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MRCP part 1 > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Main causes of hypercalcaemia

A
  1. Primary hyperparathyroidism: commonest cause in non-hospitalised patients
  2. Malignancy: the commonest cause in hospitalised patients. This may be due to number of processes, including; bone metastases, myeloma, PTHrP from squamous cell lung cancer
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2
Q

Other causes of hypercalcaemia

A 
sarcoidosis*
vitamin D intoxication
acromegaly
thyrotoxicosis
Milk-alkali syndrome
drugs: thiazides, calcium containing antacids
dehydration
Addison's disease
Paget's disease of the bone**
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3
Q

Multiple endocrine neoplasia

Type 1

MEN1 gene

Most common presentation = hypercalcaemia

A

3 P’s
Parathyroid (95%): hyperparathyroidism due to parathyroid hyperplasia
Pituitary (70%)
Pancreas (50%): e.g. insulinoma, gastrinoma (leading to recurrent peptic ulceration)

Also: adrenal and thyroid

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4
Q

Multiple endocrine neoplasia

Type 2a

RET oncogene

A

Medullary thyroid cancer (70%)

2 P’s
Parathyroid (60%)
Phaeochromocytoma

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5
Q

Multiple endocrine neoplasia

Type 2b

RET oncogene

A

Medullary thyroid cancer

1 P
Phaeochromocytoma

Marfanoid body habitus
Neuromas

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6
Q

Hypokalaemia with alkalosis

A

vomiting
thiazide and loop diuretics
Cushing’s syndrome
Conn’s syndrome (primary hyperaldosteronism)

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7
Q

Hypokalaemia with acidosis

A

diarrhoea
renal tubular acidosis
acetazolamide
partially treated diabetic ketoacidosis

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8
Q

acetazolamide

A

used to treat and prevent altitude sickness

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9
Q

Mechanism of action of Thiazolidinediones

e.g. pioglitazone, rosiglitazone

A

They are agonists to the PPAR-gamma receptor and reduce peripheral insulin resistance

The PPAR-gamma receptor is an intracellular nuclear receptor. It’s natural ligands are free fatty acids and it is thought to control adipocyte differentiation and function.

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10
Q

Adverse effects of thiazonlidinediones

A

weight gain
liver impairment: monitor LFTs
fluid retention - therefore contraindicated in heart failure. The risk of fluid retention is increased if the patient also takes insulin
recent studies have indicated an increased risk of fractures
bladder cancer: recent studies have shown an increased risk of bladder cancer in patients taking pioglitazone (hazard ratio 2.64)

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11
Q

Renal tubular necrosis

Type 1 distal

A

inability to generate acid urine (secrete H+) in distal tubule
causes hypokalaemia

complications include nephrocalcinosis and renal stones
causes include idiopathic, rheumatoid arthritis, SLE, Sjogren’s, amphotericin B toxicity, analgesic nephropathy

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12
Q

Renal tubular necrosis

Type 2 proximal

A

decreased HCO3- reabsorption in proximal tubule
causes hypokalaemia
complications include osteomalacia
causes include idiopathic, as part of Fanconi syndrome, Wilson’s disease, cystinosis, outdated tetracyclines, carbonic anhydrase inhibitors (acetazolamide, topiramate)

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13
Q

Renal tubular necrosis

Type 3 Mixed

A

extremely rare
caused by carbonic anhydrase II deficiency
results in hypokalaemia

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14
Q

Renal Tubular necosis

Type 4 Hyperkalaemic

A

reduction in aldosterone leads in turn to a reduction in proximal tubular ammonium excretion
causes hyperkalaemia
causes include hypoaldosteronism, diabetes

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15
Q

Hypothyroidism

Hashimoto’s

A

most common cause in the developed world
autoimmune disease, associated with type 1 diabetes mellitus, Addison’s or pernicious anaemia
may cause transient thyrotoxicosis in the acute phase
5-10 times more common in women

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16
Q

Hyperthyroidism

thyroxicosis

A

most common cause of thyrotoxicosis

as well as typically features of thyrotoxicosis other features may be seen including thyroid eye disease

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17
Q

Sub acute thyroiditis

de Quervain’s

A

hypothyroidism

associated with a painful goitre and raised ESR

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18
Q

Reidel’s thyroiditis

A

fibrous tissue replacing the normal thyroid parenchyma

causes a painless goitre

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19
Q

other causes of hypothyroidism

A

Postpartum thyroiditis
Drugs -lithium, amiodarone
Iodine deficiency

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20
Q

other causes of hyperthyroidism

A

Toxic multinodular goitre
autonomously functioning thyroid nodules that secrete excess thyroid hormones

Drugs
amiodarone

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21
Q

General features of hypothroidism

A

Cold intolerance
Weight gain
Lethargy

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22
Q

General features of hyperthyroidism

A

Weight loss
‘Manic’, restlessness
Palpitations
Heat intolerance

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23
Q

Skin changes in hypothyroidism

A

Dry (anhydrosis), cold, yellowish skin

Non-pitting oedema (e.g. hands, face)

Dry, coarse scalp hair, loss of lateral aspect of eyebrows

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24
Q

Skin changes in hyperthyroidism

A

Increased sweating

Pretibial myxoedema: erythematous, oedematous lesions above the lateral malleoli

Thyroid acropachy: clubbing

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25
Q

Primary hyperaldosteronism

features

A 
hypertension
hypokalaemia
e.g. muscle weakness
this is a classical feature in exams but studies suggest this is seen in only 10-40% of patients
alkalosis
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26
Q

Primary hyperaldosteronism

Investigations

A
  • plasma aldosterone/ renin ratio
    high aldosterone, low renin

-CT

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27
Q

Faconi syndrome

A

rare disorder of renal function

excess amounts of glucose, bicarb, phosphates, urate and certain amino acids are excreted in the urine.

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28
Q

Symptoms of faconi syndrome

A

kids - polydipsia, polyuria

Adults - bone pain, muscle weakness

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29
Q

Treatment of faconi syndrome

A
  • oral sodium bicarbonate
  • bone disease - bisphosphonates and vit D
  • renal transplant in kids
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30
Q

Thyroid cancer

papillary carcinoma

A

Usually contain a mixture of papillary and colloidal filled follicles
Histologically tumour has papillary projections and pale empty nuclei
Seldom encapsulated
Lymph node metastasis predominate
Haematogenous metastasis rare

70% ( often young women, excellent prognosis)

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31
Q

Thyroid cancer

Follicular adenoma

A

Usually present as a solitary thyroid nodule

Malignancy can only be excluded on formal histological assessment

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32
Q

thyroid cancer

follicular carcinoma

A

May appear macroscopically encapsulated, microscopically capsular invasion is seen. Without this finding the lesion is a follicular adenoma.
Vascular invasion predominates
Multifocal disease rare

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33
Q

Thyroid cancer

Medullary carcinoma

A

C cells derived from neural crest and not thyroid tissue
Serum calcitonin levels often raised
Familial genetic disease accounts for up to 20% cases
Both lymphatic and haematogenous metastasis are recognised, nodal disease is associated with a very poor prognosis.
Cancer of parafollicular (C) cells, secrete calcitonin, part of MEN-2

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34
Q

Thyroid cancer

anaplastic carcinoma

A

Most common in elderly females
Local invasion is a common feature
Treatment is by resection where possible, palliation may be achieved through isthmusectomy and radiotherapy. Chemotherapy is ineffective

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35
Q

thyroid cancer

lymphoma

A

associated with hashimoto’s lymphoma

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36
Q

Causes of hypocalcaemia

A

vitamin D deficiency (osteomalacia)
chronic kidney disease
hypoparathyroidism (e.g. post thyroid/parathyroid surgery)
pseudohypoparathyroidism (target cells insensitive to PTH)
rhabdomyolysis (initial stages)
magnesium deficiency (due to end organ PTH resistance)
massive blood transfusion
acute pancreatitis

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37
Q

Management of hypocalcaemia

A

acute management of severe hypocalcaemia is with intravenous replacement. The preferred method is with intravenous calcium gluconate, 10ml of 10% solution over 10 minutes
intravenous calcium chloride is more likely to cause local irritation
ECG monitoring is recommended
further management depends on the underlying cause

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38
Q

TFTs

Thyrotoxicosis (e.g. Graves’ disease)

A

TSH Low

Free T4 High

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39
Q 
TFTs 
Primary hypothyroidism (e.g. Hashimoto's thyroiditis)
A

TSH High

Free T4 Low

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40
Q

TFTs

Secondary hypothyroidism

A

TSH Low

Free T4 Low

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41
Q

TFTs

Sick euthyroid

A

TSH - low
Free T4 - low

Common in hospital inpatients. Changes are reversible upon recovery from the systemic illness and no treatment is usually needed

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42
Q

TFTs

Subclinical thyroiditis

A

TSH - High

Free T4 - Normal
This is a common finding and represents patients who are ‘on the way’ to developing hypothyroidism but still have normal thyroxine levels. Note how the TSH levels, as mentioned above, are a more sensitive and early marker of thyroid problems

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43
Q

TFTs

Poor thyroxine compliance

A

TSH High

Free T4 - normal
Patients who are poorly compliant may only take their thyroxine in the days before a routine blood test. The thyroxine levels are hence normal but the TSH ‘lags’ and reflects longer term low thyroxine levels

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44
Q

Hyponatraemia

Urinary sodium > 20 mmol/l

Sodium depletion, renal loss

A

diuretics: thiazides, loop diuretics
Addison’s disease
diuretic stage of renal failure

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45
Q

Hyponatraemia

Urinary sodium > 20 mmol/l

Patient often euvolaemic

A

SIADH (urine osmolality > 500 mmol/kg)

hypothyroidism

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46
Q

Hyponatraemia

Urinary sodium <20mmol/l

Sodium depletion, extra-renal loss

A

diarrhoea, vomiting, sweating

burns, adenoma of rectum

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47
Q

Hyponatraemia

Urinary sodium <20mmol/l

Water excess (patient often hypervolaemic and oedematous)

A

secondary hyperaldosteronism: heart failure, liver cirrhosis
nephrotic syndrome
IV dextrose
psychogenic polydipsia

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48
Q

History of primary hyperparathyroidism

A

primary hyperparathyroidism is stereotypically seen in elderly females with an unquenchable thirst and an inappropriately normal or raised parathyroid hormone level. It is most commonly due to a solitary adenoma

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49
Q

Causes of primary hyperparathyroidism

A

80%: solitary adenoma
15%: hyperplasia
4%: multiple adenoma
1%: carcinoma

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50
Q

Features of primary hyperparathyroidism

A 
polydipsia, polyuria
peptic ulceration/constipation/pancreatitis
bone pain/fracture
renal stones
depression
hypertension
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51
Q

Conditions associated with primary hyperparathyroidism

A

hypertension

multiple endocrine neoplasia: MEN I and II

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52
Q

Investigations of primary hyperparathyroidism

A

raised calcium, low phosphate
PTH may be raised or (inappropriately, given the raised calcium) normal
technetium-MIBI subtraction scan
pepperpot skull is a characteristic X-ray finding of hyperparathyroidism

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53
Q

Treatment of primary hyperparathyroidism

A

the definitive management is total parathyroidectomy
conservative management may be offered if the calcium level is less than 0.25 mmol/L above the upper limit of normal AND the patient is > 50 years AND there is no evidence of end-organ damage
calcimimetic agents such as cinacalcet are sometimes used in patients who are unsuitable for surgery

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54
Q

Causes of hypokalaemia with acidosis

A

diarrhoea
renal tubular acidosis
acetazolamide
partially treated diabetic ketoacidosis

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55
Q

Causes of hypokalaemia with alkalosis

A

vomiting
thiazide and loop diuretics
Cushing’s syndrome
Conn’s syndrome (primary hyperaldosteronism)

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56
Q

Key features of MEN I

A

peptic ulceration, galactorrhoea, hypercalcaemia

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57
Q

Key features of MEN IIa

A

medullary thyroid cancer, hypercalcaemia, phaeochromocytoma

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58
Q

Key features of Liddle’s syndrome

A

hypokalaemia, hypertension, alkalosis, family history of similar problems, low aldosterone

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59
Q

What is Liddle’s syndrome

A

Liddle’s syndrome is a rare autosomal dominant condition that causes hypertension and hypokalaemic alkalosis. It is thought to be caused by disordered sodium channels in the distal tubules leading to increased reabsorption of sodium.

Treatment is with either amiloride or triamterene

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60
Q

Thyroid cancer associatated with MEN-2

A

medullary thyroid cancer

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61
Q

Key features of Conn’s syndrome

A

hypokalaemia, hypertension, alkalosis, no similar family history, raised aldosterone

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62
Q

Key features of Addisons

A

hyperkalaemia, hyponatraemia, hypoglycaemia

hypotension, hyperpigmentation, lethargy

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63
Q

Stereotypical history of primary hyperaldosteronism

A

a 35-year-old woman is found to have a blood pressure of 180/110 mmHg. She complains of feeling tired and weak. Routine bloods show hypokalaemia

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64
Q

Stereotypical history of phaeochromocytoma

A

a 40-year-old patient with a history of hypertension presents with episodic palpitations, excessive sweating, headaches and tremor

65
Q

Treatment of hyperaldosteronism

A

spironalactone

66
Q

Causes of hypocalcaemia

A

vitamin D deficiency (osteomalacia)
chronic kidney disease
hypoparathyroidism (e.g. post thyroid/parathyroid surgery)
pseudohypoparathyroidism (target cells insensitive to PTH)
rhabdomyolysis (initial stages)
magnesium deficiency (due to end organ PTH resistance)
massive blood transfusion
acute pancreatitis

67
Q

Investigations of acromegaly

A

Serum IGF-1 levels have now overtaken the oral glucose tolerance test (OGTT) with serial GH measurements as the first-line test. The OGTT test is recommended to confirm the diagnosis if IGF-1 levels are raised.

Growth hormone levels vary throughout the day so aren’t useful

68
Q

Acromegaly OGTT

A

in normal patients GH is suppressed to < 2 mu/L with hyperglycaemia
in acromegaly there is no suppression of GH
may also demonstrate impaired glucose tolerance which is associated with acromegaly
in normal patients GH is suppressed to < 2 mu/L with hyperglycaemia
in acromegaly there is no suppression of GH
may also demonstrate impaired glucose tolerance which is associated with acromegaly

69
Q

Incretin effect

A

In normal physiology an oral glucose load results in a greater release of insulin than if the same load is given intravenously - this known as the incretin effect. This effect is largely mediated by GLP-1 and is known to be decreased in T2DM.

70
Q

Glucagon-like peptide-1 (GLP-1) mimetics (e.g. exenatide, Liraglutide)

A

Exenatide is an example of a glucagon-like peptide-1 (GLP-1) mimetic. These drugs increase insulin secretion and inhibit glucagon secretion. One of the major advances of GLP-1 mimetics is that they typically result in weight loss
Given by SC injection

71
Q

Dipeptidyl peptidase-4 (DPP-4) inhibitors (e.g. Vildagliptin, sitagliptin)

Key points

A

Dipeptidyl peptidase-4, DPP-4 inhibitors increase levels of incretins (GLP-1 and GIP) by decreasing their peripheral breakdown
oral preparation
trials to date show that the drugs are relatively well tolerated with no increased incidence of hypoglycaemia
do not cause weight gain

72
Q

Features of Kallman’s syndrome

A

‘delayed puberty’
hypogonadism, cryptorchidism
anosmia
sex hormone levels are low
LH, FSH levels are inappropriately low/normal
patients are typically of normal or above average height

73
Q

What is Kallman’s syndrome

A

a recognised cause of delayed puberty secondary to hypogonadotrophic hypogonadism. It is usually inherited as an X-linked recessive trait. Kallman’s syndrome is thought to be caused by failure of GnRH-secreting neurons to migrate to the hypothalamus.

The clue given in many questions is lack of smell (anosmia) in a boy with delayed puberty

74
Q

Kleinfelter’s syndrome

A

Klinefelter’s syndrome is associated with karyotype 47, XXY

Features
often taller than average
lack of secondary sexual characteristics
small, firm testes
infertile
gynaecomastia - increased incidence of breast cancer
elevated gonadotrophin levels
75
Q

What is androgen insensitivity syndrome

A

Androgen insensitivity syndrome is an X-linked recessive condition due to end-organ resistance to testosterone causing genotypically male children (46XY) to have a female phenotype. Complete androgen insensitivity syndrome is the new term for testicular feminisation syndrome

76
Q

Features of androgen insensitivity syndrome

A

‘primary amenorrhoea’
undescended testes causing groin swellings
breast development may occur as a result of conversion of testosterone to oestradiol

77
Q

management of androgren insufficiency syndrome

A 
counselling - raise child as female
bilateral orchidectomy (increased risk of testicular cancer due to undescended testes)
oestrogen therapy
78
Q

What are thiazolidediones?

A

Thiazolidinediones are a class of agents used in the treatment of type 2 diabetes mellitus. They are agonists to the PPAR-gamma receptor and reduce peripheral insulin resistance. Rosiglitazone was withdrawn in 2010 following concerns about the cardiovascular side-effect profile.

79
Q

Adverse effects of thiazolidediones

A

weight gain
liver impairment: monitor LFTs
fluid retention - therefore contraindicated in heart failure. The risk of fluid retention is increased if the patient also takes insulin
recent studies have indicated an increased risk of fractures
bladder cancer: recent studies have shown an increased risk of bladder cancer in patients taking pioglitazone (hazard ratio 2.64)

80
Q

Primary hypoparathyroidism

A

decrease PTH secretion
e.g. secondary to thyroid surgery*
low calcium, high phosphate
treated with alfacalcidol

81
Q

Symptoms of hypoparathyroidism secondary to hypocalcaemia

A

tetany: muscle twitching, cramping and spasm
perioral paraesthesia
Trousseau’s sign: carpal spasm if the brachial artery occluded by inflating the blood pressure cuff and maintaining pressure above systolic
Chvostek’s sign: tapping over parotid causes facial muscles to twitch
if chronic: depression, cataracts
ECG: prolonged QT interval

82
Q

pseudohypoparathryroidism

A

target cells being insensitive to PTH
due to abnormality in a G protein
associated with low IQ, short stature, shortened 4th and 5th metacarpals
low calcium, high phosphate, high PTH
diagnosis is made by measuring urinary cAMP and phosphate levels following an infusion of PTH. In hypoparathyroidism this will cause an increase in both cAMP and phosphate levels. In pseudohypoparathyroidism type I neither cAMP nor phosphate levels are increased whilst in pseudohypoparathyroidism type II only cAMP rises.

83
Q

pseudopsuedohypoparathyroidism

A

similar phenotype to pseudohypoparathyroidism but normal biochemistry

84
Q

Risk factors for urinary incontinence

A 
advancing age
previous pregnancy and childbirth
high body mass index
hysterectomy
family history
85
Q

Classification of urinary incontinence

A

overactive bladder (OAB)/urge incontinence: due to detrusor overactivity
stress incontinence: leaking small amounts when coughing or laughing
mixed incontinence: both urge and stress
overflow incontinence: due to bladder outlet obstruction, e.g. due to prostate enlargement

86
Q

Investigations of urinary incontinence

A

bladder diaries should be completed for a minimum of 3 days
vaginal examination to exclude pelvic organ prolapse and ability to initiate voluntary contraction of pelvic floor muscles (‘Kegel’ exercises)
urine dipstick and culture
urodynamic studies

87
Q

Management of urinary incontinence

A 
bladder retraining (lasts for a minimum of 6 weeks, the idea is to gradually increase the intervals between voiding)
bladder stabilising drugs: antimuscarinics are first-line. NICE recommend oxybutynin (immediate release), tolterodine (immediate release) or darifenacin (once daily preparation). Immediate release oxybutynin should, however, be avoided in 'frail older women'
mirabegron (a beta-3 agonist) may be useful if there is concern about anticholinergic side-effects in frail elderly patients
88
Q

Management of stress incontinence

A

pelvic floor muscle training: NICE recommend at least 8 contractions performed 3 times per day for a minimum of 3 months
surgical procedures: e.g. retropubic mid-urethral tape procedures
duloxetine may be offered to women if they decline surgical procedures
a combined noradrenaline and serotonin reuptake inhibitor
mechanism of action: increased synaptic concentration of noradrenaline and serotonin within the pudendal nerve → increased stimulation of urethral striated muscles within the sphincter → enhanced
contraction

89
Q

Risk factors for endometrial cancer

A 
obesity
nulliparity
early menarche
late menopause
unopposed oestrogen. The addition of a progestogen to oestrogen reduces this risk (e.g. In HRT). The BNF states that the additional risk is eliminated if a progestogen is given continuously
diabetes mellitus
tamoxifen
polycystic ovarian syndrome
hereditary non-polyposis colorectal carcinoma
90
Q

Features of endometrial cancer

A

postmenopausal bleeding is the classic symptom
premenopausal women may have a change intermenstrual bleeding
pain and discharge are unusual features

91
Q

Investigations for endometrial cancer

A

women >= 55 years who present with postmenopausal bleeding should be referred using the suspected cancer pathway
first-line investigation is trans-vaginal ultrasound - a normal endometrial thickness (< 4 mm) has a high negative predictive value
hysteroscopy with endometrial biopsy

92
Q

Management of endometrial cancer

A

localised disease is treated with total abdominal hysterectomy with bilateral salpingo-oophorectomy. Patients with high-risk disease may have post-operative radiotherapy
progestogen therapy is sometimes used in frail elderly women not consider suitable for surgery

93
Q

What is ezetimibe

A

Ezetimibe is a lipid-lowering drug which inhibits cholesterol receptors on enterocytes, decreasing cholesterol absorption in the small intestine.

Ezetimibe monotherapy is recommended as an option for treating primary hypercholesterolaemia in adults in whom initial statin therapy is contraindicated or who cannot tolerate statin therapy
Ezetimibe, coadministered with initial statin therapy, is recommended as an option for treating primary hypercholesterolaemia in adults who have started statin therapy when:
serum total or LDL cholesterol concentration is not appropriately controlled either after appropriate dose titration of initial statin therapy or because dose titration is limited by intolerance to the initial statin therapy
a change from initial statin therapy to an alternative statin is being considered.

94
Q

Management of acromegaly

A
  1. Trans-sphenoid surgery
  2. somatostatin analogue
    directly inhibits the release of growth hormone
    for example octreotide
    effective in 50-70% of patients
  3. pegvisomant
    GH receptor antagonist - prevents dimerization of the GH receptor
    once daily s/c administration
    very effective - decreases IGF-1 levels in 90% of patients to normal
    doesn’t reduce tumour volume therefore surgery still needed if mass effect
  4. dopamine agonists
    for example bromocriptine
    the first effective medical treatment for acromegaly, however now superseded by somatostatin analogues
    effective only in a minority of patient
95
Q

What is Gitelman’s syndrome

A

Gitelman’s syndrome is due to a defect in the thiazide-sensitive Na+ Cl- transporter in the distal convoluted tubule.

96
Q

Features of Gitelman’s syndrome

A 
normotension
hypokalaemia
hypocalciuria
hypomagnesaemia
metabolic alkalosis
97
Q

Causes of Cushing’s syndrome

ACTH dependent causes

A

Cushing’s disease (80%): pituitary tumour secreting ACTH producing adrenal hyperplasia
ectopic ACTH production (5-10%): e.g. small cell lung cancer is the most common causes

98
Q

Causes of Cushing’s syndrome

ACTH independent causes

A

iatrogenic: steroids
adrenal adenoma (5-10%)
adrenal carcinoma (rare)
Carney complex: syndrome including cardiac myxoma
micronodular adrenal dysplasia (very rare)

99
Q

Causes of Cushing’s syndrome

Pseudo-Cushing’s

A

mimics Cushing’s
often due to alcohol excess or severe depression
causes false positive dexamethasone suppression test or 24 hr urinary free cortisol
insulin stress test may be used to differentiate

100
Q

Congenital adrenal hyperplasia

21-hydroxylase deficiency features

A

virilisation of female genitalia
precocious puberty in males
60-70% of patients have a salt-losing crisis at 1-3 wks of age

101
Q

Congenital adrenal hyperplasia

11-beta hydroxylase deficiency features

A

virilisation of female genitalia
precocious puberty in males
hypertension
hypokalaemia

102
Q

Congenital adrenal hyperplasia

17-hydroxylase deficiency features

A

non-virilising in females
inter-sex in boys
hypertension

103
Q

Endocrine side effects of corticosteroids

A

impaired glucose regulation, increased appetite/weight gain, hirsutism, hyperlipidaemia

104
Q

Cushing side effects of corticosteroids

A

moon face, buffalo hump, striae

105
Q

Musculoskeletal side effects of corticosteroids

A

osteoporosis, proximal myopathy, avascular necrosis of the femoral head

106
Q

Immunosuppression side effects of corticosteroids

A

increased susceptibility to severe infection, reactivation of tuberculosis

107
Q

Psychiatric side effects of corticosteroids

A

insomnia, mania, depression, psychosis

108
Q

Gastro-intestinal side effects of corticosteroids

A

peptic ulceration, acute pancreatitis

109
Q

Ophthalmic side effects of corticosteroids

A

glaucoma, cataracts

110
Q

other side effects of corticosteroids

A

suppression of growth in children
intracranial hypertension
neutrophilia

111
Q

Mineralocorticoid side-effects

A

fluid retention

hypertension

112
Q

Bartter’s Syndrome

A

Bartter’s syndrome is an inherited cause (usually autosomal recessive) of severe hypokalaemia due to defective chloride absorption at the Na+ K+ 2Cl- cotransporter (NKCC2) in the ascending loop of Henle. It should be noted that it is associated with normotension (unlike other endocrine causes of hypokalaemia such as Conn’s, Cushing’s and Liddle’s syndrome which are associated with hypertension).

113
Q

Barrter’s syndrome features

A 
usually presents in childhood, e.g. Failure to thrive
polyuria, polydipsia
hypokalaemia
normotension
weakness
114
Q

What is Riedel’s thyroiditis

A

Riedel’s thyroiditis is a rare cause of hypothyroidism characterised by dense fibrous tissue replacing the normal thyroid parenchyma. On examination a hard, fixed, painless goitre is noted. It is usually seen in middle-aged women. It is associated with retroperitoneal fibrosis.

115
Q

MODY 3

A

60% of cases
due to a defect in the HNF-1 alpha gene
is associated with an increased risk of HCC

116
Q

MODY 2

A

20% of cases

due to a defect in the glucokinase gene

117
Q

MODY 5

A

rare
due to a defect in the HNF-1 beta gene
liver and renal cysts

118
Q

Features of MODY

A

typically develops in patients < 25 years
a family history of early onset diabetes is often present
ketosis is not a feature at presentation
patients with the most common form are very sensitive to sulfonylureas, insulin is not usually necessary

119
Q

Features of phaeochromocytoma

A 
Features are typically episodic
hypertension (around 90% of cases, may be sustained)
headaches
palpitations
sweating
anxiety
120
Q

Management of phaeochromocytoma

A

Surgery is the definitive management. The patient must first however be stabilized with medical management:
alpha-blocker (e.g. phenoxybenzamine), given before a
beta-blocker (e.g. propranolol)

121
Q

Investigations of phaeochromocytoma

A

24 hr urinary collection of metanephrines (sensitivity 97%*)

this has replaced a 24 hr urinary collection of catecholamines (sensitivity 86%)

122
Q

Features of Addison’s

A

lethargy, weakness, anorexia, nausea & vomiting, weight loss, ‘salt-craving’
hyperpigmentation (especially palmar creases)*, vitiligo, loss of pubic hair in women, hypotension, hypoglycaemia
hyponatraemia and hyperkalaemia may be seen
crisis: collapse, shock, pyrexia

123
Q

Mechanism of action: propylthiouracil

A

Blocks thyroid peroxidase from coupling and iodinating the tyrosine residues on thyroglobulin –> reducing thyroid hormone production + inhibits 5’-deiodinase which reduces peripheral conversion of T4 to T3

124
Q

Stereotypical history of primary hyperaldosteronism

A

a 35-year-old woman is found to have a blood pressure of 180/110 mmHg. She complains of feeling tired and weak. Routine bloods show hypokalaemia

125
Q

Stereotypical history of Addison’s disease

A

a 40-year-old woman presents with lethargy, weakness and weight loss. On examination her blood pressure is 80/50 mmHg and there is hyperpigmentation of the skin

126
Q

Features of primary hyperaldosteronism

A 
hypertension
hypokalaemia
e.g. muscle weakness
this is a classical feature in exams but studies suggest this is seen in only 10-40% of patients
alkalosis
127
Q

Stereotypical history of 5-alpha reductase deficiency

A

a baby is born with ambiguous genitalia, exhibiting labioscrotal folds with clitoromegaly. At 13 years of age the child undergoes virilization with facial hair and deepening of the voice

128
Q

Key features of Liddle’s syndrome

A

hypokalaemia, hypertension, alkalosis, family history of similar problems, low aldosterone

129
Q

Adverse effects of sulfonylureas

A 
hypoglycaemia
weight gain 
hyponatraemia 
hepatotoxicity 
bone marrow suppression 
peripheral neuropathy
130
Q

what are meglitinides

A

increase pancreatic insulin secretion
like sulfonylureas they bind to an ATP-dependent K+(KATP) channel on the cell membrane of pancreatic beta cells
often used for patients with an erratic lifestyle
adverse effects include weight gain and hypoglycaemia (less so than sulfonylureas)

131
Q

Complications of subclinical hypothyroidism

A

Dementia
AF
osteoporosis

132
Q

Mechanism of action: Gliptins (DPP-4 inhibitors)

A

Reduce the peripheral breakdown of incretins such as GLP-1

133
Q

9am serum cortisol > 500 nmol/l

A

makes Addison’s very unlikely

134
Q

9am serum cortisol 100-500 nmol

A

Is inconclusive - needs short synacthen test

135
Q

9am serum cortisol <100

A

Diagnosis of Addisons

136
Q

Electrolyte abnormalities in addisons

A

hyperkalaemia
hyponatraemia
hypoglycaemia
metabolic acidosis

137
Q

Management of acute hyponatraemia with severe symptoms (drunk, drinking lots, reduced GCS

A

Hypertonic saline (3%)

138
Q

Management of hypervolaemic hyponatraemia

A

fluid restrict to 500–1000 mL/day
consider loop diuretics
consider vaptans

139
Q

Management of euvolaemic hyponatraemia

A

fluid restrict to 500–1000 mL/day
consider medications:
demeclocycline
vaptans (vasopressin/ADH receptor antagonists) - can be hepatoxic and make pts thirstier

140
Q

Management of hypovolaemic hyponatraemia

A

normal, i.e. isotonic, saline (0.9% NaCl)
this may sometimes be given as a trial
if the serum sodium rises this supports a diagnosis of hypovolemic hyponatraemia
if the serum sodium falls an alternative diagnosis such as SIADH is lik

141
Q

Causes of pseudohyperkalaemia

A
  • high blood cell turnover (e.g. essential thrombocytosis)
  • haemolysis during sampling
  • delayed processing
  • familial causes
142
Q

Features of a thyroid storm

A 
fever > 38.5ºC
tachycardia
confusion and agitation
nausea and vomiting
hypertension
heart failure
abnormal liver function test - jaundice may be seen clinically
143
Q

Management of thryroid storm

A

symptomatic treatment e.g. paracetamol
treatment of underlying precipitating event
beta-blockers: typically IV propranolol
anti-thyroid drugs: e.g. methimazole or propylthiouracil
Lugol’s iodine
dexamethasone - e.g. 4mg IV qds - blocks the conversion of T4 to T3

144
Q

Thyroid MALT lymphoma

A

follows an indolent course and often presents as a neck lump without typical ‘B’ symptoms such as fever, night sweats and weight loss. Some patients may report compression symptoms such as dysphagia and dyspnoea.

145
Q

Anosmia hypogonadotrophic hypogonadism

A

Kallman’s syndrome

146
Q

Features of Addison’s

A

lethargy, weakness, anorexia, nausea & vomiting, weight loss, ‘salt-craving’
hyperpigmentation (especially palmar creases)*, vitiligo, loss of pubic hair in women, hypotension, hypoglycaemia
hyponatraemia and hyperkalaemia may be seen
crisis: collapse, shock, pyrexia

147
Q

Secondary causes of hypertriglyceridaemia

A 
diabetes mellitus (types 1 and 2)
obesity
alcohol
chronic renal failure
drugs: thiazides, non-selective beta-blockers, unopposed oestrogen
liver disease
148
Q

secondary causes of hypercholesterolaemia

A

nephrotic syndrome
cholestasis
hypothyroidism

149
Q

Indications for Meglitinides in T2DM

A

stimulate insulin release - good for erratic lifestyle- take them shortly before meals

150
Q

Investigations of Cushing’s

A

24 hour urine cortisol

151
Q

Prolactin and Dopamine

A

Dopamine continuously suppresses prolactin

152
Q

Geitelman’s syndrome - features

A

normotension, hypokalaemia + hypocalciuria
hypomagnesaemia
metabolic alkalosis

153
Q

Pathophysiology of Geitelman’s syndrome

A

a defect in the thiazide-sensitive Na+ Cl- transporter in the distal convoluted tubule.

154
Q

Features of primary hyperaldosteronism

A

hypertension
hypokalaemia - e.g. muscle weakness
alkalosis
bilateral idiopathic adrenal hyperplasia is the cause in up to 70% of cases

155
Q

de Queverian’s thryoiditis

A

sub acute hyperthyroiditis followed by hypothyroidism

156
Q

Formula for working out averabge BM from HbA1c

A

average plasma glucose = (2 * HbA1c) - 4.5

157
Q

Management of acromegaly: adjunct to surgery

A

Octreotide

158
Q

Fibrates

A

Used in management of hyperlipidaemia
Increase risk of VTE
work through activating PPAR alpha receptors resulting in an increase in LPL activity reducing triglyceride levels.

159
Q

Cause of congenital adrenal hyperplasia

A

due to 21-hydroxylase deficiency

MRCP part 1 (15 decks)

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