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Year 2 BRS Endo > endo all > Flashcards

endo all Flashcards

1
Q

what projects signals to posterior pituitary?

A

magnocellular neurons in hypothalamus

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2
Q

Pituitary cells?

A

Somatatrophs : somatostatin , growth hormones

corticotrophs; Adrenocorticotropic hormone

lactotrophs : prolactin

thyrothrophs: TSH
gonadotrophs: FSH,LH

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3
Q

primary hypothyroidism?

A

defect in the gland - autoimmune

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4
Q

secondary hypothyroidism

A

disorder of thyrotrophs - anterior pituitary

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5
Q

why is anterior piuitary more susceptible to sheehans ?

A

the blood supply to anterior-pituitary is at increased risk of damage because it is supplied mainly by long hypophyseal vessels and portal capillaries in pituitary stalk and blood supply to posterior gland is less susceptible to damage as it is supplied by short hypophyseal vessels.

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6
Q

Pituitary apoplexy

A

is severe bleeding in or loss of blood flow to the pituitary gland

associated with pituitary blood supply

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7
Q

presentation

of Pituitary apoplexy

A

Severe sudden onset headache
Visual field defect – bitemporal hemianopia, diplopia, ptosis
↓ Secretion of hormones

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8
Q

how does hypopituitarism present - fsh/lh impacts ?

A

reduced libido
secondary amenorrhoea
Erectile dysfunction
Reduced pubic hair

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9
Q

Presentation of Hypopituitarism

ACTH

A

ACTH
Fatigue
NB Not a salt losing crisis (renin-angiotensin)

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10
Q

Presentation of Hypopituitarism TSH

GH

PRL

A

Reduced quality of life
NB short stature only in children

fatigue

Inability to breastfeed

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11
Q

why are MRI preferred for imaging the pituitary?

A

Pituitary MRI (CT not so good at delineating pituitary gland)

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12
Q

Biochemical markers for hypopituitarism

A

[basal plasma]
T4 - long half life about 3 months

fsh/Lh - cyclical

Gh/ACTH - pulsatile

take with caution as variable

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13
Q

functioning pituitary tumours

A

prolactinoma
acromegaly
cushings disease

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14
Q

Presentation of Prolactinoma

A

Lactotroph pituitary adenoma galactorrhea
fatigue
erectile dysfunction

reduced libido
impacts menstrual cycle
subfertility

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15
Q

why does having a prolactinoma impact sex?

A

reduced libido, erectile dysfunction and vaginal dryness
impotence

  • due to prolactin reducing FSH/LH production - so decreased oestrogen and testosterone = low sperm count and ovulation
  • inhibition of kisspeptin neuron
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16
Q

treatment for Prolactinoma?

A

Dopamine receptor agonist, e.g. BROMOCRIPTINE, CABERGOLINE

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17
Q

why are dopamine receptor agonist used to treat Prolactinoma?

A

physiologically dopamine binds to d2 receptors on anterior pituitary lactotrophs and inhibits prolactin release; so dopamine receptor agonist do the same thing and eventually shrink the tumour

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18
Q

acromegaly

presentation

physical signs

complaints

A

excess growth hormone
somatotrophs

=overgrowth : tongue,nose,jaw,hand/feet size

Bi-temporal hemianopia
headaches
excessive sweating

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19
Q

diagnosis of Acromegaly

A

serum IGF-1 raised

oral glucose tolerance test

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20
Q

why is a glucose test done on someone with suspected acromegaly?

A
  • GH is a stress hormone so is released in response to low glucose in blood

if glucose is given and there is no suppression of GH that is abnormality

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21
Q

why is IGF-1 measure not GH? What is IGF-1?

A
  • insulin like growth factor 1

when GH travels to liver- produces IGF-1 so a good serum marker to see release of GH

GH itself is pulsatile so not useful to measure randomly

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22
Q

treatment of acromegaly?

A

CVd risk so need to treat

  • transphenoidal surgery
    Inhibition of GH release by somatostatin analogues
    dopamine agonists: expression of dopamine receptors on these tumours mean gd target and dopamine inhibits GH
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23
Q

Cushing Disease

A

excess cortisol
- too much ACTH

proximal myopathy 
depression 
High BP
diabetes 
osteoporosis
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24
Q

diagnosis of Cushing

A

24h urine free cortisol test will show continually elevated cortisol, high late night cortisol

oral DEXAMETHASONE : cortisol still not suppressed

25
Q

why is oral dexamethasone given to test for cushing?

A

oral dexamethasone acts like a synthetic cortisol

so should cause suppression of cortisol release from adrenal cortex but in someone with hypercortisolism it wont be suppressed

26
Q

non -functioning pit adenoma

A

bitemporal hemianopia

compression of optic chiasm

27
Q

ADh promotes water reabsoroption from where?

A

renal collecting ducts via V2 receptors

28
Q

Stimuli for vasopressin release are:

______sensed by ______ in the hypothalamus ; Process: ______are special neurons in the hypothalamus that sense _____

A
  • increased plasma osmolality (concentration)
  • osmoreceptors
  • osmoreceptors

-
plasma osmolality

29
Q

Diabetes insipidus

polyuria, nocturia & polydipsia

A

inability to make vasopressin

30
Q

Desmopressin test

A

Desmopressin is a synthetic VP

so if cranial - giving DDAVP would concentrate urine and increase water reabsorption

if nephrogenic -rarer- no response to DDAVP

31
Q

how to treat nephrogenic

cranial

DI?

A
  • thiazide diuretics

- desmopressin

32
Q

if someone has a low urine osmolality after DDAVP administration what does it mean?

A

low urine osmolality means urine is not concentrated = Lots of water loss

if no response to DDAVP then it means they have Nephrogenic diabetes insipidus

33
Q

SIADH?

A

Syndrome of inappropriate antidiuretic hormone secretion

34
Q

SIADH pathophysiology and presentation?

A

too much adh
> water reabsorption [alot]
> blood volume is HIGH hypervolemic

> sodium loss?? hyponatraemia

35
Q

other actions of Vasopressin?

A

vasoconstrictor - V1 receptor

stim ACTH release anterior pituitary

36
Q

non osmotic stimuli for ADH?

A

Decrease in atrial pressure sensed by atrial stretch receptors

37
Q

why can nuclei of posterior pituitary respond to systemic circulatory changes?

[osmoreceptors- 3rd ventricle]

A

no blood brain barrier

38
Q

why is the non osmotic stimuli for ADh important?

such as reduction in circulating volume

A

restore blood volume in case of haemorrhage

by increasing water reabsorption

vasoconstriction via v1 receptors also

39
Q

cause of Nephrogenic diabetes

A

genetic : mutated V2, aquoporin 2

drugs : lithium

40
Q

management of SIADH?

A

Fluid restriction

Vaptan (vasopressin antagonist (binds to v2 receptors))

41
Q

causes of SIADH

A 
CNS
- Head injury, stroke, tumour, 
Pulmonary disease
- Pneumonia, bronchiectasis
Malignancy
- Lung cancer (small cell)
Drug-related
- Carbamazepine, - Serotonin Reuptake Inhibitors (SSSRIs)
Idiopathic
42
Q

management of hyperthyroidism

drugs

A

First 3 drugs reduce thyroid hormone synthesis
β blockers help with symptoms

Thionamides 🡪 inhibit thyroid peroxidase and hence inhibit T3/T4 synthesis
B-blockers e.g. propranolol reduce tremor, tachycardia
Potassium iodine inhibits

43
Q

how does potassium iodine work?

A

fills up thyroid with stable iodine so radioactive iodine cannot be taken up - reduces T4/T3 production

44
Q

radioiodine moa?

what is it used for?

A

Hyperthyroidism
destroys cells in thyroid gland
= reduces thyroxine levels and size of gland
radiation destroys the overactive cells

45
Q

Cushing diagnosis?

A

24hr urine free cortisol
blood diurnal levels
low dose dexamethasone suppression test

> dexamethasone acts like cortisol so upon administration normal physiological response would be for serum cortisol to go down- failure to suppress= cushing

46
Q

what tumour can cause cushings syndrome?

A

ectopic ACTH lung cancer

adrenal adenoma secreting cortisol

pituitary tumour - Cushing disease

47
Q

High acth

A

cushings disease

48
Q

low ACTH : cushings syndrome?

A

steroid medication

adrenal adenoma

49
Q

Ketoconazole = antifungal; risk of hepatotoxicity (possibly fatal liver damage) so use is not advised but it is still prescribed. Mainly blocks 17α hydroxylase, inhibiting cortisol production. control of cushings syndrome prior to surgery

A

= antifungal; risk of hepatotoxicity (possibly fatal liver damage) so use is not advised but it is still prescribed. Mainly blocks 17α hydroxylase, inhibiting cortisol production. control of cushings syndrome prior to surgery

50
Q

Metryrapone

A

Metryrapone = inhibition of 11β-hydroxylase; steroid synthesis in the zona fasciculata [and reticularis] is arrested at the 11-deoxycortisol stage

51
Q

Conns syndrome

A

benign adrenal corticol tumour

= ALDOSTERONE secretions increased

52
Q

which condition increases aldosterone secretion?

A

Conns

Primary aldosteronism

53
Q

treatment for Conns ?

A

Competitive Mineralocorticoid antagonists
Spironolactone
Epleronone

blocks aldosterone from binding

54
Q

phaeochromocytoma

hyperadrenalism of what?

what part of adrenal gland?

A

XS catecholamines
adrenaline/noradrenaline

medulla

55
Q

Symptoms

of phaeo?

A 
palpitations
headache 
sweating
 chest pains, nausea, tremor, 
anxiety, 
hypertension, 
pallor, 
tachycardia,
fever, 
weight loss

due to
stimulates alpha and beta adrenergic receptors

56
Q

what heart condition can Phaeo lead to?

A

Hypertension > MI/Stroke

ventricular fibrillation = death

57
Q

management of Phaeo

A

Alpha blockade
IV fluids
Beta blockade
Surgery to remove tumour

58
Q

Hypoadrenalism?

A

Addisons

Congenital adrenal hyperplasia

Year 2 BRS Endo (1 decks)

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