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Phase 2A > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What is the aetiology of T1DM?

A

Insulin deficiency from B cell destruction of insulin secreting pancreatic beta cells, associated with HLA DR3

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2
Q

What is the pathophysiology involved in T1DM?

A

There is inadequate insulin secretion relative to the needs of the body leading to hyperglycaemia and deranged metabolism

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3
Q

What are the symptoms of T1DM?

A

Polyuria, weight loss, fatigue, thirst, visual blurring, genital thrush, lethargy

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4
Q

What are the signs of T1DM?

A

Ketonuria, recurrent infections, drowsiness, coma, normal body weight

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5
Q

What tests are used to diagnose T1DM?

A

Abnormal plasma glucose (random >/= 11.1 mmol/L or fasting >/= 7 mmol/L) in the presence of symptoms
In asymptomatic people with an abnormal random glucose 2x fasting plasma glucose (ranges still the same)
Oral glucose tolerance test

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6
Q

What is the treatment for T1DM?

A

Diabetes education and lifestyle advice

Insulin

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7
Q

What are the possible complications of T1DM?

A

Vascular disease, neuropathy, retinopathy, cataracts, glaucoma, ketoacidosis, foot ulcers, nephropathy

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8
Q

What is the aetiology of T2DM?

A

There is impaired insulin secretion and insulin resistance

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9
Q

What are the risk factors for T2DM?

A

Obesity, lack of exercise, calorie and alcohol excess, PCOS

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10
Q

What is the pathophysiology involved in T2DM?

A

There is diminished effectiveness of endogenous insulin leading to hyperglycaemia and deranged metabolism

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11
Q

What ethnicities have an increased risk of T2DM?

A

Asian, African, Polynesian

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12
Q

What are the symptoms of T2DM?

A

May be asymptomatic or present with complications e.g. MI

Polyuria, thirst, lethargy, boils

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13
Q

What are the signs of T2DM?

A

There are no obvious physical signs - the patient is usually overweight

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14
Q

What tests are used to diagnose T2DM?

A

HbA1c >48 (6.5%)
Fasting glucose >/= 7 mmol/L (>6.5 - impaired glucose tolerance)
Oral GTT @ 2 hours >/= 7.8 mmol/L (>6.1 - impaired glucose tolerance)

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15
Q

What is the treatment for T2DM?

A

Metformin (increases insulin sensitivity and helps weight)
If HbA1c >/= 53 16 weeks later add: sulfonylurea e.g. glicazide
If HbA1c >/= 57 at 6 months, consider: insulin, glitazone or sulfonylurea receptor binders
Education and lifestyle advice e.g. reduce weight, start a statin, control BP

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16
Q

What are the complications of T2DM?

A

Hyperosmolar hyperglycaemic state - severe hyperglycaemia and marked serum hyperosmolarity
Chronic: vascular disease, nephropathy, retinopathy, cataracts, glaucoma, ketoacidosis, foot ulcers, neuropathy

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17
Q

What is the aetiology of DKA?

A

Infection, discontinuation of insulin, inadequate insulin, cardiovascular disease, drugs e.g. steroids, thiazides

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18
Q

What is the pathophysiology involved in DKA?

A

There is uncontrolled hyperglycaemia and a catabolic state leading to ketones being produced as the body requires glucose in cells causing acidosis

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19
Q

What are the symptoms of DKA?

A

Polyuria, polydipsia, vomiting, weakness, lethargy, altered mental state including coma

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20
Q

What are the signs of DKA?

A

Dehydration, tachycardia and weak pulse, hypotension, ketotic breath - “pear drops”, deep breathing - Kussmaul respiration

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21
Q

What tests are used to diagnose DKA?

A

ECG, CXR, MSU - dipstick
Bloods - capillary and plasma glucose, ketones U&Es, HCO3-, amylase, osmolality, FBC, culture, ABG/VBG - ketonaemia (++), hyperglycaemia (>11), venous ph (<7.3) HCO3- (<16)

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22
Q

What is the treatment of DKA?

A

ABCDE
Fluid replacement - 500ml of 0.9% NaCl bolus
Insulin 0.1u/kg/hr of Actrapid IV
When glucose <14 mmol/L start 10% glucose 125ml/H
Monitor U&Es
Find and treat the cause of DKA e.g. infection

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23
Q

What is the aim of DKA treatment?

A

Decrease ketones by 0.5 mmol/L/hour
OR
Rise in venous bicarb of 3 mmol/L/hour

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24
Q

What is the aetiology of hypothyroidism?

A

Primary (low T4): primary atrophic hypothyroidism, Hashimoto’s thyroiditis (anti-TSHR, anti-Tg, anti-TPO antibodies & goitre), iodine deficiency, post-thyroidectomy/radioiodine/antithyroid drugs, drugs e.g. lithium
Secondary (low TSH): hypopituitarism

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25
Q

What is the pathophysiology involved in hypothyroidism?

A

There is insufficient secretion of thyroid hormones and can be due to various abnormalities

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26
Q

What is the epidemiology of hypothyroidism?

A

Women>men

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27
Q

What are the symptoms of hypothyroidism?

A

Tiredness, weight gain, lethargy, low mood, cold intolerance, goitre, constipation, hoarse voice, myalgia, decreased memory/cognition, menorrhagia

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28
Q

What are the signs of hypothyroidism?

A 
BRADYCARDIC! 
Bradycardic
Reflexes relax slowly 
Ataxia (cerebellar)
Dry thin hair/skin
Yawning/drowsy/coma
Cold hands ± low temperature
Ascites
Round puffy face
Defeated demeanour
Immobile ± ileus
CCF
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29
Q

What tests are used to diagnose hypothyroidism?

A

Bloods: FBC (macrocytosis), TFTs (high TSH, low T4), lipids/cholesterol (raised), antibodies (anti-TPO, anti-thyroglobulin

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30
Q

What is the treatment of hypothyroidism?

A

Levothyroxine (T4) - review at 12 weeks, adjust 6 weekly

Give smaller doses to elderly patients as there’s a risk of angina/MI

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31
Q

What is the aetiology of hyperthyroidism?

A

Graves’ disease (IgG bind to and stimulate the TSH receptors
Toxic mulitnodular goitre, toxic adenoma, ectopic thyroid tissue, exogenous (iodine excess), DeQuervain’s thyroiditis (post-viral)

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32
Q

What is the pathophysiology of hyperthyroidism?

A

Excess thyroid hormone is usually due to gland hyperfunction leading to thyrotoxicosis

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33
Q

What is the epidemiology of hyperthyroidism?

A

Female>male

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34
Q

What are the symptoms of hyperthyroidism?

A

Palpitations, diarrhoea, heat intolerance, low weight, increased appetite, oligomennorrhoea ± infertility

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35
Q

What are the signs of hyperthyroidism?

A

Palmar erythema, warm moist skin, fine tremor, tachycardia, SBT, AF, thin hair, lid lag/retraction, goitre, nodules, bruit

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36
Q

What tests are used to diagnose hyperthyroidism?

A

Bloods: FBC (normocytic anaemia), TFTs (low TSH, high T3, T4) LFTs (increased), ESR (increased), Calcium (increased), thyroid autoantibodies, visual fields, acuity and eye movements

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37
Q

What is the treatment for hyperthyroidism?

A

Drugs: beta-blockers or carbimazole

Radioiodine or thyroidectomy

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38
Q

What is thyroid eye disease?

A

Retro-orbital inflammation and lymphocyte infiltration results in swelling of the orbit

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39
Q

What is the management for thyroid eye disease?

A

Conservative e.g. stop smoking, sunglasses
IV methylprednisolone
Surgical decompression or eyelid surgery

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40
Q

What are some risk factors for thyroid cancer?

A

Exposure to ionising radiation, history of goitre, thyroid nodules or thyroiditis, female gender, genetics

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41
Q

What are the different types of thyroid cancer?

A 
Papillary (60%)
Follicular (<25%)
Medullary (5%)
Lymphoma (5%)
Anaplastic
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42
Q

What are the symptoms of thyroid cancer?

A

Thyroid nodule usually non-tender

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43
Q

What are the signs of thyroid cancer?

A

Thyroid nodule - hard and fixed nodules are more suggestive of malignancy, usually non-tender to palpation
Firm cervical masses - ?regional lymph node mets
Vocal cord paralysis - involvement of the recurrent laryngeal nerve

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44
Q

What tests are used to diagnose thyroid cancer?

A

TFTs - normal in most patients
USS, fine needle aspiration cytology, radionuclide imaging
CT/MRI scans

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45
Q

What is the treatment for thyroid cancer?

A

Surgery: total or subtotal thyroidectomy
Radiotherapy or radioiodine ablation therapy
Chemotherapy: sorafenib (multi kinase inhibitor)

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46
Q

What is the aetiology of Cushing’s syndrome?

A

Pituitary adenoma (then called Cushing’s disease), exogenous glucocorticoids, adrenal adenoma, adrenal carcinoma, ectopic ACTH production (e.g. small cell lung cancer

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47
Q

What is the pathophysiology of Cushing’s syndrome?

A

There is chronic glucocorticoid excess, loss of the normal feedback mechanisms and loss of circadian rhythm of cortisol secretion

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48
Q

What is the epidemiology of Cushing’s syndrome?

A

Higher incidence in patients with DM, HTN, obesity

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49
Q

What are the symptoms of Cushing’s syndrome?

A

Increased weight, depression, lethargy, irritability, psychosis, acne, proximal weakness, gonadal dysfunction (irregular menses, ED, hirsutism)

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50
Q

What are the signs of Cushing’s syndrome?

A

Central obesity, buffalo neck hump, moon face, purple striae on the abdomen, supraclavicular fat distribution, skin and muscle atrophy, bruises, osteoporosis, hypertension, hyperglycaemia, infection - prone/poor healing

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51
Q

What tests are used to diagnose Cushing’s syndrome?

A

Bloods (increased plasma cortisol)
Overnight dexamethasone suppression test (no suppression in Cushing’s)
48 hour dexamethasone suppression test (no suppression in Cushing’s)
Circadian rhythm plasma cortisol levels
Imaging - adrenal CT or MRI, pituitary MRI

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52
Q

What is the treatment for Cushing’s syndrome?

A

Iatrogenic - stop steroids
Cushing’s disease - trans-sphenoidal surgery or bilateral adrenalectomy (causes Nelson’s syndrome)
Adrenal adenoma - adrenalectomy
Adrenal carcinoma - adrenalectomy, radiotherapy and adrenolytics (mitotane)
Ectopic ACTH - surgery if localised

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53
Q

What is the aetiology of Addison’s disease?

A

Autoimmunity, TB, surgical removal of the adrenal glands, haemorrhage or infarction, infiltration, Schilder’s disease

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54
Q

What is the pathophysiology involved in Addison’s disease?

A

There is destruction of the entire adrenal cortex so the production of glucocorticoid, mineralocorticoid and sex steroids are all reduced

55
Q

What is the epidemiology of Addison’s disease?

A

Female > male

56
Q

What are the symptoms of Addison’s disease?

A

Weight loss, anorexia, malaise, weakness, fever, depression, nausea and vomiting, abdo pain, constipation/diarrhoea, dizzy, faints

57
Q

What are the signs of Addison’s disease?

A

Pigmented palmar creases and buccal mucosa, vitiligo, postural hypotension, shock (low BP, high HR, coma)

58
Q

What tests are used to diagnose Addison’s disease?

A

Bloods: FBC (anaemia, eosinophilia), U&Es (low Na, high K, high Ca, high urea), low BM
Short ACTH stimulation test - Addison’s excluded if 30 min cortisol >550 nmol/l
9am ACTH levels - inappropriately high in Addison’s
21-hydroxylase adrenal autoantibodies

59
Q

What is the treatment for Addison’s disease?

A

Replace steroids with hydrocortisone daily
Replace mineralocorticoids with fludrocortisone
IV fluids if dehydrates

60
Q

What is secondary adrenal insufficiency?

A

A lack of ACTH and therefore cortisol.

The most common cause is iatrogenic - long term steroid therapy suppresses the HPA axis

61
Q

What is the aetiology of Conn’s syndrome?

A

A solitary aldosterone-producing adenoma

62
Q

What is the pathophysiology involved in Conn’s syndrome?

A

Excess production of aldosterone, independent of RAAS causes increased sodium and water retention and decreased renin release

63
Q

What are the symptoms of Conn’s syndrome?

A

Weakness, cramps, paraesthesiae, polyuria, polydipsia - can be asymptomatic

64
Q

What are the signs of Conn’s syndrome?

A

Hypertension

65
Q

What tests are used to diagnose Conn’s syndrome?

A

Bloods: FBC, U&Es (hypokalaemia, hypernatraemia), renin and aldosterone levels (high aldosterone, low renin
ECG - arrhythmias from electrolyte imbalance
Imaging - CT or MRI to locate adenoma

66
Q

What is the treatment for Conn’s syndrome?

A

Laparoscopic adrenalectomy

Spironolactone for 4 weeks pre-op to control BP and K+

67
Q

What is the aetiology of acromegaly?

A

Excess growth hormone from a pituitary tumour or an ectopic GHRH carcinoid tumour

68
Q

What is the pathophysiology involved in acromegaly?

A

Growth hormone stimulates bone and soft tissue growth through increased secretion of insulin-like growth factor 1

69
Q

What are the symptoms of acromegaly?

A

Acroparaesthesiae, amenorrhoea, decreased libido, headache, increased sweating, snoring

70
Q

What are the signs of acromegaly?

A

Increased growth of hands, feet and jaw, coarsening face, wide nose, macroglossia, obstructive sleep apnoea, big supraorbital ridges

71
Q

What tests are used to diagnose acromegaly?

A

Bloods: IGF1 and OGTT (normally GH secretion is suppressed by glucose), increased BP, increased calcium, phosphate
MRI of the pituitary fossa
Visual fields and acuity

72
Q

What is the treatment of acromegaly?

A

Trans-sphenoidal surgery to remove the tumour, somatostatin analogue

73
Q

What is the aetiology of diabetes insipidus?

A

Cranial - decreased secretion of ADH

Nephrogenic - renal tubules are insensitive to vasopressin

74
Q

What is the pathophysiology involved in diabetes insipidus?

A

ADH is synthesised in the hypothalamus and then transported to the posterior pituitary. It’s release is governed by plasma osmolarity. Failure causes the inability to concentrate urine in the distal renal tubules leading to the passage of copious amounts of dilute urine (>3L/24 hours)

75
Q

What are the symptoms of diabetes insipidus?

A

Polyuria, polydipsia, dehydration, nocturia, symptoms of hypernatraemia - weakness, irritability, confusion, fits and coma

76
Q

What are the signs of diabetes insipidus?

A

Signs of dehydration, palpable bladder (grossly enlarged)

77
Q

What tests are used to diagnose diabetes insipidus?

A

Bloods: U&Es, Ca, glucose (to exclude DM), serum and urine osmolarities
24 hour urine collection to measure volume
Fluid deprivation test with response to desmopressin
MRI of the pituitary and hypothalamus
USS of the kidneys

78
Q

What is the treatment for diabetes insipidus?

A

Cranial - physiological replacement with desmopressin, mild cases can be managed by ingestion of water to quench thirst
Nephrogenic - if daily urine volume <4L/24h and patient isn’t severely dehydrated then definitive treatment isn’t always necessary
Treat with thiazide diuretics (e.g. hydrochlorothiazide) and omiloride
Both - treat underlying cause if detected

79
Q

What is the aetiology of SIADH?

A

CNS: infection, mass/bleed, GBS/MS, paraneoplastic syndrome (SCLC)
Pulmonary: infection, abscess, asthma, CF
Drug side effects: SSRIs, MDMA, morphine, amitriptyline

80
Q

What is the pathophysiology involved in SIADH?

A

Inappropriate secretion of ADH leads to water retention and hyponatraemia

81
Q

What are the symptoms of SIADH?

A

Confusion, nausea, irritability, anorexia, aches and weakness, tremor

82
Q

What are the signs of SIADH?

A

Myoclonus, reflex changes, tremor, ataxia, focal or generalised seizures, raised JVP (hypervolaemia)

83
Q

What tests are used to diagnose SIADH?

A

Fluid status - usually euvolaemic or hypervolaemic
Bloods: U&Es (low Na, <135 mmol/L), plasma osmolality (low), TFTs (hypothyroidism can cause SIADH)
Urine osmolality (high), urine sodium (high)
Imaging - detect causes e.g. SCLC

84
Q

What is the treatment for SIADH?

A

Fluid restriction

Medication: Tolvaptan (V2 vasopressin blocker) or demococycline (potent ADH blocker - causes photosensitivity)

85
Q

What is the aetiology of primary hyperparathyroidism?

A

80% of cases are due to a solitary adenoma

20% of cases are due to hyperplasia of all glands

86
Q

What is the pathophysiology of primary hyperparathyroidism?

A

Excess PTH is produced by one or more of the parathyroid glands causing hypercalcaemia

87
Q

What group of people mostly get primary hyperparathyroidism?

A

Post menopausal women

88
Q

What are the symptoms of primary hyperparathyroidism?

A

Bone pain, pathological fractures (due to osteoporosis), renal colic, muscle weakness, fatigue, anorexia, nausea and vomiting, constipation

89
Q

What are the signs of primary hyperparathyroidism?

A

Renal calculi, haematuria, hypertension, confusion, dementia, inability to concentrate, memory problems

90
Q

What tests are used to diagnose primary hyperparathyroidism?

A

Bloods: U&Es, calcium (high), phosphate (low), PTH (high), vitamin D levels
24 hour urinary calcium excretion (high)
Imaging: abdo XR for calculi, USS of the parathyroid gland, CT, MRI or radioisotope scanning

91
Q

What is the treatment for primary hyperparathyroidism?

A

If mild: advise patient to increase their fluid intake, avoid thiazides, high Ca or vitamin D
Surgery to remove adenoma if symptomatic or asymptomatic with grossly abnormal test results

92
Q

What is the aetiology of secondary hyperparathyroidism?

A

CKD, vitamin D deficiency, GI diseases e.g. Crohn’s or a gastric bypass

93
Q

What is the pathophysiology involved in secondary hyperparathyroidism?

A

PTH is high in an attempt to correct a persistently low Ca level

94
Q

What are the symptoms of secondary hyperparathyroidism?

A

Usually asymptomatic in the early stages

Symptoms are predominantly bony - osteomalacia, bone pain

95
Q

What are the signs of secondary hyperparathyroidism?

A

Signs of renal disease e.g. hypertension

96
Q

What tests are used to diagnose secondary hyperparathyroidism?

A

Bloods: normal-low calcium, high PTH, phosphate levels depend on aetiology (low in vit D deficiency, high in CKD)
Radiology can show evidence of bone disease

97
Q

What is the treatment for secondary hyperparathyroidism?

A

Treat the underlying cause e.g. correct vit D deficiency

CKD: Ca2+ supplements, phosphate restriction ± phosphate binders, vit D analogues, calcimimetics e.g. cinacalcet

98
Q

What is the aetiology of tertiary hyperparathyroidism?

A

Prolonged, uncorrected secondary hyperparathyroidism; long standing kidney disease is the most common cause

99
Q

What is the pathophysiology of tertiary hyperparathyroidism?

A

The glands become autonomous, producing excessive PTH even after the hypocalcaemia has been corrected

100
Q

What are the symptoms of tertiary hyperparathyroidism?

A

Tiredness, malaise, dehydration, bone pain, abdo pain

101
Q

What are the signs of tertiary hyperparathyroidism?

A

Renal colic, renal calculi, haematuria, hypertension, confusion, inability to concentrate

102
Q

What tests are used to diagnose tertiary hyperparathyroidism?

A

Bloods: high calcium, high phosphate, high PTH

103
Q

What is the treatment for tertiary hyperparathyroidism?

A

Cinacalcet

Total or subtotal parathyroidectomy

104
Q

What is the aetiology of hypoparathyroidism?

A

Transient in neonates
Congenital: DiGeorge’s syndrome, PTH gene mutations, calcium receptor mutations, autoimmune
Acquired: neck surgery, radiation, drugs, haemochromatosis, Wilson’s disease, Mg deficiency

105
Q

What is the pathophysiology involved in hypoparathyroidism?

A

Reduced PTH secretion can be due to gland failure, low levels of PTH cause Ca to drop and PO4 to rise

106
Q

What are the symptoms of hypoparathyroidism?

A

Muscle pain, bone pain, abdominal pain, paraesthesiae of the face, fingers and toes, facial twitching, syncope, lethargy, headaches, convulsions

107
Q

What are the signs of hypoparathyroidism?

A

Carpopedal spasm, stridor, hyper-reflexia, dry rough skin, brittle nails with transverse grooves, Chvostek’s sign, Trousseau’s sign, dental abnormalities

108
Q

What tests are used to diagnose hypoparathyroidism?

A

Bloods: low Ca, high PO4, low PTH, normal alk phos, Mg (may be low), U&Es (exclude CKD), vitamin D levels
ECG - prolonged QT
Echo
USS of the kidneys

109
Q

What is the treatment for hypoparathyroidism?

A

If severe symptoms - IV calcium
Dietary advice - diet rich in Ca and vitamin D
Medication: calcium and vitamin D supplements (e.g. AdCal D3)

110
Q

What are the complications of hypoparathyroidism?

A

QT interval changes can lead to syncope, arrhythmias and death

111
Q

What is the aetiology of hypocalcaemia?

A

Actual vitamin D deficiency (e.g. malabsorption)
Functional vitamin D deficiency (e.g. liver or renal disease)
Mg deficiency
Hypoparathyroidism

112
Q

What is the pathophysiology of hypocalcaemia?

A

It may be due to deficiencies of calcium homeostasis, secondary to high phosphate or other causes

113
Q

What are the symptoms of hypocalcaemia?

A

Symptoms generally correlate with the magnitude and speed of fall in calcium
Paraesthesiae, tetany, anxious, irritable, muscle cramps

114
Q

What are the signs of hypocalcaemia?

A

Carpopedal spasm, Chvostek’s sign (when the course of CN5 is tapped is produces muscle spasm), Trousseau’s sign (inflate BP cuff >systolic - produces carpopedal spasm), seizures, prolonged QT, laryngospasm, bronchospasm

115
Q

What tests are used to diagnose hypocalcaemia?

A

Bloods: fasted Ca, U&Es, amylase, serum CK, Mg and PO4, PTH, vitamin D levels
ECG

116
Q

What is the treatment for hypocalcaemia?

A

Acute: treat if <1.8 or <2.0 with symptoms - give 10ml of 10% calcium gluconate by slow IV injection (can also give orally)
If hypomagnesaemic - correct
Give vitamin D if likely to be persistent
Persistent: calcium and vitamin D supplementation

117
Q

What is the aetiology of hyperkalaemia?

A

Renal causes e.g. AKI or CKD

Increased circulation of K e.g. tumour lysis syndrome, burns, crush syndrome, trauma, DKA, fresh water drowning

118
Q

What levels of K denote mild, moderate and severe hyperkalaemia?

A

Mild: 5.5-5.9
Moderate: 6.0-6.4
Severe: >6.5 mmol/L MEDICAL EMERGENCY

119
Q

What are the symptoms of hyperkalaemia?

A

Non-specific, include weakness and fatigue, muscular paralysis, shortness of breath, palpitations or chest pain

120
Q

What are the signs of hyperkalaemia?

A

Bradycardia, tachypnoea, muscle weakness, flaccid paralysis, depressed or absent tendon reflexes, fast irregular pulse

121
Q

What tests are used to diagnose hyperkalaemia?

A

An unexpected result should be repeated
Bloods: FBC, U&Es, capillary and plasma glucose, ABG (look for metabolic acidosis) (digoxin levels)
ECG: tall tented T waves, small P waves, widening of QRS

122
Q

What is the treatment for hyperkalaemia?

A

ABCDE
Stop further K accumulation - stop K+ conserving drugs
Protect cardiac membrane - 10ml of 10% calcium gluconate (only if ECG changes)
Shift K into cells - insulin and glucose infusion, salbutamol nebs
Remove K from the body - calcium polystyrene sulfonate resin and regular lactulose
Non-urgent - treat the underlying case, review medications and polystyrene sulfonate resin (binds K in gut)

123
Q

What is the aetiology of hypokalaemia?

A

Diuretics, D&V, pyloric stenosis, rectal villous adenoma, intestinal fistula, Cushing’s syndrome, Conn’s syndrome, alkalosis, renal tubular failure

124
Q

What levels of K denote mild, moderate and severe hypokalaemia?

A

Mild: 3.1-3.5
Moderate: 2.5-3.0
Severe: <2.5

125
Q

What are the symptoms of hypokalaemia?

A

Mild forms tend to be asymptomatic

Severe - muscle weakness, cramps, constipation, paraesthesia, palpitations

126
Q

What are the signs of hypokalaemia?

A

Hypotonia, hyporeflexia, tetany, salt cravings, ileus (due to GI muscle involvement)

127
Q

What tests are used to diagnose hypokalaemia?

A

Bloods: U&Es, HCO3, serum glucose, Cl, Mg
ECG - flat T waves, ST depression, prominent U waves
ABG
Urine potassium, sodium and osmolality

128
Q

What is the treatment for hypokalaemia?

A

If mild: give oral K supplement, review K after 3 days. If taking thiazide diuretic, swap to K sparing diuretic (or repeat test)
If severe: give IV K cautiously. No more than 20 mmol/h and not more concentrated than 40mmol/L. Don’t give if oligouric

129
Q

What is the aetiology of prolactinaemia?

A

Excess production from the pituitary e.g. prolactinoma, disinhibition by compression of the pituitary stalk or use of dopamin antagonists

130
Q

What is the pathophysiology of prolactinaemia?

A

Increased prolactin levels leads to hypogonadism, infertility and osteoporosis by inhibiting the release of GnRH

131
Q

What are the symptoms of prolactinaemia?

A

Women: amenorrhoea or oligomenorrhoea, infertility, galactorrhoea, decreased libido, increased weight, dry vagina
Men: erectile dysfunction, decrease in facial hair, galactorrhoea

132
Q

What are the signs of prolactinaemia?

A

Visual disturbances e.g. bitemporal hemianopia, cranial nerve palsies, osteoporosis

133
Q

What tests are used to diagnose prolactinaemia?

A

Bloods: TFTs, beta hCG (exclude pregnancy), basal serum prolactin
Visual field tests, MRI pituitary

134
Q

What is the treatment for prolactinaemia?

A

Dopamine agonists e.g. bromocriptine or cabergoline
Surgery is rarely needed
Urgent referral if vision deteriorates

Phase 2A (11 decks)

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