Endo Flashcards

1
Q

Define acromegaly

A

Constellation of signs and symptoms caused by hypersecretion of GH in adults

note: most are caused by a pituitary adenoma

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2
Q

Outline the signs of acromegaly

A

coarsening of facial features
soft-tissue and skin changes - rings and shoes becoming tight
carpal tunnel syndrome
joint pain and dysfunction
snoring
alterations in sexual functioning
Can also get hyperprolactinaemia symptoms

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3
Q

List some appropriate investigations for acromegaly

A

serum insulin-like growth factor 1 (IGF-1) [lacks specificity]
oral glucose tolerance test (OGTT) - CONFIRMATORY [failure of GH suppression after 75g glucose load]
random serum growth hormone (GH)

Consider visual field testing
Consider MRI pituitary

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4
Q

Generate a management plan for acromegaly

A

1st line = transphenoidal surgery + consider radiotherapy
2nd line = somatostatin analogues (octreotide, lanreotide)
3rd line = dopamine agonists (cabergoline)
3rd line = GH receptor antagonists (pegvisomant - recombinant GH analogue)

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5
Q

What hormones does the adrenal gland produce and where are they produced?

A

CORTEX:
Mineralocorticoid (aldosterone) - zona glomerulosa
Glucocorticoids (cortisol) - zona fasciculata
Androgens (DHEA) - zona reticularis

MEDULLA:
adrenaline/noradrenaline

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6
Q

List some risk factors for adrenal insufficiency

A

Primary - Addison’s disease (usually autoimmune)
Secondary - hypothalamic/pituitary failure
Infections - TB
Infiltrative - mets, amyloidosis, lymphoma
Iatrogenic - sudden cessation of long term steroid therapy

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6
Q

Outline the presenting symptoms of adrenal insufficiency

A

Chronic Presentation - the symptoms tend to be VAGUE and NON-SPECIFIC
Dizziness
Anorexia
Weight loss
Diarrhoea and Vomiting
Abdominal pain
Lethargy
Weakness
Depression
INCREASED PIGMENTATION

Acute Presentation (Addisonian Crisis)
Acute adrenal insufficiency
Major haemodynamic collapse: shock, N+V, hypothermia and abdo pain
Precipitated by stress (e.g. infection, surgery)

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7
Q

List some appropriate investigations for adrenal insufficiency

A

morning serum cortisol (< 100 nmol/L is diagnostic)
plasma adrenocorticotrophic hormone (ACTH)
serum electrolytes
urea and creatinine
FBC
TFTs

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8
Q

What is the difference between the short synacthen and long synacthen test?

A

Short Synacthen Test
-Give IM 250 µg tetrocosactrin (synthetic ACTH)
-Serum cortisol < 550 nmol/L at 30 mins indicates adrenal failure

Long Synacthen Test
-1 mg synthetic ACTH administered
-Measure serum cortisol at 0, 30, 60, 90 and 120 minutes
-Then measure again at 4, 6, 8, 12 and 24 hours
-Patients with primary adrenal insufficiency show no increased after 6 hours

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9
Q

Generate a management plan for an Addisonian crisis

A

A-E approach
1. Rapid IV fluid rehydration
2. 50 mL of 5% dextrose to correct hypoglycaemia
3. IV or Im 100 mg hydrocortisone bolus
4. Followed by 100 mg 6 hourly hydrocortisone until BP is stable
5. Treat precipitating cause (e.g. antibiotics for infection)
Monitor

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10
Q

How is ongoing adrenal insufficiency managed?

A

Replacement:
-Glucocorticoids with hydrocortisone (3/day)
-Mineralocorticoids with fludrocortisone
[Hydrocortisone dosage needs to be increased during times of acute illness or stress]

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11
Q

Define carcinoid syndrome

A

Constellation of symptoms (esp liver mets) caused by systemic release of humoral factors from carcinoid tumours (slow-growing type of neuroendocrine tumours)

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12
Q

List the presenting symptoms of carcinoid syndrome

A

Paroxysmal FLUSHING
Diarrhoea
Crampy abdominal pain
Wheeze – due to bronchospasm
Sweating
Palpitations
Telangiectasia

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13
Q

List some appropriate investigations for carcinoid syndrome

A

serum chromogranin A/B (will be elevated)
urinary 5-hydroxyindoleacetic acid
metabolic panel
liver function tests
full blood count
CT/PET scan to localise tumour

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14
Q

Generate a management plan for carcinoid syndrome

A

Surgical resection + perioperative octreotide infusion

For unresectable - somatostatin analogue or interferon alpha
Consider chemotherapy, radiotherapy and immunotherapy
Consider palliative debulking

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15
Q

What are the risk factors for Cushing’s syndrome

A

ACTH dependent:
-pituitary adenoma (Cushing’s disease)
-ectopic ACTH from lung cancer/carcinoid tumours

ACTH independent
-adrenal adenoma
-adrenal carcinoma

Taking STEROIDS

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16
Q

Outline the presenting symptoms of Cushing’s syndrome

A

Myalgia
Thin skin/easy bruising
Poor wound healing
Weight gain - central obesity
Moon face
Interscapular fat bad
Hirsuitism
Acne
Menstrual irregularities

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17
Q

List the appropriate investigations for Cushing’s syndrome

A
  1. Urine pregnancy test (if appropriate)
  2. Bloods (U+Es, LFTs, BMs, CRP)
  3. 1 mg overnight dexamethasone suppression test
  4. Late-night salivary cortisol
  5. 24hr urinary free cortisol
    Can also do low dose dexamethasone test (over 48hrs)

Consider ix for cause:
-pituitary MRI
-high dose dexamethasone suppression test
-petrosal sinus sampling
-ACTH levels

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18
Q

Generate a management plan for Cushing’s syndrome

A

If iatrogenic - discontinue steroids

Medical:
-inhibit cortisol synthesis with metyrapone or ketoconazole

Surgical:
-pituitary adenoma - trans-sphenoidal resection
-adrenal adenoma - surgical removal

If refractory Cushing’s disease - bilateral adrenalectomy

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19
Q

List some complications of Cushing’s syndrome

A

Diabetes
Osteoporosis
HTN
Pre-disposition to infections

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20
Q

Define diabetes insipidus

A

Diabetes insipidus is a metabolic disorder characterised by an absolute or relative inability to concentrate urine due inadequate secretion or of insensitivity to vasopressin (ADH)

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21
Q

List some causes of diabetes insipidus

A

Central:
-Idiopathic
-Tumours e.g. pituitary
-Infiltrative (e.g. sarcoidosis)
-Infection (e.g. meningitis)
-Vascular (e.g. aneurysms, Sheehan syndrome)
-Trauma (e.g. head injury, neurosurgery)

Nephrogenic:
-Idiopathic
-Drugs (e.g. lithium)
-Post-obstructive uropathy
-Pyelonephritis
-Pregnancy
-Osmotic diuresis (e.g. diabetes mellitus)

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22
Q

Outline the presenting symptoms of diabetes insipidus

A

Polyuria
Nocturia
Polydipsia
Enuresis (in children)

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23
Q

List some appropriate investigations for diabetes insipidus

A
  1. Bloods (U+Es - Na, Ca, K, glucose)
  2. urine osmolality (decreased)
  3. serum osmolality (increased)
  4. urine dipstick (negative for glucose)
  5. water deprivation test
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24
Q

Explain the results of a water deprivation test

A

Water restricted for 8 hrs and then desmopression given and osmolality measured.

Normally water restriction = increased urine osmolality (>600 mosmol/kg)

DI = urine osmolality is LOW (<400 mosmol/kg)
Cranial DI - urine osmolality rises >50% after desmopressin
Nephrogenic DI - osmolality rises <45% after desmopressin

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25
Q

Generate a management plan for diabetes insipidus

A

A-E
1. Give IV fluids if hypernatraemic (5% dextrose may be necessary)
2. Desmopressin
3. Maintenance of fluid balance

If nephrogenic then can give thiazide diuretics or NSAIDs (these inhibit prostaglandin synthesis and prostaglandin inhibits ADH)

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26
Q

What HLA associations are linked to T1DM?

A

HLA-DQ, HLA-DR3/4

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27
Q

List some causes of T2DM

A

MODY (maturity onset diabetes of the young) – autosomal dominant
Pancreatic disease e.g. chronic pancreatitis, pancreatic ca.
Endocrinopathies e.g. Cushing’s syndrome, acromegaly, PCOS
Drugs e.g. corticosteroids

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28
Q

Give some risk factors for T2DM

A

Genetic predisposition
Older age
Physical inactivity
Obesity - ↑FFAs, hyperglycaemia
Hypertension
Dysplipidaemia
Cardiovascular disease

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29
Q

List some appropriate investigations for suspected diabetes

A
  1. Urine dip
  2. Blood glucose
  3. HbA1c (>48 mmol/mol or 6.5%)
  4. Urine albumin:creatinine ratio
  5. eGFR
  6. U+Es
  7. Lipids

[If suspecting DKA then do ABG and ketones]

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30
Q

What are the blood glucose cut offs for diagnosing diabetes?

A

Fasting blood glucose >7
2hr post OGTT >11.1
Random >11.1

For diagnosis need:
-Symptomatic + 1 positive result
-Asymptomatic + 2 positive results

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31
Q

Generate a management plan for T1DM

A

Patient education
MDT
Diabetes specialist nurse
DAFNE (dose adjusted for normal eating)
Glycaemic control insulin (either basal bolus regimen or insulin pump)

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32
Q

Generate a management plan for DKA

A

IV fluid replacement with 0.9% saline
Start IV dextrose when glucose reaches 15mmol/l
Insulin infusion
Potassium (in fluids)

Monitor blood glucose, ketones, urine output and VBG

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33
Q

What advice is given for T2DM

A

Patient education
Lifestyle measures - diet, weight loss, exercise
BP control (ACEi +/- diuretic)
Statins
Smoking cessation

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34
Q

Outline the medication pathway for T2DM

A
  1. Metformin
    (if C/I then usually start on sulfonylurea)
  2. Metformin + sulfonylurea
    (or sulfonylurea + DDP4i)
  3. Metformin + sulfonylurea + SGLT2/DPP4i/Pioglitazone
  4. Substitute least effective of the three with GLP-1 (NOTE: do NOT give DPP4 and GLP 1 in combo)
  5. Add in insulin
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35
Q

Generate a management plan for HHS/HONK

A

IV isotonic saline fluid replacement (unless 0.45% saline if Na+ >155mmol/l)
Start IV dextrose when glucose reaches 15mmol/l
Insulin infusion 3 U/hour
Potassium (in fluids)
Monitor blood glucose, ketones, urine output and venous blood gases

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36
Q

Outline the main complications of diabetes

A

Diabetic kidney disease
Impaired vision (diabetic retinopathy)
Peripheral vascular disease
Peripheral neuropathy
IHD
Stroke/TIA
Gangrene
Infection
Impotence/ED

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37
Q

Define Grave’s disease

A

Hyperthyroidism due to presence of TSH receptor stimulating antibodies
(most common cause of hyperthyroidism in UK)

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38
Q

List the presenting symptoms of Grave’s disease

A

Heat intolerance
Sweating
Weight loss
Palpitations
Tremor
Exopthalmos
Pretibial myxoedema
Diffuse goitre
Anxiety
Oligomenorrhoea/Amenorrhoea

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39
Q

List some appropriate investigations for Grave’s disease

A
  1. Thyroid examination
  2. TFTs (low TSH + high T3/T4)
  3. Autoantibodies (Anti-TSHr, Anti-TPO, anti-thyroglobulin)
  4. Imaging (thyroid uptake scan - diffuse)
  5. CRP

Can do biopsy - will show tall follicles with scalloped borders

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40
Q

Generate a management plan for Grave’s disease

A
  1. Carbimazole or PTU (in pregs) - block organification of iodine - Risk of AGRANULOCYTOSIS
  2. Beta blocker for HR
  3. Radioactive iodine if treatment failure
  4. Consider thyroid surgery (risk of damage to recurrent laryngeal nerve)
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41
Q

Generate a management plan for a thyroid storm

A
  1. A-E approach
  2. IV fluids + analgesia
  3. Propranolol
  4. Steroids
  5. High dose carbimazole/PTU
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42
Q

What are the different types of hyperparathyroidism?

A

Primary - increased secretion of PTH independent to plasma Ca
Secondary - increased PTH secretion secondary to hypocalcaemia
Tertiary - autonomous PTH secretion following chronic secondary hyperparathyroidism

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43
Q

Outline some causes of primary hyperparathyroidism

A

Parathyroid adenoma
Parathyroid hyperplasia
Parathyroid carcinoma
MEN syndrome

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44
Q

Outline some causes of secondary hyperparathyroidism

A

Chronic renal failure
Vitamin D deficiency
Malabsorption syndromes

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45
Q

List the presenting symptoms of primary hyperparathyroidism

A

Signs of hypercalcaemia:
-Polyuria
-Renal calculi
-Constipation
-Depression/anxiety
-Fatigue
-Memory loss
-Paraesthesia

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46
Q

List the presenting symptoms of secondary hyperparathyroidism

A

Signs of hypocalcaemia or underlying cause
-Tingling in fingers/toes
-Myoclonus
-Muscle cramps
-Chvostek’s sign
-Trousseau’s sign

47
Q

List some appropriate investigations for hyperparathyroidism

A
  1. serum calcium
  2. Serum PTH
  3. vitamin D level
  4. U+Es + LFTs (albumin)
  5. serum phosphate
  6. ALP
  7. 24 urinary calcium
  8. Consider ABG
  9. X ray (pepper pot skull in primary, rachitic rosary in secondary)
  10. Renal ultrasound (if suspected calculi)
48
Q

Generate a management plan for hyperparathyroidism

A

Managing the hypercalcaemia:
-IV fluids
-Consider bisphosphonate if Ca still high

1st line - parathyroidectomy + monitoring + vit D supplementation

For secondary hyperparathyroidism - treat underlying cause (e.g. phosphate restriction for CKD)

49
Q

List some complications of primary and secondary hyperparathyroidism

A

Primary:
-Osteoporosis
-Bone fractures

Secondary:
-Osteitis fibrosa cystica
-Uraemia

50
Q

List some causes of hypothyroidism

A

Acquired:
-Hashimoto’s thyroiditis (AI)
-Iatrogenic (post-surgery, radioiodine, hyperthyroid meds)
-Iodine excess (Wolff-Chaikoff effect)

Congenital:
-Thyroid agenesis

51
Q

Outline the presenting symptoms of hypothyroidism

A

Cold intolerance
Weight gain
Lethargy
Dry skin
Memory issues
Hair loss
Ataxia
Paraesthesia
Menstrual irregularities

Myxoedema coma - hypoventilation, hypothermia, hyponatraemia, confusion, coma, heart failure

52
Q

List some appropriate investigations

A
  1. Thyroid exam
  2. TFTs (high TSH, low T3/4)
  3. Antibodies (anti-TPO, anti-TG, AMA)
  4. U+Es
  5. lipids
  6. Uptake scan
53
Q

Generate a management plan for hypothyroidism

A
  • low dose levothyroxine (25-200 mcg/day)

NOTE: rule out underlying adrenal insufficiency before starting thyroid medication

54
Q

Generate a management plan for myxoedema coma

A

Oxygen
Rewarming
Rehydration
IV T4/T3
IV hydrocortisone
Treat underlying cause (e.g. infection)

55
Q

What are the features of MEN1?

A

Parathyroid tumours
Pituitary adenomas
Pancreatic islet cell tumours

56
Q

What are the features of MEN2a and MEN2b?

A

MEN2a:
Parathyroid tumours
Phaeochromocytomas
Medullary thyroid cancer

MEN2b:
Mucosal neuromas (e.g. GI tract)
Medullary thyroid cancer
Phaeochromocytomas

57
Q

List some appropriate investigations for MEN1/2

A

serum calcitonin (MEN2)
serum CEA (MEN2)
plasma metanephrines (MEN2)
serum parathyroid hormone and calcium (MEN1/2)
fasting serum gastrin (MEN1)
serum chromogranin A (MEN1)
serum prolactin (MEN1)
insulin-like growth factor-1 (MEN1)
24-hour urine metanephrines and catecholamines (MEN2)
24-hour urine calcium (MEN1/2)
thyroid biopsy (MEN2)

58
Q

Generate a management plan for MEN1/2

A

Treat the symptoms:
-Hyperparathyroidsm - hypercalcaemia pharmacotherapy + surgery
-Gastrinoma - PPI + surgery
-Non-functioning pituitary adenomas - monitor + surgery
-Prolactinomas - dopamine agonists
-Thyroid cancer - surgery + hormone replacement
-Phaeo - surgery + consider short term alpha 1 antagonists and steroid replacement.

59
Q

How is obesity defined?

A

BMI >30kg/m^2

60
Q

Define osteomalacia

A

Metabolic bone disease characterised by incomplete mineralisation of the underlying mature organic bone matrix following growth plate closure in adults

note: in kids it is referred to as Rickets

61
Q

List some risk factors for osteomalacia

A

Dietary Ca and Vit D deficiency
CKD
Limited sunlight exposure
Anticonvulsant therapy

62
Q

Outline the presenting symptoms of osteomalacia

A

diffuse bone pain and tenderness
fractures
proximal muscle weakness

63
Q

List some appropriate investigations for osteomalacia

A

-Serum Ca
-Serum vit D
-Serum phosphate
-U+Es
-PTH
-ALP
-24 hr urinary calcium
-bone x rays/DEXA

64
Q

Generate a management plan for osteomalacia

A

Calcium and vitamin D supplementation
Monitoring

65
Q

Define osteoporosis

A

Skeletal disease characterised by low bone density and micro-architectural defects in bone tissue causing increased bone fragility.
Defined as a T score ≤-2.5

66
Q

List some risk factors for osteoporosis

A

Smoking
Excess alcohol use
Premature menopause
Low BMI
Drugs (steroids, thyroxine)
Cushing’s

67
Q

Outline the presenting symptoms of osteoporosis

A

Usually asymptomatic
May present with fractures
Back pain/loss of height over time (due to vertebral fractures)

68
Q

List some appropriate investigations for osteoporosis

A

DEXA
Bloods - U+Es, Ca, ALP, Albumin, Vit D, PTH, TFTs
Consider X rays

69
Q

What is the difference between a T score and a Z score?

A

T-scores reflect how bone density compares with that of a typical, young, healthy person, whereas Z-scores uses an age-matched control

70
Q

Generate a management plan for osteoporosis

A

Lifestyle measures - increased exercise, weight loss
1st line - Bisphosphonates
Calcium and Vit D supplementation
2nd line - terparatide
3rd line - denusomab

71
Q

What side effect is associated with bisphosphonate treatment?

A

Jaw necrosis

72
Q

Define Paget’s disease of bone

A

A chronic bone disorder that is characterised by focal areas of increased bone remodelling, resulting in overgrowth of poorly organised bone.

73
Q

What are the 3 distinct phases of Paget’s disease?

A
  1. Initial short-lived burst of osteoclastic activity –> bone resorption
  2. Mixed phase of osteoclastic and osteoblastic activity –> abnormally structured bone
  3. Chronic sclerotic phase (bone formation outweighs bone resorption
74
Q

Outline the presenting symptoms/signs of Paget’s disease of bone

A

Mostly asymptomatic
Gradual bone pain (most likely pelvis, long bones + skull)
Frontal bossing (increased size of headwear)
Prognathism
Facial pain + HEARING loss (if skull involvement)

75
Q

List some appropriate investigations for Paget’s disease of bone

A
  1. Examination
  2. Plain X ray
  3. Bone scans
  4. Serum Ca
  5. BONE specific ALP (used for treatment response)
  6. serum ALP
  7. Vit D (this should be normal)
76
Q

What would X rays show in Paget’s disease of bone?

A

lytic changes
fractures
sclerotic picture (later stages)

77
Q

Generate a management plan for Paget’s disease of bone

A

If asymptomatic:
-Observe, regular f/u
-Consider bisphosphonate or calcitonin

Symptomatic:
1st line = bisphosphonate or calcitonin
Physiotherapy
Walking aids
Hearing aids

78
Q

Define phaeochromocytoma

A

Catecholamine-producing tumours that usually arise from chromaffin cells of the adrenal medulla

note: it is NOT an adenoma like in Cushing’s/Conn’s

79
Q

Which genetic syndromes can cause phaeochromocytomas?

A

MEN2a and MEN2b
von Hippel-Lindau syndrome
Neurofibromatosis type 1

80
Q

Outline the presenting symptoms of phaeochromocytomas

A

PAROXYSMAL episodes
Headache (due to malignant hypertension)
Palpitations
Chest pain
Dyspnoea
Sweating
GI sx - N+V, epigastric pain, constipation
Neuro sx - Weakness, tremor, anxiety

81
Q

List some appropriate investigations for phaechromocytomas

A
  1. 24 hr urinary catecholamine/metanephrine collection
  2. Plasma free metanephrines and catecholamines
  3. Genetic testing
  4. Consider MRI or CT adrenal protocol for tumour localisation
82
Q

Generate a management plan for phaeochromocytoma

A

If hypertensive crisis (>180/120) - 1st line phentolamine

If no hypertensive crisis:
1st line = alpha blockers (phenoxybenzamine)
THEN beta blockers (for reflexive tachycardia)
IV fluids
Surgical excision of tumour

83
Q

What are the key presenting features of a non-functioning pituitary adenoma?

A

Headaches
Bitemporal hemianopia
Can have panhypopituitarism

84
Q

What are the Rotterdam criteria for PCOS?

A
  1. Oligomenorrhoea/Amenorrhoea (>2 years)
  2. Hyperandrogenism (biochemical/clinical)
  3. Evidence of cysts on ovaries on USS:
    -≥ 12 follicles in one ovary measuring 2-9mm in diameter
    -Ovarian volume > 10cm3

need 2 of the 3 criteria

85
Q

List some risk factors for PCOS

A

Strong FHx
premature adrenarche
obesity
low birth weight

86
Q

Outline the presenting symptoms of PCOS

A
  • Irregular or absent menstruation
  • Infertility
  • Hirsutism
  • Acne
  • Overweight/ obese
  • Scalp hair loss
    -Depression and other psych factors
    -ACANTHOSIS NIGRICANS
87
Q

List some appropriate investigations for PCOS

A
  1. Hormone profile (progesterone, oestrogen, testosteron, LH, FSH, DHEAS)
  2. Prolactin
  3. TFTs
  4. OGTT
  5. Fasting lipids panel
  6. Pelvic ultrasound/TVUSS
88
Q

Generate a management plan for PCOS

A

Conservative:
-Weigh loss, lifestyle advice

Medical:
If NOT planning pregnancy - COCP, LNG-IUS or Co-cyprindol (useful for hirsuitism)

If planning pregnancy - Clomiphene (+/- metformin)

Surgical:
Not planning pregnancy - laser/electrolysis
Planning pregnancy - laparoscopic ovarian drilling, IVF

89
Q

Outline some complications of PCOS

A

Infertility
T2DM
Pregnancy complications
CVD
NAFLD
Endometrial cancer
HTN
OSA

NOTE: NO INCREASED RISK OF BREAST OR OVARIAN CANCER

90
Q

List some causes of primary aldosteronism

A

Adrenal adenoma (Conn’s syndrome)
Adrenal cortex hyperplasia
Adrenal carcinoma producing aldosterone

91
Q

Outline the pathophysiology of hyperaldosteronism

A

Excess aldosterone leads to increased Na+ and water retention
This leads to hypertension
It also causes increased renal K+ loss leading to hypokalaemia
Renin is suppressed due to NaCl retention

92
Q

Outline the presenting symptoms of primary hyperaldosteronism

A

Usually asymptomatic
HTN
Can get symptoms of hypokalaemia:
-Muscle weakness
-Polyuria/polydipsia
-Parasthesia
-Lethargy
-Tetany
-Mood disturbances

93
Q

List some appropriate investigations for primary hyperaldosteronism

A
  1. Ambulatory blood pressure monitoring
  2. Serum K (LOW)
  3. Serum Na (usually normal because of associated water resorption)
  4. Urinary K (HIGH)
  5. Aldosterone:renin ratio (HIGH due to renin supression)

Consider the following confirmatory tests:
-Salt loading
-CT adrenal/MRI
-Posture stimulation testing

94
Q

Generate a management plan for primary hyperaldosteronism

A

Unilateral:
-adrenalectomy + postop aldosterone antagonists

Bilateral hyperplasia:
-Spironolactone OR Eplerenone OR amiloride

94
Q

What are the different types of prolactinoma?

A

Microadenomas: < 1 cm
Macroadenomas: > 1 cm
Giant Pituitary Adenomas: > 4 cm
Malignant Prolactinoma (RARE)

95
Q

Outline the presenting symptoms of a prolactinoma

A

Women
○ Amenorrhoea/oligomenorrhoea
○ Galactorrhoea
○ Infertility
○ Hirsuitism
○ Reduced libido
Men
○ Symptoms are subtle and develop slowly
○ Reduced libido
○ Reduced beard growth
○ Erectile dysfunction

Note: both can have sx caused by tumour size (headaches, bitemporal hemianopia, cranial nerve palsies)

96
Q

List some appropriate investigations for a prolactinoma

A
  1. Neuro exam
  2. Pregnancy test (if appropriate)
  3. Serum prolactin (>5000mU/L suggests true prolactinoma)
  4. TFTs (hypothyroid stimulates prolactin release)
  5. Pituitary MRI
97
Q

Generate a management plan for a prolactinoma

A

1st line = dopamine agonist (cabergoline)
2nd line = COCP

If macroadenoma or medical treatment ineffective - transphenoidal resection

98
Q

What is SIADH characterised by?

A

Hypotonic hyponatraemia
Concentrated urine
Euvolaemic state

99
Q

Which drugs can cause SIADH?

A

Vincristine
Opiates
Carbamazepine
Chlorpropamide

100
Q

List some causes of SIADH

A

Brain:
-Haemorrhage/thrombosis
-Meningitis
-Abscess
-Trauma
-GBS

Lung:
-Pneumonia
-TB

Tumours:
-SCLC
-Breast cancer
-Lymphoma
-Leukaemia

Metabolic:
-Porphyria
-Alcohol withdrawal

101
Q

Outline the presenting symptoms of SIADH

A

Can be ASYMPTOMATIC
Headache
N+V
Muscle cramp/weakness
Confusion
Drowsiness
Convulsions
Coma

102
Q

List some appropriate investigations for SIADH

A
  1. Serum Na (LOW)
  2. Serum osmolality (LOW)
  3. Serum urea, creatinine
  4. Urine osmolality (HIGH)
  5. Urine Na (HIGH)
  6. Glucose, serum protein and lipids - to rule out pseudohyponatraemia
  7. TFTs
103
Q

Generate a management plan for SIADH

A

1st line: Treat underlying cause
1st line: Fluid restriction to 1L per day
2nd line: Vasopressin receptor antagonists (e.g. tolvaptan)
3rd line: NaCl + furosemide
4th line: demeclocycline

In SEVERE/ACUTE cases - slow IV hypertonic saline and furosemide with close monitoring

104
Q

Give some differentials for SIADH

A

Pseudohyponatraemia
Psychogenic polydipsia
Renal failure
Addison’s disease
Hypothyroidism

105
Q

What complication can be caused by correcting SIADH?

A

Central pontine myelinolysis (demylination of pons) - occurs with rapid correction of hyponatraemia

Characterised by:
-Quadriparesis
-Respiratory arrest
-Fits

106
Q

What are the types of thyroid cancer (from most common to least)

A

Papillary – well-differentiated developed from follicular cells and spreads to N [Psammoma bodies, Orphan Anne nuclei]
Follicular – well-diff developed from follicular cells and rarely spreads to N [Hurthle cells]
Medullary – develops from C cells
Anaplastic – v. rare – fast growing and poorly diff

107
Q

List the presenting features of thyroid cancer

A

Slow-growing neck lump
Discomfort swallowing
Hoarse voice - RED FLAG!!
Cervical lymphadenopathy

108
Q

List some appropriate investigations for thyroid cancer

A
  1. Examination
  2. TFTs (usually normal)
  3. Bone profile
  4. Markers:
    -Thyroglobulin - papillary and follicular
    -Calcitonin - medullary
  5. Thyroid US
  6. Fine-Needle Aspiration Cytology (FNA)
  7. Excision Lymph Node Biopsy

Consider CT/MRI - for staging

109
Q

Generate a management plan for thyroid cancer

A

Surgery
Thyroid hormone replacement

Consider chemotherapy and external radiation

110
Q

Define thyroiditis

A

Inflammation of thyroid gland

111
Q

What are the main types of thyroiditis

A

Hashimoto’s - AI
de Quervain’s - viral
Postpartum
Drug-induced
Ridel’s - fibrosis (woody/craggy lump)

112
Q

What happens to TFTs in thyroiditis

A

Increase in thyroid hormone synthesis causes hyperthyroidism
Then the stores run out and pt becomes HYPOthyroid

113
Q

Outline the presenting symptoms of thyroiditis

A

neck pain
tender, firm, enlarged thyroid
fever
palpitations
sx of hypothyroid
sx due to thyroid gland enlargement (dyspnoea, dysphagia)

114
Q

List some appropriate investigations for thyroiditis

A
  1. Examination of thyroid
  2. TFTs (TSH raised)
  3. ESR/CRP
  4. Antibodies (Anti-TPO, Anti-thyroglobulin, AMA)
  5. Thyroid US
  6. Radionucleotide isotope scanning (usually LOW)
115
Q

Generate a management plan for thyroiditis

A

Mainly supportive care
Thyroid supplementation
Analgesia
Consider corticosteroid

If severe thyrotoxicosis - potassium iodide + pred