Endo part 1 Flashcards

1
Q

typical biochemical pattern for primary hyperparathyroidism

A
  • excessive autonomous secretion of PTH
  • from parathyroid gland
  • results in usually mild hypercalcaemia
  • and low serum phosphate
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2
Q

74 y/o lady, 6 month history of

  • worsening confusion
  • unintentional weigh tloss
  • low back pain

PMH
- hypothyroidism managed with levothyroxine

blood results show

  • raised calcium
  • raised urea
  • normocytic anaemia

most likely cause of hypercalcaemia?

A

Multiple myeloma

  • combo of hypercalcaemia, normocytic anaemia and renal failure seen more so in MM situation
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3
Q

why does hypercalcaemia arise in patients with mulitiple myeloma?

A
  • aar of tumour induced osteoclastic bone destruction
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4
Q

which type of diuretics are shown to worsen hypercalcaemia?

A
  • indapamide

- thiazide

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5
Q

carpal spasm on inflation of BP cuff to pressure above systolic is known as

A

trousseau’s sign

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6
Q

phalens sign seen in

A

carpal tunnel syndrome

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7
Q

chvosteks sign indicates

A

hypocalcaemia

tap over parotid cn7

causes facial muscles to twitch

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8
Q

froments sign is seen in

A

ulnar nerve palsy

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9
Q

describe primary hypoparathyroidism

A
  • decrease in PTH secretion
  • e.g. secondary to thyroid surgery
  • leads to low calcium
  • leads to high phosphate
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10
Q

how may primary hypothyroidism be treated?

A
  • with alfacalcidol (vit d)
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11
Q

summarise main symptoms of hypoparathyroidism secondary to hypocalcaemia

A
  • tetany (muscle twitching, cramping and spasm)
  • perioral paraesthesia
  • trousseaus sign
  • chvosteks sign
  • if chronic: depression, cataracts
  • prolonged QT interval on ECG
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12
Q

hypocalcaemia as seen on ECG

A
  • prolonged QT interval on ECG
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13
Q

how does psuedohypoparathyroidism come about?

A
  • target cells being insensitive to PTH
  • due to abnormality in a G protein
  • low calcium, high phosphate , high PTH
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14
Q

pseudohypoparathyroidism associated with what three clinical features

A
  • low IQ
  • short stature
  • shortened 4th and 5th metacarpals
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15
Q

how is diagnosis of psuedohypoparathyroidism made?

A
  • measuring urinary cAMP and phosphate following infusion of PTH

In pseudohypoparathyroidism type I neither cAMP nor phosphate levels are increased whilst in pseudohypoparathyroidism type II only cAMP rises.

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16
Q

Pseudopseudohypoparathyroidism

A

similar phenotype to pseudohypoparathyroidism but normal biochemistry

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17
Q

which medication may result in galactorrhoea and why?

A
  • metoclopramide
  • its a dopamine receptor antagonist (migraines)
  • dopamine normally inhibits prolactin
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18
Q

spironolactone is

A
  • aldosterone antagonist

- known to cause gynaecomastia

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19
Q

what is Kallman’s syndrome

A
  • delayed puberty secondary to hypogonadotrophic hypogonadism
  • LH and FSH are low or normal
  • sex hormone levels are low
  • often have lack of smell
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20
Q

21-hydroxylase deficiency occurs due to

A
  • congenital adrenal hyperplasia

- characterised by virilisation of female genitalia and precocious puberty in males

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21
Q

what is klinefelter syndrome?

A

47, XXY

  • infertility
  • small poorly functioning testicles
  • characterised by low testosterone
  • increased levels of FSH and LH
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22
Q

what is androgen insensitivity syndorme?

A
  • x-linked recessive
  • due to end organ resistance to testosterone
  • genotypically male children 46 XY will tend to have female phenotype
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23
Q

key features of kallman’s syndrome

A
  • delayed puberty
  • hypogonadism, cryptorchidism
  • anosmia (lack of smell)
  • sex hormone slow
  • LH, FSH inappropriately low
  • patients often normal or above average height
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24
Q

what is a characteristic x-ray finding of hyperparathyoidism in the head?

A

pepperpot skull

  • excess PTH
  • excess osteoclastic acitivity
  • osteolytic lesions on skull
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25
Q

pregnant women with hypothyroidism may need to have what management done?

A
  • increase in their thyroid hormone replacement dose by up to 50%
  • woman’s need for levothyroxine will increase during pregnancy
26
Q

what is firstline investigation in suspected primary hyperaldosteronism?

A
  • plasma aldosterone / renin ratio
27
Q

which test is used to diagnose cushings syndrome?

A
  • dexamethasone suppression test
28
Q

patients with cushings typically present with?

A
  • central obesity
  • abdominal striae
  • hypertension
  • hyperglycaemia
29
Q

which test used to diagnose Addison’s disease?

A
  • short synacthen test
30
Q

addisons disease characterised by

A
  • hypoaldosteronism

- patients presenting with weakness, anorexia, weight loss, hyperpigmentation, hyponatraemia and hyperkalaemia

31
Q

primary hyperalodsteronism thought to be caused by :

A
  • commonly by adrenal adenoma known as Conns syndrome
32
Q

what is hashimoto’s thyroiditis?

A
  • autoimmune cause of hypothyroidism

- caused by autoantibodies attacking thyroid (anti-thyroid peroxidase, antithyroglobulin)

33
Q

features of hashimoto’s thyroiditis

A
  • weight gain
  • tiredness
  • cold intolerance
  • pooor concentration
  • nontender goitre on examination
34
Q

where is calcitonin made?

A
  • peptide hormone

- made and secreted by parafollicular cells

35
Q

calcitonin role

A
  • inhibit osteoclasts

- oppose PTH

36
Q

papillary carcinoma notes

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

37
Q

Follicular adenoma notes

A

Usually present as a solitary thyroid nodule

Malignancy can only be excluded on formal histological assessment

38
Q

Follicular carcinoma notes

A

May appear macroscopically encapsulated,
microscopically capsular invasion is seen.

Without this finding the lesion is a follicular adenoma.

Vascular invasion predominates
Multifocal disease raree

39
Q

medullary carcinoma notes

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.

40
Q

Anaplastic carcinoma notes

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.

41
Q

34 y/o female patient

  • feeling thirsty all the time
  • polyuria pale urine
  • weakness in arms
  • occassional palpitations
  • low potassium
A

primary hyperaldosteronism suspected

42
Q

describe subacute thyroiditis aka de quervains thydroiditis

A
  • thought to occur post viral infection

features

  • hyperthyroisim
  • painful goitre
  • raised ESR
  • globally reduced uptake on iodine-131 scan
43
Q

drug used to treat hyperthyroidism

A

carbimazole

44
Q

worsening fatigue, thirst, anorexia, constipation, and general aches and pains are all indicative to

A

hypercalcaemia

45
Q

tertiary hyperparathyroidism

A
  • usually occurs after prolonged secondary hyperparathyroidism
  • glands become autonomous
  • produce excessive PTH even after initial cause of hypocalcaemia has been corrected
46
Q

If there is clubbing with hyperthyroidism, think

A

Grave’s disease

47
Q

In type 1 diabetics, a general HbA1c target of ……. should be used

A

48 mmol/mol

48
Q

treatment of choice for toxic multinodular goitre

A

radioactive iodine

49
Q

A 42-year-old man presents to the emergency department with a headache, sweating and palpitations. These symptoms have been ongoing for the last hour and he feels they are worsening.

On examination, his blood pressure is found to be 180/90 mmHg and a fine tremor is noted in both hands. His urine is sampled and shows raised levels of urinary metanephrines

Given this man’s presentation, what is the most appropriate first-line treatment?

A

Phaeochromocytoma

  • raised BP
  • raised urinary metanephrines
  • palpitations, tremor and headache
50
Q

what type of drug is amlodipine

A

calcium channel blocker

51
Q

propranolol is a

A

beta blocker

52
Q

action of metformin

A
  • reduces peripheral insulin sensitivity

- reduces gluconeogenesis

53
Q

myxoedema coma typically presents with

A

confusion and hypothermia

54
Q

In type 1 diabetics, blood glucose targets:

on waking
before meals at other times of the day

A

5-7 mmol/l on waking

4-7 mmol/l before meals at other times of the day

55
Q

The symptoms of polyuria, nocturia and chronic thirst, combined with a pre-existing diagnosis of chronic kidney disease (CKD) suggests

A

nephrogenic diabetes insipidus

56
Q

how does nephrogenic diabetes insipidus result

A
  • renal insensitivity to ADH
  • preventing the concentration of urine
  • water deprivation test should be done
57
Q

how does the short synacthen test worth

A
  • synacthen is a synthetic ACTH analogue

- should stimulate cortisol secretion from the adrenal glands

58
Q

The primary mode of action of orlistat is to …

A

inhibit pancreatic lipases

in turn will decrease absorption of lipids from the intestine

59
Q

A 19-year-old with type 1 diabetes presents to the Emergency Department feeling unwell. She states she has had vomiting and diarrhoea for 2 days and has not been taking her full insulin doses as she has been off her food. Her capillary glucose is 37 mmol/l and there are 4+ ketones on urinalysis.

classic presentation of

A

diabetic ketoacidosis

60
Q

Whipple’s triad of symptoms are hallmark for an…

A

insulinoma

61
Q

what is Whipple’s triad of symptoms?

A
  1. hypoglycaemia with fasting or exercise
  2. reversal of symptoms with glucose
  3. recorded low BMs at time of symptoms