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Finals > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Most common type of thyroid cancer?

A

papillary (70%)

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2
Q

Types of thyroid cancer?

A

Papillary (70%)
Follicular (20%)
Medullary (5%)
Anaplastic (1%)

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3
Q

Thyroid cancer which secretes calcitonin?

A

Medullary

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4
Q

Thyroid cancer associated with MEN-2?

A

Medullary

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5
Q

Thyroid cancer not responding to treatment?

A

anaplastic

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6
Q

Thyroid cancer causing pressure symptoms?

A

Anaplastic

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7
Q

Management of Papillary or follicular thyroid cancer?

A
  1. Thyroidectomy
  2. radioiodine to kill residual cells
  3. yearly thyroglobulin levels to detect early recurrance
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8
Q

Management of addisionian crisis?

A

hydrocortisone 100mg IM or IV
Fluids

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9
Q

Causes of Addisionian crisis?

A
  • surgery or sepsis causing acute exacerbation of chronic insufficiency (Addisions, hypopituitarism)
  • adrenal haemorrhage
  • steroid withdrawal
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10
Q

How does addisionian crisis present?

A
  • reduced consciousness
  • hypotension
  • hypoglycaemia, hyponatraemia, hyperkalaemia
  • very unwell patient
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11
Q

TFT pattern for primary hyperthyroidism?

A
  • Low TSH
  • high T4 + T3
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12
Q

TFT pattern for secondary hyperthyroidism?

A
  • High TSH
  • High T4 + T3
    (no negative feedback)
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13
Q

First line hyperthyroidism treatment?

A
  1. symptomatic relief
  2. Carbimazole
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14
Q

causes of primary hyperaldosteronism?

A
  • bilateral idiopathic adrenal hyperplasia (60-70%)
  • adrenal adenoma (Conn syndrome - 20-30%)
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15
Q

features of primary hyperaldosteronism?

A

hypertension
hypokalaemia
metabolic acidosis

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16
Q

investigation for primary hyperaldosteronism?

A

aldosterone/renin ratio = first line (high aldosterone + low renin)

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17
Q

management for primary hyperaldosteronism?

A

depends on cause:
- bilateral adrenal hyperplasia - aldosterone antagonist e.g. spironolactone
- adrenal adenoma (conn syndrome) - surgical

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18
Q

Management of Addisons disease (primary adrenal insufficiency)?

A

hydrocortisone (used to replace cortisol) + flucocortisone (used to replace aldosterone)

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19
Q

Investigations for Cushings syndrome?

A

overnight dexamethasone suppression test
24 hr urinary free cortisol

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20
Q

important side effect of carbimazole + which test?

A

agranulocytosis - FBC

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21
Q

hypothyroid primary TFT pattern?

A

TSH high
low T3+T4

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22
Q

secondary hypothyroid TFT pattern?

A

TSH low
T3+4 low

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23
Q

Treatment for hypothyroid?

A

levothyroxine

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24
Q

Hashimoto/Graves associated antibodies?

A

Anti-TPO (both)
Antithyroglobulin Antibodies (both)
TSH Receptor Antibodies (graves)

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25
Q

Causes of high MCV?

A

hypothyroidism
vit B12/folate
alcohol excess

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26
Q

Kallman syndrome hormone pattern?

A

low LH/FSH + low testosterone (sex hormones)

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27
Q

Kallman syndrome clinical presentation?

A

Delayed puberty,
lack of smell,
hypogonadism,
cryptorchidism,
cleft palate, visual / hearing defects
low LH/FSH
low sex hormones

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28
Q

Management of Kallman syndrome?

A
  • testosterone supplementation
  • gonadotrophin supplementation may result in sperm production if fertility is desired later in life
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29
Q

Hormones released by anterior pituitary?

A

TSH
Adrenocorticotropic Hormone (ACTH)
FSH and LH
Growth Hormone (GH)
Prolactin

30
Q

Hormones released by posterior pituitary?

A

Oxytocin
Antidiuretic Hormone (ADH)

31
Q

Difference between Cushings syndrome and Cushings disease?

A

Cushing’s Syndrome is prolonged abnormal elevation of cortisol.

Cushing’s Disease is where a pituitary adenoma (tumour) secretes excessive ACTH.

32
Q

Investigation for adrenal insufficiency?

A

short synacthen test - cortisol levels should at least double after 1hour… if not then primary insufficency (addisons)

33
Q

Hyperthyroidism with pyrexia, tachycardia and delirium (followed by surgery/infection/traume) - what is it?

A

Thyroid storm

34
Q

Management of Cushings syndrome?

A

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
Q

Clinical features of antiphospholipid syndrome (CLOT)?

A

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
Q

How is antiphospholipid syndrome diagnosed?

A

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
Q

Anti-histone antibodies most likely diagnosis?

A

Drug induced lupus

38
Q

Anti-RNA polymerase + Anti-topoisomerase-1 (Scl-70) antibodies - most likely diagnosis?

A

diffuse cutaneous systemic sclerosis

39
Q

Anti-dsDNA antibodies - most likely diagnosis?

A

SLE

40
Q

Anti- centromere antibodies - most likely diagnosis?

A

CREST syndrome

41
Q

What is systemic sclerosis?

A

Auto-immune condition that causes scleroderma (skin thickening) and vascular injury.

There are two types- limited and diffuse systemic sclerosis.

42
Q

Another name for limited systemic sclerosis?

A

CREST syndrome (Calcinosis, Raynaud’s, oEsophageal dysmotility, Sclerodactyly and Telangiectasia)

43
Q

Which areas of the body does limited systemic sclerosis affect?

A

hands / feet / face

44
Q

what is Sjogren’s syndrome?

A

inflammatory autoimmune disorder characterised by decreased lacrimal and salivary gland secretion, which manifests as dry eyes and dry mouth.

45
Q

Autoantibodies associated with Sjogren’s syndrome?

A

ANA antibodies - non specific
rheumatoid factor - 90% of patients
Anti-Lo and anti-RO (40-90%)

46
Q

what is Schirmer’s test and what does it help diagnose?

A

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
Q

Toxic multinodular goitre management?

A

radioiodine therapy

48
Q

Diabetic neuropathy first line?

A

amitripyline
duloxetine
gabapentin
pregablin

49
Q

thyroid storm management?

A

corticosteroids, PTU and propanolol

50
Q

What is diabetes insipidus/what are the types?

A

Decreased secretion of antidiuretic hormone (ADH) from the pituitary (cranial DI)

OR

an insensitivity to antidiuretic hormone (nephrogenic DI).

51
Q

Investigations for diabetes insipidus?

A

Osmolarity - high serum, low urine (>700 mOsm/kg excludes)

water deprivation test

52
Q

Management of nephrogenic diabetes insipidus?

A

thiazides
low salt/protein diet

53
Q

Management of cranial diabetes insipidus?

A

desmopressin

54
Q

Causes of nephrogenic diabetes insipidus?

A
  • Medications - lithium
  • Genetic mutations in the ADH receptor gene (X-linked recessive inheritance)
  • Hypercalcaemia
  • Hypokalaemia
  • Kidney diseases (e.g., polycystic kidney disease)
55
Q

Causes of cranial diabetes insipidus?

A
  • 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
Q

How does Addison’s disease (primary adrenal insufficiency) present?

A

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
Q

Management of DKA?

A
  • Fluid replacement - first line even if acidotic
  • IV insulin at 0.1 unit/kg/hour
  • correction of electrolyte disturbances
58
Q

What is acromegaly?

A

too much growth hormone usually due to pituitary tumour

59
Q

Investigations for acromegaly?

A

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
Q

Management of acromegaly?

A

trans-sphenoidal surgery - first line

61
Q

Types of hyperparathyroidism?

A

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
Q

Primary / Tertiary hyperparathyroidism management?

A

Cinacalcet (a calcimimetic that mimics the action of calcium on tissues)

Total or subtotal parathyroidectomy

63
Q

Secondary hyperparathyroidism management?

A

treat underlying cause (e.g. vit D supplementation or renal transplant)

64
Q

Patterns of PTH / calcium for primary / secondary / tertiary hyperparathyroidism?

A

Primary - PTH high, calcium high
Secondary - PTH high, calcium low/normal
Tertiary - PTH high, calcium high

65
Q

Presentation of prolactinoma?

A

Headache
Visual disturbance
Females - amenorrhoea, infertility, galactorrhoea, osteoporosis
Males - impotence, loss of libido, galactorrhoea

66
Q

Investigation for prolactinoma?

A

MRI

67
Q

Management of prolactinoma?

A

Medical - dopamine agonists (e.g. cabergoline, bromocriptine)

Surgery - trans-sphenoidal

68
Q

Hypercalcaemia 1st line investigation?

A

PTH level

69
Q

Which drug should be given before removing a pheochromacytoma?

A

phenoxybenzamine (as removal of tumour can release large amount of catecholamines causing refractory hypertension - by pre-blocking the alpha receptors this is prevented.)

70
Q

Complication of fluid resuscitation in DKA (particularly in children)?

A

Cerebral oedema - due to high glucose rapidly falling causing all the water to be sucked out the brain

Finals (18 decks)

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