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Hard stuff to remember > Endocrine > Flashcards

Endocrine Flashcards

1
Q

which receptor type do amines e.g. adrenaline bind to?

A

G protein coupled receptor

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2
Q

what activates nuclear hormone receptors?

A
  • steroid hormones

- thyroid hormones

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3
Q

what receptor does growth hormone work on?

A

tyrosine kinase receptors

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4
Q

What does somatostatin do?

A

-inhibits glucagon and insulin secretion
-decreases stomach acid secretion and production
-inhibits secretion of growth hormone and TSH
(basically inhibits secretion of growth and metabolic hormones)

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5
Q

How is insulin secreted? (5 steps)

A
  1. Glucose enters B cells through GLUT2
  2. if enough glucose enters cell will be phosphorylated by glucokinase (Km = 5mM)
  3. B cell metabolises glucose to ATP
  4. ATP inhibits K+ channels -> cell membrane depolarises
  5. Ca2+ channels open, Ca2+ enters cell and stimulates release of vesicles full of insulin
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6
Q

How does DKA work?

A
  1. no glucose is available so FA oxidised to provide energy giving Acetyl-CoA
  2. if no oxaloacetate available (from glycolysis) to accept Acetyl-CoA in krebs cycle then Acetyl-CoA is diverted to become ketone bodies
  3. accumulation of ketones -> acidosis
  4. insulin cannot move out of blood as no insulin so excreted in urine -> dehydration
  5. lack of insulin meant K+ cannot move into cells -> hyperkalaemia
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7
Q

Diagnosis criteria for diabetes (type 1 or 2)

A
  • HbA1C over 48m/m
  • fasting glucose over 7
  • 2h OGTT or random glucose over 11.1 mmom/L
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8
Q

Some of more common MODY mutations

A
  • mutation in glucokinase meaning its Km is 7 or 8
  • mutations in GLUT-2 channels
  • mutations in Kir6.2 subunit of Katp channels
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9
Q

treatment for Graves/hyperthyroidism in pregnancy

A

propylthiouracil

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10
Q

Hashimoto’s thyoroiditis antibodies

A

anti thyroid peroxidase (anti TPO)

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11
Q

What is de quervain’s/ giant cell thyroiditis?

A
  • transient presence of anti thyroid antibodies
  • post viral infection
  • painful goitre
  • symptoms of hyper then hypo
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12
Q

Genes associated with papillary thyroid cancer

how common is it?

A
  • RET
  • BRAF
  • most common thyroid cancer
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13
Q

Risk factors for papillary carcinoma

A

-exposure to ionising radiation during childhood

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14
Q

histological features of papillary thyroid cancer

A
  • finger-like projections of follicle cells
  • Orphan Annie nuclei (empty nuclei)
  • psammoma bodies (calcium deposits)
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15
Q

where is papillary thyroid cancer going to metastasise to first?

A

-lymphatic vessels and lymph nodes

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16
Q

genes associated with follicular carcinoma

how common is it?

A
  • RAS
  • deactivation of PTEN (tumour suppressor gene)

-second most common thyroid cancer

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17
Q

risk factors fro follicular carcinoma

A

-low dietary iodine intake

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18
Q

what does follicular carcinoma metastasise to first?

A
  • breaks through thyroid fibrous capsule
  • blood vessels
  • liver, bone, brain
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19
Q

Genes associated with medullary carcinoma

A
  • RET

- MEN2a and MEN2b

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20
Q

histological features of medullary carcinoma

A
  • spindle shaped cells

- fibrous deposits around C cells (excessive production of calcitonin)

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21
Q

Whats unusual about medullary thyroid cancer?

A

-can release ectopic hormones e.g. serotonin, VIP

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22
Q

what is the most aggressive thyroid cancer?

A

-anaplastic thyroid cancer

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23
Q

symptoms of thyroid cancer

A
  • solitary painless nodule in thyroid gland
  • usually cold i.e. it doesn’t secrete anything
  • large tumours may compress other structures
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24
Q

What is the Guthrie test?

A
  • newborn screening test
  • detects neonatal metabolic conditions
  • heel prick onto blotting paper
  • from this can get TSH and T4 levels (lack of indicates congenital hypothyroidism)
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25
Q

Addison’s disease biochemistry

A
  • hyponatraemia

- hyperkalaemia

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26
Q

what does zona glomerulosa secrete

A
  • aldosterone

- regulated by K+ and AII

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27
Q

what does zona fasciculata secrete?

A
  • glucocorticoids

- regulated by ACTH

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28
Q

what does zona reticularis secrete?

A

-sex steroids

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29
Q

what does adrenal medulla secrete?

A
  • adrenaline

- noradrenaline

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30
Q

investigations for acromegaly

A
  • comparing IGF1 values to age and sex

- glucose tolerance test (acromegaly is confirmed if glucose does not suppress GH secretion)

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31
Q

examples of dopamine agonists used in the treatment of prolactinoma

A
  • cabergoline

- dostinex

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32
Q

primary aldosteronism features

A
  • hypertension
  • hyperkalaemia
  • alkalosis
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33
Q

investigation for primary aldosteronism

A
  • plasma aldosterone to renin ratio (is aldosterone proportional to renin?)
  • saline suppression test
34
Q

where do neuroblastoma most commonly occur?

A
  • adrenal glands

- young kids

35
Q

10% rule of pheochromocytoma

A
  • 10% extra adrenal
  • 10% bilateral
  • 10% malignant
  • 10% not associated with hypertension
  • 25% familial
36
Q

medical treatment of pheochromocytoma

A

-phenoxybenzamine
-propanolol
(alpha then beta blockade)

37
Q

Defective enzyme in congenital adrenal hyperplasia

A

-21 hydroxylase

38
Q

investigation for congenital adrenal hyperplasia

A

-basal 17-OH progesterone (precursor to aldo and cortico before 21 hydroxylase action)

39
Q

MEN1 tumours

A
  • pituitary
  • parathyroid*
  • bronchial carcinoid
  • enteropancreatic
40
Q

MEN2 tumours

A
  • nerve
  • thyroid C cell (medullary)
  • pheochromocytoma
41
Q

What is McCune-Albright syndrome?

A
  • mutation in gene needed for G protein signalling (GNAS1)
  • autonomous hyper secretion from endocrine glands
  • cafe au lait patches
42
Q

What is Kallman’s syndrome

A
  • hypogonadotrophic hypogonadism
  • failure of production of gonadotrophin releasing hormone
  • no puberty, infertility and no sense of smell
43
Q

how do parathyroid hormones work?

A
  • stimulate osteoblast proliferation and expression of RANK ligand
  • RANK ligand on osteoblasts can stimulate pre-osteoclasts to mature
  • active osteoclasts can then release enzymes which break down bone and release Ca2+
  • PTC also increase reabsorption of Ca2+ in distal convoluted tubule
44
Q

what does calcidiol do?

active vitamin D

A

-increase G.I tract Ca2+ absorption

45
Q

causes of hypocalcamia

A
  • increased phosphate levels e.g. CKD
  • hypoparathyroidism e.g. post thyroidectomy, digeorge syndrome
  • vitamin D deficiency e.g. osteomalacia/rickets
  • drugs e.g. calcitonin, biphosphonates
  • hypomagnasemia
46
Q

why does hypomagnesemia cause hypocalcaemia

A
  • magnesium is needed for cells to release calcium
  • if Mg2+ low then intracellular calcium is too high
  • also inhibits PTH -> hypocalcaemia
47
Q

symptoms of hypocalceamia

A
  • parasthesia -finger, toes, perioral
  • muscle cramps, weakness tetony
  • fatigue
  • bronchospasm
  • QT prolongation
48
Q

Acute hypocalcaemia treatment

A

EMERGENCY!

  • IV calcium gluconate 10ml
  • IV infusate (+/- magnesium)
49
Q

what is a normal bone mineral density?

A

BMD within 1 SD of young adult mean

50
Q

osteopenia definition

A

BMD greater than 1SD below the adult mean

51
Q

osteoporosis definition

A

BMD greater than 2.5 SD deviations below the adult mean

52
Q

What is pagets disease

A

abnormal osteoclastic activity followed by increase osteoblastic activity

53
Q

which cells produce testosterone?

A

leydig cells

54
Q

what do sertoli cells do?

A
  • take up most of testosterone in body

- nourishes developing sperm cells

55
Q

what stimulates testosterone production?

A

LH

56
Q

what stimulates spermatogenesis

A

FSH

57
Q

how long is the follicular phase and what happens in it?

A
  • days 1-14 after menstruation (but variable)
  • growth/increase in ovarian follicles, oestrogen release
  • mediated by FSH
58
Q

how long is luteal phase and what happens in it?

A
  • days 14-28 after menstruation
  • ovulation (day 14), corpus luteum formation and progesterone secretion
  • mediated by LH
59
Q

high frequency of GnRH pulses stimulates what?

A

LH release

60
Q

low frequency of GnRH pulses stimulates what?

A

FSH release

61
Q
  • Low GnRh
  • low FSH and LH
  • oestrogen deficiency
A

hypothalamic pituitary failure (group 1)

e.g. v low BMI

62
Q
  • normal GnRH?
  • normal FSH, raised or normal LH
  • normal oestrogen
A

hypothalamic pituitary dysfunction (type 2)

e.g. PCOS

63
Q
  • normal/increase GnRH?
  • normal/raised FSH and LH
  • oestrogen deficiency
A 
ovarian failure (group 3)
e.g. menopause
64
Q

first line for patient with PCOS seeking fertility treatment

A

clomifine citrate (increase FSH and LH secretion)

65
Q

what is a progesterone challenge test?

A
  • give patient progesterone then stop giving it
  • this should induce a withdrawal bleed
  • no withdrawal bleed suggests low oestrogen as no lining thickening occurring e.g. in hypothalamic hypogonadism
66
Q

what is hydrosalpinx?

A

when fallowing tube becomes blocked and fills with serous fluid

67
Q

mechanism of metformin

A
  • decreases hepatic gluconeogenesis
  • increases peripheral glucose uptake (up-regulates insulin signalling)
  • reduces carbohydrate absorption
  • increases fatty acid oxidation
68
Q

examples of sulphonylureas

A
  • gliclazide (long acting)

- tolbutamide (short acting)

69
Q

mechanism of sulphonylureas

A
  • displace ADP-Mg2+ from SUR1 subunit of KATP channel
  • KATP channel closes which allows beta cell to depolarise
  • depolarisation stimulates insulin release
70
Q

example of Thiazolidinediones (TZDs)

A

-piaglitazone

glitazones

71
Q

Mechanism of TZDs

A
  • activates PPAR gamma
  • PPAR gamma is an transcription factor for insulin signalling and lipid metabolism proteins
  • so enhances action of insulin
72
Q

when are TZDs used?

why might they not be so helpful?

A

-add on to metformin in T2DM

  • weight gain!
  • hepatotoxicity
  • fluid retention (don’t use in those with poor renal function)
  • increased fracture risk
73
Q

Examples of SGLT2 inhibitors

A
  • dapagliflzin
  • canagliflozin
  • empagliflozin
74
Q

where do SGLT2 inhibitors act on kidney?

A
  • sodium glucose transport protein 2

- proximal tubule

75
Q

examples of DPP-4 inhibitors

A

-sitagliptin

gliptins

76
Q

mechanism of DPP-4 inhibitors

A
  • after meal GLP1 and GLP2 released to stimulate release of insulin
  • DDP-4 inhibitors stop GLP proteins being broken down so they have prolonged action
77
Q

examples of GLP-1 receptor agonists

A
  • extenatide
  • liraglutide

note: must be given sub cut

78
Q

GLP-1 receptor agonists mechanism

A
  • mimic action of GLP1
  • GLP1 stimulates insulin secretion
  • longer lasting than endogenous GLP1 as resistant to DPP-4 enzyme
79
Q

Which diabetic meds cause weight gain?

A
  • sulphonylureas
  • pioglitazone
  • insulin
80
Q

which diabetic meds cause weight loss

A
  • metformin (only sometimes)

- SGLT2 inhibitors

Hard stuff to remember (10 decks)

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