bone resorption inhibitors, tumour lysis, osteoblstic metastases, toxic shock syndrome

264

DD of hypocalcaemia?

CKD, hypoparathyroidism, pseydohypoparathyroidism, vit D deficiency

265

Management of hypocalcaemia?

correct magnesium level, oral calcitrol

mild - calcium 5mmol/6h and daily plasma calcium levels, vit d and calcium supplements if persistent
severe - 10ml calcium gluconate with IV
CKD - alfacalcidol to maintain serum calcium

266

What is Chvostek's sign?

detects latent tetany, tap 5th facial nerve in front of ear with patients mouth slightly open to cause contraction of facial muscles

267

Prevention of hypocalcaemia?

ensure adequate dietary intake, avoid total parenteral nutrition, ensure magnesium and calcium levels check twice a week (more if ill), 1,25-dihydroxyvitmainD and calcium before parathyroidectomy

268

What is classed as mild and severe hypocalcaemia?

mild = 2-2.12mmol/L
severe =

269

Investigations in hypoparathyroidism?

ECG - prolonged QT interval
renal US to look for renal calculi
imaging - shortened metacarpals
brain MRI - basal ganglia calcification
24 hour urinary calcium is low
TSH and ACTH levels
25-hydroxyvitamine D3 and 1,25-dihydroxyvitamin D3 to look for vitamin D deficiency

270

What is DiGeorge's syndrome?

abnormal parathyroid gland development from third and fourth pouches