1
Q
Most common type of thyroid cancer?
A
papillary (70%)
2
Q
Types of thyroid cancer?
A
Papillary (70%)
Follicular (20%)
Medullary (5%)
Anaplastic (1%)
3
Q
Thyroid cancer which secretes calcitonin?
A
Medullary
4
Q
Thyroid cancer associated with MEN-2?
A
Medullary
5
Q
Thyroid cancer not responding to treatment?
A
anaplastic
6
Q
Thyroid cancer causing pressure symptoms?
A
Anaplastic
7
Q
Management of Papillary or follicular thyroid cancer?
A
- Thyroidectomy
- radioiodine to kill residual cells
- yearly thyroglobulin levels to detect early recurrance
8
Q
Management of addisionian crisis?
A
hydrocortisone 100mg IM or IV
Fluids
9
Q
Causes of Addisionian crisis?
A
- surgery or sepsis causing acute exacerbation of chronic insufficiency (Addisions, hypopituitarism)
- adrenal haemorrhage
- steroid withdrawal
10
Q
How does addisionian crisis present?
A
- reduced consciousness
- hypotension
- hypoglycaemia, hyponatraemia, hyperkalaemia
- very unwell patient
11
Q
TFT pattern for primary hyperthyroidism?
A
- Low TSH
- high T4 + T3
12
Q
TFT pattern for secondary hyperthyroidism?
A
- High TSH
- High T4 + T3
(no negative feedback)
13
Q
First line hyperthyroidism treatment?
A
- symptomatic relief
- Carbimazole
14
Q
causes of primary hyperaldosteronism?
A
- bilateral idiopathic adrenal hyperplasia (60-70%)
- adrenal adenoma (Conn syndrome - 20-30%)
15
Q
features of primary hyperaldosteronism?
A
hypertension
hypokalaemia
metabolic acidosis
16
Q
investigation for primary hyperaldosteronism?
A
aldosterone/renin ratio = first line (high aldosterone + low renin)
17
Q
management for primary hyperaldosteronism?
A
depends on cause:
- bilateral adrenal hyperplasia - aldosterone antagonist e.g. spironolactone
- adrenal adenoma (conn syndrome) - surgical
18
Q
Management of Addisons disease (primary adrenal insufficiency)?
A
hydrocortisone (used to replace cortisol) + flucocortisone (used to replace aldosterone)
19
Q
Investigations for Cushings syndrome?
A
overnight dexamethasone suppression test
24 hr urinary free cortisol
20
Q
important side effect of carbimazole + which test?
A
agranulocytosis - FBC
21
Q
hypothyroid primary TFT pattern?
A
TSH high
low T3+T4
22
Q
secondary hypothyroid TFT pattern?
A
TSH low
T3+4 low
23
Q
Treatment for hypothyroid?
A
levothyroxine
24
Q
Hashimoto/Graves associated antibodies?
A
Anti-TPO (both)
Antithyroglobulin Antibodies (both)
TSH Receptor Antibodies (graves)
25
Causes of high MCV?
hypothyroidism
vit B12/folate
alcohol excess
26
Kallman syndrome hormone pattern?
low LH/FSH + low testosterone (sex hormones)
27
Kallman syndrome clinical presentation?
Delayed puberty,
lack of smell,
hypogonadism,
cryptorchidism,
cleft palate, visual / hearing defects
low LH/FSH
low sex hormones
28
Management of Kallman syndrome?
- testosterone supplementation
- gonadotrophin supplementation may result in sperm production if fertility is desired later in life
29
Hormones released by anterior pituitary?
TSH
Adrenocorticotropic Hormone (ACTH)
FSH and LH
Growth Hormone (GH)
Prolactin
30
Hormones released by posterior pituitary?
Oxytocin
Antidiuretic Hormone (ADH)
31
Difference between Cushings syndrome and Cushings disease?
Cushing’s Syndrome is prolonged abnormal elevation of cortisol.
Cushing’s Disease is where a pituitary adenoma (tumour) secretes excessive ACTH.
32
Investigation for adrenal insufficiency?
short synacthen test - cortisol levels should at least double after 1hour... if not then primary insufficency (addisons)
33
Hyperthyroidism with pyrexia, tachycardia and delirium (followed by surgery/infection/traume) - what is it?
Thyroid storm
34
Management of Cushings syndrome?
treat underlying cause - surgery usually.
if surgical removal of cause not available then surgically remove both adrenal glands + long standing steroid replacement
Metyrapone - reduces production of cortisol (occasionally used)
35
Clinical features of antiphospholipid syndrome (CLOT)?
Clots - PE or DVT
Livedo reticularis - A mottled, lace-like appearance of the skin on the lower limbs.
Obstetric loss - miscarriages, pre-eclampsia and premature birth
Thrombocytopenia
(+cardiac valve disease)
36
How is antiphospholipid syndrome diagnosed?
One or more of the following positive blood tests are needed on 2 occasions, 12-weeks apart to diagnose APS:
1. Anti-cardiolipin antibodies.
2. Anti-beta2-GPI antibodies.
3. Positive lupus anticoagulant assay.
37
Anti-histone antibodies most likely diagnosis?
Drug induced lupus
38
Anti-RNA polymerase + Anti-topoisomerase-1 (Scl-70) antibodies - most likely diagnosis?
diffuse cutaneous systemic sclerosis
39
Anti-dsDNA antibodies - most likely diagnosis?
SLE
40
Anti- centromere antibodies - most likely diagnosis?
CREST syndrome
41
What is systemic sclerosis?
Auto-immune condition that causes scleroderma (skin thickening) and vascular injury.
There are two types- limited and diffuse systemic sclerosis.
42
Another name for limited systemic sclerosis?
CREST syndrome (Calcinosis, Raynaud's, oEsophageal dysmotility, Sclerodactyly and Telangiectasia)
43
Which areas of the body does limited systemic sclerosis affect?
hands / feet / face
44
what is Sjogren's syndrome?
inflammatory autoimmune disorder characterised by decreased lacrimal and salivary gland secretion, which manifests as dry eyes and dry mouth.
45
Autoantibodies associated with Sjogren's syndrome?
ANA antibodies - non specific
rheumatoid factor - 90% of patients
Anti-Lo and anti-RO (40-90%)
46
what is Schirmer's test and what does it help diagnose?
demonstrates reduced tear production using a strip of filter paper on the lower eyelid, with wetting of <5 mm being positive
+ve in Sjogren's syndrome
47
Toxic multinodular goitre management?
radioiodine therapy
48
Diabetic neuropathy first line?
amitripyline
duloxetine
gabapentin
pregablin
49
thyroid storm management?
corticosteroids, PTU and propanolol
50
What is diabetes insipidus/what are the types?
Decreased secretion of antidiuretic hormone (ADH) from the pituitary (cranial DI)
OR
an insensitivity to antidiuretic hormone (nephrogenic DI).
51
Investigations for diabetes insipidus?
Osmolarity - high serum, low urine (>700 mOsm/kg excludes)
water deprivation test
52
Management of nephrogenic diabetes insipidus?
thiazides
low salt/protein diet
53
Management of cranial diabetes insipidus?
desmopressin
54
Causes of nephrogenic diabetes insipidus?
- Medications - lithium
- Genetic mutations in the ADH receptor gene (X-linked recessive inheritance)
- Hypercalcaemia
- Hypokalaemia
- Kidney diseases (e.g., polycystic kidney disease)
55
Causes of cranial diabetes insipidus?
- Brain tumours
- Brain injury
- Brain surgery
- Brain infections (e.g., meningitis or encephalitis)
- Genetic mutations in the ADH gene (autosomal dominant inheritance)
- Wolfram syndrome (a genetic condition also causing optic atrophy, deafness and diabetes mellitus)
- haemochromatosis
56
How does Addison's disease (primary adrenal insufficiency) present?
Fatigue
Muscle weakness
Muscle cramps
Dizziness and fainting
Thirst and craving salt
Weight loss
Abdominal pain
Depression
Reduced libido
Hyperpigmentation
hypotension
hyponatraemia and hyperkalaemia
57
Management of DKA?
- Fluid replacement - first line even if acidotic
- IV insulin at 0.1 unit/kg/hour
- correction of electrolyte disturbances
58
What is acromegaly?
too much growth hormone usually due to pituitary tumour
59
Investigations for acromegaly?
measure insulin-growth factor 1 (IGF-1)
If raised then OGTT - check if GH suppressed (if no then acro)
MRI when confirmed to see tumour size
60
Management of acromegaly?
trans-sphenoidal surgery - first line
61
Types of hyperparathyroidism?
Primary - one parathyroid gland (or more) produces excess PTH - usually due to tumour.
Secondary - there is increased secretion of PTH in response to low calcium because of kidney, liver, or bowel disease (e.g. vit D deficiency, CKD)
Tertiary - happens when secondary hyperparathyroidism continues for an extended period, after which the underlying cause is treated - this is due to growth of the gland.
62
Primary / Tertiary hyperparathyroidism management?
Cinacalcet (a calcimimetic that mimics the action of calcium on tissues)
Total or subtotal parathyroidectomy
63
Secondary hyperparathyroidism management?
treat underlying cause (e.g. vit D supplementation or renal transplant)
64
Patterns of PTH / calcium for primary / secondary / tertiary hyperparathyroidism?
Primary - PTH high, calcium high
Secondary - PTH high, calcium low/normal
Tertiary - PTH high, calcium high
65
Presentation of prolactinoma?
Headache
Visual disturbance
Females - amenorrhoea, infertility, galactorrhoea, osteoporosis
Males - impotence, loss of libido, galactorrhoea
66
Investigation for prolactinoma?
MRI
67
Management of prolactinoma?
Medical - dopamine agonists (e.g. cabergoline, bromocriptine)
Surgery - trans-sphenoidal
68
Hypercalcaemia 1st line investigation?
PTH level
69
Which drug should be given before removing a pheochromacytoma?
phenoxybenzamine (as removal of tumour can release large amount of catecholamines causing refractory hypertension - by pre-blocking the alpha receptors this is prevented.)
70
Complication of fluid resuscitation in DKA (particularly in children)?
Cerebral oedema - due to high glucose rapidly falling causing all the water to be sucked out the brain
Finals
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