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Phase 2a > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What is an endocrine hormone?

A

blood borne and acts at distant sites

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2
Q

What is a paracrine hormone?

A

acting on adjacent cells

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3
Q

What is an autocrine hormone?

A

feedback on the same cell that secreted the hormone

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4
Q

What is an endocrine gland?

A

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

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5
Q

What is an exocrine gland?

A

secretes through a duct (pancreas amylase and lipase)

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6
Q

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

A

fat soluble

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7
Q

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

A

fat - protein bound

water - unbound

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8
Q

Where do peptides store hormones?

A

in secretary granules

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9
Q

What are the different classes of hormones?

A

peptides, amines, idothyronines, cholesterol derivatives and steroids

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10
Q

Synthesis of T3 and T4?

A

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

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11
Q

How do adrenocortical and gonadal steroids work?

A

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

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12
Q

How is hormone secretion controlled?

A

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

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13
Q

What is synergism?

A

combined effects of two hormones amplified

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14
Q

What is permissiveness?

A

a hormone needed for another’s full potential effect

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15
Q

Function of the thyroid hormone?

A

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

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16
Q

Function of growth hormone?

A

stimulates production of IGF-1 to induce metabolic changes

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

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17
Q

What hormone stimulates GH?

A

GHRH (grehlin increased GH secretion)

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18
Q

What hormone inhibits GH?

A

somatostatin

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19
Q

What is acromegaly?

A

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

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20
Q

What is giantism?

A

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

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21
Q

What causes acromegaly?

A

benign pituitary GH producing adenoma or GHRH producing bronchial carcinoid

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22
Q

Symptoms of acromegaly?

A

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

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23
Q

Investigations for acromegaly?

A

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

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24
Q

What is the diagnostic test for acromegaly?

A

glucose tolerance test

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

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25
Q

What is IGFBP-3?

A

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

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26
Q

Management of acromegaly?

A

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

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27
Q

How does pegvisomant treat acromegaly?

A

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

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28
Q

How does somatostatin analogues treat acromegaly?

A

inhibit GH secretion

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29
Q

side effect of long term dopamine agonists for acromegaly?

A

cardiac fibrosis - need regualr ECHO

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30
Q

Why is stereotactic radiotherapy better than radiotherapy in acromegaly?

A

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

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31
Q

Complications of acromegaly?

A

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

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32
Q

Prognosis of acromegaly?

A

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

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33
Q

What are carcinoid tumours?

A

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

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34
Q

Where do carcinoid tumours usually occur?

A

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

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35
Q

What condition is carcinoid tumours related to?

A

carcinoid syndrome

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36
Q

Symptoms of carcinoid tumours?

A

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

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37
Q

What is carcinoid syndrome?

A

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

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38
Q

Presentation of carcinoid syndrome?

A

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

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39
Q

What is the common size of a carcinoid syndrome?

A

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

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40
Q

Investigations of carcinoid syndrome?

A

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

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41
Q

Complications of carcinoid tumours?

A

MEN1, appendicitus, intussception, bowel obstruction, metastatic spread

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42
Q

Management of carcinoid tumour and syndrome?

A

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

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43
Q

What is carcinoid crisis?

A

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

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44
Q

Treatment for carcinoid crisis?

A

octrotidem supportive measure, fluid balance managment

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45
Q

Prognosis of carcinoid crisis?

A

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

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46
Q

What is hypothyroidism?

A

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

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47
Q

Symptoms of hypothyroidism?

A

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

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48
Q

What are the complications of hypothyroidism in pregnancy?

A

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

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49
Q

How common is hypothyroidism?

A

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

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50
Q

Causes of hypothyroidism?

A

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)

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51
Q

Risk factors for autoimmune hypothyroidism?

A

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

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52
Q

Diagnosis of hypothyroidism?`

A

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

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53
Q

What is subclinical hypothyroidism?

A

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

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54
Q

Treatment of hypothyroidism?

A

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

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55
Q

Complications of levothryoxine?

A

angina pain worsens, hyperthyroidism

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56
Q

How dose levothyroxine treat hypothyroidism?

A

replaces thyroxine production and normalises serum TSH concentrations

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57
Q

What is myxoedema coma?

A

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

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58
Q

Treatment of myxoedema coma?

A

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

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59
Q

What is borderline hypothyroidism?

A

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

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60
Q

What is Hashimoto’s disease?

A

autoimmune hypothyroidism with a goitre

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61
Q

Examples of thyroid diet foods?

A

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

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62
Q

Cause of Hashimoto’s disease?

A

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

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63
Q

In who is Hashimoto’s disease most common?

A

women aged 60-70

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64
Q

Symptoms of Hashimoto’s disease?

A

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

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65
Q

Investigations of Hashimoto’s disease?

A

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

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66
Q

Whats the difference between a hot and cold thyroid nodule?

A

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

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67
Q

Treatment of Hashimoto’s disease?

A

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

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68
Q

Complications of Hashimoto’s disease?

A

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

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69
Q

Prognosis of Hashimoto’s disease?

A

good and most achieve normal thyroid levels

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70
Q

What is hyperthyroidism?

A

raised thyroid level from overactive thyroid gland

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71
Q

Causes of hyperthyroidism?

A

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

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72
Q

What is De Quervains thyroiditis?

A

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

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73
Q

Symptoms of hyperthyroidism?

A

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

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74
Q

Complications of hyperthyroidism?

A

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

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75
Q

How common is hyperthyroidism?

A

10x more common in women, 20-40years

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76
Q

What does hyperthyroidism show in investigations?

A

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

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77
Q

Treatment of hyperthyroidism?

A

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

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78
Q

Side effect of carbimazole?

A

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

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79
Q

Precautions during radioactive iodine treatment?

A

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

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80
Q

Symptoms of ophthalmic Grave’s disease?

A

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

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81
Q

What is exophthalmos and opthalmoplegia?

A

retro orbital inflammation, causing eye popping, worse in smokers

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82
Q

Treatment of ophthalmic Grave’s disease?

A

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

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83
Q

Triggers of ophthalmic Grave’s disease?

A

stress, infection, childbirth, hyperthyroid

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84
Q

Pathophysiology of ophthalmic Grave’s disease?

A

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

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85
Q

How common is thyroid cancer?

A

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

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86
Q

Symptoms of thyroid cancer?

A

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

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87
Q

What are different types of thyroid cancer?

A

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

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88
Q

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

A

papillary - women aged 35-40

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89
Q

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

A

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

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90
Q

What causes follicular thyroid cancer?

A

areas of low iodine

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91
Q

In who is follicular thyroid cancer most common?

A

women 30-30years

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92
Q

Where does medullary thyroid cancer arise from?

A

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

mainly autosomal dominant inherited

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93
Q

Who gets thyroid lymphomas?

A

women aged 50 with Hashimoto’s

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94
Q

Symptoms of thyroid lymphoma?

A

dyspnoea, dysphagia, non Hodgkin’s,

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95
Q

Treatment of hurthle cell carcinoma?

A

surgery, postoperative radioative iodine 131, levotyroxine, external radiotherapy

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96
Q

What kind of thyroid cancers are more aggressive ?

A

medullar and anaplastic

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97
Q

Where do anaplastic thyroid cancers arise from?

A

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

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98
Q

Risk factors of thyroid cancer?

A

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

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99
Q

TNM staging?

A

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

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100
Q

Presentation of thyroid cancer?

A

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

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101
Q

Investigations of thyroid cancer?

A

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

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102
Q

Treatment of thyroid cancer?

A

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

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103
Q

Complications of thyroid cancer?

A

laryngeal nerve palsy, hypoparathyroidism, nerve damage

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104
Q

What is Cushing’s syndrome?

A

increased glucocorticoid in the body

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105
Q

How common is Cushing’s syndrome?

A

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

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106
Q

Functions of cortisol?

A

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

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107
Q

Causes of Cushing’s syndrome?

A

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

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108
Q

Cushing’s syndrome symptoms?

A

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

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109
Q

Investigations for Cushing’s syndrome?

A

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
Q

Treatment of Cushing’s syndrome?

A

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
Q

What is Conn’s syndrome?

A

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
Q

What is the most common cause of secondary hypertenision?

A

primary hyperaldosterone

113
Q

What is primary hyperaldosterone?

A

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

114
Q

What are the 2 forms of familial hyperaldosterone?

A

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
Q

What can type 1 familial hyperaldosteronism lead to?

A

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

116
Q

Symptoms of hyperaldosteronism?

A

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

117
Q

What can Conn’s syndrome lead to?

A

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

118
Q

What will investigations show in hyperaldosteronism?

A

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
Q

When should tests for hyperaldosteronism be done?

A

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
Q

How should aldosterone and renin levels be measured?

A

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

121
Q

How is the salt loading done for hyperaldosteronism diagnosis?

A

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
Q

DD for hyperaldosteronism?

A

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
Q

Treatment of Conn’s?

A

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
Q

Treatment of BAH?

A

aldosterone antangonists e.g. amiloride, spironolactone, eplerenone

125
Q

Treatment of GRA?

A

steroids to reduce aldosterone productioon drive, dexamethasone

spironolactone if hypertension persists after

126
Q

Treatment of adreanl carcinoma?

A

surgery with post operative adrenolytic therapy with mitotane

127
Q

What is secondary hyperaldosteronism?

A

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

128
Q

Causes of secondary hyperaldosteronism?

A

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

129
Q

Complications of secondary hyperaldosteronism?

A

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

130
Q

Treatment of secondary hyperaldosteronism?

A

lifelong antihypertensive therapy, aldosterone antagonists

131
Q

side effects of spironolactone?

A

gynaecomastia, menstural problems and erectile dysfunction

132
Q

Which aldosterone antagonists is best to prevent hypokalaemia?

A

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

133
Q

Which aldosterone antagonist is selctive?

A

eplerenone

134
Q

What is Addison’s disease?

A

lack of steroid hormone rlease form the adrenal glands

135
Q

How common is Addison’s disease?

A

8000 people in the UK, age 30-50 normally

136
Q

What makes steroid hormones?

A

adrenal cortex

137
Q

What controls steroid release?

A

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

138
Q

What makes adrenaline and noradrenaline?

A

adrenal medulla

139
Q

Causes of adrenal insufficiency?

A

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

140
Q

Symptoms of Addison’s disease?

A

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
Q

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

A

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

142
Q

When would Addison’s crisis occur?

A

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

143
Q

Tests for Addison’s disease?

A

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
Q

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

A

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

145
Q

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

A

primary adrenal insufficiency

146
Q

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

A

secondary or tertiary adrenal insufficiency

147
Q

Treatment of Addison’s disease?

A

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
Q

Treatment of Addison’s crisis?

A

hydrocortisone injections and fluids to increase BP, may need ICU

149
Q

When are cortisol level highest?

A

in the morning

150
Q

Complications of Addison’s disease?

A

other autoimmune disease, adrenal crisis, osteoporosis

151
Q

What is secondary adrenal insufficiency?

A

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

152
Q

What is critical illness related corticosteroid insufficiency (CIRCI)?

A

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

153
Q

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

A

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

154
Q

How is secondary adrenal insufficiency diagnosed?

A

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
Q

Management of secondary adrenal insufficiency?

A

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

156
Q

Prognosis of adrenal insufficiency?

A

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

157
Q

What diabetes insipidus?

A

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
Q

Where is ADH made?

A

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

159
Q

What is gestational diabetes insipidus?

A

results from degradation of ADH by a placental vasopressinase

160
Q

What is dipsogenic diabetes insipidus?

A

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

161
Q

What are the two types of diabetes insipidus?

A

cranial - decreased ADH secretion

nephrogenic - resistance to ADH in kidney

162
Q

Causes of cranial diabetes insipidus?

A

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
Q

Causes of nephrogenic diabetes insipidus?

A

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
Q

Symptoms of diabetes insipidus?

A

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
Q

DD of diabetes insipidus?

A

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

166
Q

Investigations in diabetes insipidus?

A

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
Q

What is the water deprivation test for diabetes insipidus?

A

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
Q

Management of cranial diabetes insipidus?

A

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
Q

Management of nephrogenic diabetes insipidus?

A

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
Q

Complications of nephrogenic diabetes insipidus treatment?

A

desmopressin can worsen MI

171
Q

prognosis of diabetes insipidus?

A

rare death form dehydration, hypernatraemia, fever, CV etc

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

good prognosis

172
Q

What is hyponatraemia?

A

excess of water in relation to serum sodium which is

173
Q

What is SIADH?

A

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

174
Q

Who is most at risk of hyponatraemia?

A

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
Q

Presentation of hyponatraemia?

A

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
Q

Diagnostic features of SIADH?

A

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
Q

Causes of SIADH?

A

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
Q

What will investigations show in SIADH?

A

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
Q

Management of SIADH?

A

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
Q

Complications of vaptans?

A

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

181
Q

Complications of hyponatraemia?

A

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
Q

Symptoms of pontine myelinolysis?

A

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

183
Q

What is hypokalaemia?

A

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

184
Q

What are the classifications of hypokalaemia causes?

A

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

185
Q

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

A

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
Q

Causes of hypokalaemia from transcellular shift

A

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

187
Q

Causes of hypokalaemia from decreased intake?

A

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

188
Q

Presentation of hypokalaemia?

A

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
Q

What is the most common cause of hypokalaemia?

A

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
Q

Investigations in hypokalaemia?

A

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
Q

What do ECGs show in hypokalaemia?

A

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
Q

Treatment of hypokalaemia?

A

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
Q

Complications of hypokalaemia?

A

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
Q

Prevention of hypokalaemia?

A

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

195
Q

What is hyperkalaemia?

A 
mild = 5.5-5.9mmol/L
moderate = 6-6.6mmol/L
severe = >6.5mmol/L
196
Q

How much of potassium is intracellular?

A

98%

197
Q

Who is most at risk of hyperkalaemia?

A

young and elderly, hopsital, men

198
Q

What is artefactual hyperkalaemia and what causes it?

A

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
Q

What classifications of hyperkalaemia are there?

A

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

200
Q

What are renal causes of hyperkalaemia?

A

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

201
Q

What can cause an increase of potassium in the circulation?

A

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

202
Q

What causes a shift of potassium from intracellular to extracelullar?

A

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

203
Q

What can give unexpectedly high results of potassium?

A

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
Q

Why can diabetic patients get hyperkalaemia?

A

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
Q

Symptoms of hyperkalaemia?

A

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
Q

What will and ECG show in hyperkalaemia?

A

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

207
Q

What will blood show in hyperkalaemia?

A

normocytic normochromic anaemia, thrombocytosis, leukocytosis

208
Q

Management of hyperkalaemia?

A

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
Q

Treatment of resistant hyperkalaemia?

A

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

210
Q

Prognosis of hyperkalaemia?

A

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

211
Q

Prevention of hyperkalaemia?

A

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

212
Q

What is crush syndrome?

A

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
Q

Cause of crush syndrome?

A

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
Q

Pathophysiology of crush syndrome?

A

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
Q

How is crush syndrome characterised?

A

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

216
Q

Complications of crush syndrome?

A

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
Q

Symptoms of crush syndrome?

A

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
Q

Initial management of crush syndrome?

A

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
Q

What is rhabdomyolysis?

A

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

220
Q

Investigations for crush syndrome?

A

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
Q

Further management in crush syndrome?

A

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
Q

Prevention of crush syndrome?

A

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

223
Q

What is hyperparathyroidism?

A

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

224
Q

Effects of parathyroid hormone?

A

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

225
Q

Effects of calcium?

A

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
Q

What is primary hyperparathyroidism and the causes?

A

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
Q

What is secondary hyperparathyroidism and the causes?

A

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
Q

What is tertiary hyperparathyroidism and the causes?

A

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
Q

Symptoms of primary and tertiary hyperparathyroidism?

A

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
Q

Complications of hyperparathyroidism?

A

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

231
Q

hyperparathyroidism investigations?

A

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
Q

Treatment of primary hyperparathyroidism?

A

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
Q

Treatment of secondary hyperparathyroidism?

A

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
Q

Treatment of tertiary hyperparathyroidism?

A

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
Q

Complications of parathyroidectomy?

A

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

236
Q

Prognosis of hyperparathyroidism?

A

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

237
Q

How common is hypercalcaemia?

A

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

238
Q

Presentation of hypercalcaemia?

A

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

239
Q

Causes of hypercalcaemia?

A

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
Q

Investigations of hypercalcaemia?

A

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
Q

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

A

hyperparathyroidism

242
Q

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

A

malignancy

243
Q

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

A

vitmain D excess

244
Q

Management of hypercalcaemia?

A

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
Q

What does a raised calcitonin level in hypercalcaemia suggest?

A

B cell lymphoma

246
Q

What does a raised alk phos with hypercalcaemia suggest?

A

bony metastases, sarcoidosis, thyrotoxicosis

247
Q

What is hypoparathyroidism?

A

characterised as hypocalcaemia, hyperphosphateaemia, low or inappropriately normal PTH

248
Q

What 3 things are involved in calcium regulation?

A

calcitrol, PTH, 1,25-dihydroxyvitamin D3

249
Q

What causes calcium absorption?

A

1,25 dihydroxyvitamin D3

250
Q

What stimulated calcium release from bone?

A

1,25-dihydroxyvitamin D3 and PTH

251
Q

What is transient hypoparathyroidism in the neonatal period?

A

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

252
Q

What causes hypocalcaemia in neonates?

A

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

253
Q

Causes of hypoparathyroidism?

A

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
Q

Presentation of hypoparathyroidism?

A

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
Q

Typical blood result in hypoparathyroidism?

A

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

256
Q

Typical blood results in pseudohypoparathyroidism?

A

low serum calcium and normal or high PTH

257
Q

What is pseudohypoparathyroidism?

A

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
Q

Treatment of hypoparathyroidism?

A

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
Q

Complications of hypoparathyroidism?

A

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
Q

How common is hypocalcaemia?

A

very common, in up to 88% of ICU patients

261
Q

Symptoms of hypocalcaemia?

A

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
Q

What is Trousseau’s sign?

A

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
Q

Causes of hypocalcaemia?

A

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
Q

DD of hypocalcaemia?

A

CKD, hypoparathyroidism, pseydohypoparathyroidism, vit D deficiency

265
Q

Management of hypocalcaemia?

A

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
Q

What is Chvostek’s sign?

A

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

267
Q

Prevention of hypocalcaemia?

A

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
Q

What is classed as mild and severe hypocalcaemia?

A

mild = 2-2.12mmol/L

severe =

269
Q

Investigations in hypoparathyroidism?

A 
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
Q

What is DiGeorge’s syndrome?

A

abnormal parathyroid gland development from third and fourth pouches

Phase 2a (15 decks)

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