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Ned's PassMed notes 2019/20 > Endocrine need to know > Flashcards

Endocrine need to know Flashcards

1
Q

which pancreatic cells produce insulin

A

beta cells

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2
Q

what is the antagonist of insulin

A

glucagon

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3
Q

a random blood glucose of what would diagnose diabetes

A

> 11.1

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4
Q

name the slow onset version of T1DM

A

LADA

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5
Q

name 3 signs of DKA

A

Ab pain
vomiting
signs of systemic shock

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6
Q

what is the target HbA1c for T1DM

A

48-58

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7
Q

what are the 2 main factors contributing to T2DM

A

genetics

diet and lifestyle resulting in obiesity

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8
Q

what is the underlying pathology in T2DM

A

insulin resistance

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9
Q

what is the target HbA1c for T2DM

A

48-53

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10
Q

which 2 drugs can cause type 3 diabetes

A

steroids and anti-psychotics

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11
Q

which 3 endocrine disorders can cause type 3 diabetes

A

cushings

phaeochromocytoma, acromegaly

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12
Q

what is the inheritance pattern of MODY and what distinguishes it form T1DM

A

AD

no auto antibodies present
mild onset of symptoms over months

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13
Q

which drug is used to treat MODY

A

sulphonylureas

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14
Q

define hypoglycaemia

A

blood sugar <4mmol

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15
Q

what are the 3 biochemical markers of DKA

A

hyperglycaemia
ketones in blood
high anon gap acidosis

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16
Q

how is DKA defined

A

a state of insulin DEFICIENCY causing hyperglycaemia and dehydration

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17
Q

which type of diabetes is DKA seen in

A

T1DM

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18
Q

which type of diabetes is Hyperglycemic hyperosmolar syndrome seen in

A

T2DM

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19
Q

how is the presentation of HHS different from DKA

A

HHS is slow onset (days/weeks) and affects mainly elderly

HHS only associated with dehydration, no ketoacidosis as there is residual insulin

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20
Q

tx for HHS

A

insulin sliding scale

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21
Q

what is the most active form of thyroid hormone

A

T3 - needs to be transported bound to a plasma protein (thyroid binding globulin is the main one)

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22
Q

how does graves disease cause hyperthyroidism

A

an AI disease- production of antibodies that. mimic TSH to release T3/T4 in the absence of TSH

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23
Q

what are the 3 antibodies seen in grave’s disease

A

TRAB stimulating
anti-thyroid perioxidase
anti-thyroglobuin

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24
Q

what are 3 specific signs of grave’s

A

pre tibial myxoedema
bilateral exophthalmus
ophthalmoplegia

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25
Q

which cause of hyperthyroidism occurs post virus and how is it treated

A

sub-acute deQuervains thyroiditis

Tx = NSAIDS

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26
Q

what are the TFT results in primary hyperthyroidism

A

high T3/T4

low TSH

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27
Q

what are the TFT results in secondary hyperthyroidism

A

high T3/T4
high TSH

(suggests problem is in the hypothalamus)

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28
Q

what is used to treat hyperthyroidism and what is the major side effect

A

carbimazole - antithyroid medication

agranulocytosis

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29
Q

hashimito’s thyroiditis causes an associated risk of what cancer

A

B cell NHL

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30
Q

what antibody is most commonly seen in hashimoto’s

A

anti-thyroid peroxidase (anti-TPO)

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31
Q

what is the most common cause of hypothyroidism

A

atrophic thyroiditis

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32
Q

what is the tx for hypothyroidism

A

levothyroxine - T4

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33
Q

name the 5 types of thyroid cancer

A
  1. follicular
  2. papillary
  3. medullary
  4. anaplastic
  5. lymphoma
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34
Q

what is the most common type of thyroid cancer

A

papillary

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35
Q

which thyroid cancer presents with orphan Annie nuclei and calcified psammoma bodies on histology

A

papillary

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36
Q

describe the differences in age of patients in papillary vs follicular

A

papillary - younger patients - 20-30y/o

follicular - older patients- >50y/o

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37
Q

which thyroid cancer is associated with abnormal secretion of calcitonin and hypercalcemia

A

medullary

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38
Q

which thyroid cancer is almost always associated with an underlying AI disease (eg-hashimotos)

A

lymphoma

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39
Q

what is the gold standard diagnostic test for thyroid malignancy

A

US guided FNA

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40
Q

what is the name of the enzyme responsible for the production of hydroxyapatite in bone

A

alkaline phosphatase (ALP)

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41
Q

what causes the release of parathyroid hormone

A

it is released in response to lowering of serum calcium

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42
Q

what is the net affect of PTH release

A

increased calcium and reduced phosphate

increased osteoclastic activity and bone resorption (breakdown)

decreased phosphate resorption in the kidneys

stimulation of biologically active vit d

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43
Q

what is the biologically active form of vit D called

A

calcitriol

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44
Q

what is the role of vit D in terms of reabsorption

A

it increases reabsorption of calcium and phosphate in the small intestine and -ivley feedback on PTH release

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45
Q

what is the method of action of biphosphonates

A

prevent bone resorption by killing off osteoclasts

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46
Q

what is the metabolic picture seen in pagets disease of the bone

A

increased osteoblastic and osteoclastic activity causing disorganised and weakened bone formation

47
Q

what is the difference between osteoporosis and osteomalacia/rickets

A

osteoporosis has a low bone mass

osteomalacia/rickets has a normal bone mass but a LOW mineral content within the bone

48
Q

what is the most common cause of primary hyperparathyroidism

A

a solitary parathyroid adenoma (80%)

49
Q

how does hyperparathyroidism present

A

hypertension
bone pain
hypercalcemia - kidney stones, sore bones, stomach groans, and psychiatric moans

50
Q

describe secondary and tertiary hyperparathyroidism

A

elevated PTH in response to hypocalcemia

51
Q

what is the difference between secondary and tertiary hyperPTH

A

secondary is physiological

tertiary is when there is HYPERPLASTIC CHANGES in parathyroid glands due to PROLONGED hypocalcemia

52
Q

causes of 2ndry or tertiary hyperPTH

A

vit D deficiency

CKD

53
Q

what is the biochemical profile of secondary and tertiary hyperPTH

A

Secondary: low Ca, High PTH and PO4.

Tertiary: high calcium, very high PTH, low PO4

54
Q

which 3 cancers can can cause release of PTH and what is the biochemical profile

A

small cell lung
renal
breast

make a protein that mimics PTH

High Ca, low PTH

55
Q

what metabolic imbalance can dehydration cause

A

hypercalcemia
raised albumin
raised urea

56
Q

what does MEN stand for

A

multiple endocrine neoplasia

57
Q

what is MEN

A

a group of genetic endocrine disorders that are associated with the development of multiple hormone secreting tumours

58
Q

what are the 3 types of MEN

A

MEN 1 - 3P’S
MEN 2A - 2P’S
MEN 2B- 1P

59
Q

what 3 tumours are associated with MEN 1 (3P’s)

A

Parathyroid
Pituitary
Pancreas

60
Q

what 3 tumours are associated with MEN 2A (2P’s)

A

parathyroid
pheochromocytoma
thyroid medullary carcinoma

61
Q

what 3 tumours are associated with MEN 2 (1P)

A

pheochromocytoma
medullary thyroid carcinoma
mucosa neuroma
marfanoid appearance

62
Q

where does the pituitary sit

A

the sella turcica of the sphenoid bone

63
Q

what hormones are stored in the posterior pituitary

A

ADH

Oxytocin

64
Q

what hormones are produced and released from the anterior pituitary

A

TSH, LH, FSH, ACTH, GH, prolactin

65
Q

what provides negative control over prolactin release

A

dopamine

66
Q

what test is used to measure GH and ACTH axis

A

insulin tolerance test

67
Q

what should happen to GH and ACTH when you give IV insulin

A

insulin is a natural stimulator of GH and ACTH - there should be cortisol release from ACTH

68
Q

how is an ACTH deficiency and adrenal cortical function tested

A

short synthACTHen test

69
Q

pituitary tumours are almost always what type

A

benign adenomas

70
Q

what is the most common benign pituitary adenoma

A

prolactinoma

71
Q

what is the 1st Line surgical management for a pituitary adenoma

A

trans sphenoidal surgery +/- radiotherapy

72
Q

what is a craniopharngioma

A

a tumour of rathkes pouch, where the pituitary originates

73
Q

what tumour is most likely the causative in 5-15y/os who present with growth retardation

A

craniopharyngioma

74
Q

what drugs can induce a hyperprolactinoma

A

drugs that inhibit dopamine

  1. anti-emetics (metoclopramide, domperidone)
  2. anti-psychotics (typical and atypical)
75
Q

name the 1st line dopamine agonists given in hyperprolactinoma

A

cabergoline and bromocriptine

76
Q

which cancer is associated with acromegaly

A

bowel cancer

77
Q

what CV risks are associated with acromegaly

A

hypertension
LV hypertrophy and failure
increased risk of IHD

78
Q

what is the gold standard diagnosis in acromegaly

A

glucose tolerance test

79
Q

in a physiological GTT, what should happen to the GH levels

A

GH is suppressed by the glucose

80
Q

describe the effect insulin and glucose have on GH and cortisol secretion

A

insulin- increases their secretion

glucose - inhibits their secretion

81
Q

what structural pathology causes acromegaly

A

MACROadenoma

82
Q

what is 1st line management of acromegaly

A

surgical removal of pit tumour +/- radiotherapy

83
Q

what is the 2nd line Pharma management of acromegaly and describe its MOA

A

somatostatin analogue - it is the natural analogue of GH

reduces GH secretion by providing negative feedback and blocking peripheral action

84
Q

describe the difference between central and nephrogenic diabetes insidious

A

central DI = failure to produce ADH

nephropgenic DI = failure of kidneys to respond to the ADH

85
Q

what drug can cause nephrogenic DI

A

lithium

86
Q

how is diabetes insipidus defined

A

passage of large volumes (>3l) of water per day

87
Q

what is the gold standard test for DI and how does it work

A

water deprivation test - will indicate if body is able to concentrate urine

if urine cannot be concentrated then DI can be diagnosed (osmolality >600 is indicative)

88
Q

what is the action of ADH

A

it stimulates aquaporins to open and reabsorb water

89
Q

after water deprivation test, how is central DI differentiated from nephrogenic DI

A

synthetic ADH is given.
If concentration of urine is seen, it suggests central DI

No concentration of urine suggests nephrogenic DI

90
Q

how is central DI treated

A

desmopressin (synthetic ADH )

91
Q

how is nephrogenic DI treated

A

thiazide diuretics - generate hyponatremia and drive water reabsorption

92
Q

what is produced in the zona glomerulosa of adrenal gland (outer layer)

A

mineralocorticoids

93
Q

what is produced in the zona fasciculata of adrenal gland (middle layer)

A

glucocorticoids

94
Q

what is produced in the zona reticularis of adrenal gland (inner layer)

A

androgen precursors

95
Q

what is produced in the medulla of the adrenal gland

A

catchecolamines (adrenaline and noradrenaline)

96
Q

what is the pathophysiology of primary adrenal dysfunction

A

failure within the adrenal glands so reduced cortisol and aldosterone released

97
Q

what is the most common cause of primary adrenal dysfunction

A

AI - Addison’s disease

98
Q

what causes the hyperpigmentation of skin in primary adrenal insufficiency

A

increased levels of ACTH

ACTH is upregulated in an attempt to increase cortisol production

99
Q

what is the Na, K and glucose in primary adrenal dysfunction

A

Low Na, glucose

high K+

100
Q

what is the diagnostic test for primary adrenal insufficiency

A

short synACTHen test

101
Q

what is the treatment of primary adrenal deficiency

A

mostly steroid replacement

aldosterone def - give fludrocortisone

cortisol def - hydrocortisone

102
Q

what should be done on sick days with steroid treatment

A

double the dose of steroids for at least 1 week

103
Q

what is raised 17 hydroxyprogesterone diagnostic of

A

bilateral adrenal hyperplasia

104
Q

what can long term, excessive steroid use cause

A

secondary adrenal insufficiency - synthetic steroids cause dampening down of the steroid axis

105
Q

in secondary adrenal insufficiency, are both steroid types reduced

A

NO - only corticosteroids

mineralocorticoids are under control of RAAS so aren’t affected by ACTH deficiency

106
Q

what makes secondary adrenal insufficiency clinically different from primary

A

no dehydration

no skin pigmentation - the ACTH isnt being produced

107
Q

what is the treatment of secondary adrenal insufficiency

A

oral hydrocortisone

108
Q

what is the diagnostic test for primary hyperaldosteronism

A

plasma aldosterone:renin ratio >750

saline suppression test - inability to suppress aldosterone production by >50% following water consumption

109
Q

what is the diagnostic test in cushing’s

A

48 hour dexamethasone suppression test

110
Q

what is the screening test for cushing’s

A

overnight dexamethasone suppression test

111
Q

what do phaeochromocytoms mostly produce

A

noradrenaline

112
Q

what are the 4 main symptoms of a pheochromocytoma

A

headache e
palpitations
sweating
hypertension

113
Q

before surgery can be carried out for a pheochromocytoma, what needs to be done

A

protect blood pressure!

give alpha blocker FOLLOWED BY beta blocker

Ned's PassMed notes 2019/20 (17 decks)

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