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(58 cards)

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
why is oral dexamethasone given to test for cushing?
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
non -functioning pit adenoma
bitemporal hemianopia | compression of optic chiasm
27
ADh promotes water reabsoroption from where?
renal collecting ducts via V2 receptors
28
Stimuli for vasopressin release are: | ______sensed by ______ in the hypothalamus ; Process: ______are special neurons in the hypothalamus that sense _____
- increased plasma osmolality (concentration) - osmoreceptors - osmoreceptors - plasma osmolality
29
Diabetes insipidus | polyuria, nocturia & polydipsia
inability to make vasopressin
30
Desmopressin test
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
how to treat nephrogenic cranial DI?
- thiazide diuretics | - desmopressin
32
if someone has a low urine osmolality after DDAVP administration what does it mean?
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
SIADH?
Syndrome of inappropriate antidiuretic hormone secretion
34
SIADH pathophysiology and presentation?
too much adh > water reabsorption [alot] > blood volume is HIGH hypervolemic > sodium loss?? hyponatraemia
35
other actions of Vasopressin?
vasoconstrictor - V1 receptor | stim ACTH release anterior pituitary
36
non osmotic stimuli for ADH?
Decrease in atrial pressure sensed by atrial stretch receptors
37
why can nuclei of posterior pituitary respond to systemic circulatory changes? [osmoreceptors- 3rd ventricle]
no blood brain barrier
38
why is the non osmotic stimuli for ADh important? such as reduction in circulating volume
restore blood volume in case of haemorrhage by increasing water reabsorption vasoconstriction via v1 receptors also
39
cause of Nephrogenic diabetes
genetic : mutated V2, aquoporin 2 drugs : lithium
40
management of SIADH?
Fluid restriction | Vaptan (vasopressin antagonist (binds to v2 receptors))
41
causes of SIADH
``` CNS - Head injury, stroke, tumour, Pulmonary disease - Pneumonia, bronchiectasis Malignancy - Lung cancer (small cell) Drug-related - Carbamazepine, - Serotonin Reuptake Inhibitors (SSSRIs) Idiopathic ```
42
management of hyperthyroidism | drugs
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
how does potassium iodine work?
fills up thyroid with stable iodine so radioactive iodine cannot be taken up - reduces T4/T3 production
44
radioiodine moa? | what is it used for?
Hyperthyroidism destroys cells in thyroid gland = reduces thyroxine levels and size of gland radiation destroys the overactive cells
45
Cushing diagnosis?
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
what tumour can cause cushings syndrome?
ectopic ACTH lung cancer adrenal adenoma secreting cortisol pituitary tumour - Cushing disease
47
High acth
cushings disease
48
low ACTH : cushings syndrome?
steroid medication | adrenal adenoma
49
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
= 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
Metryrapone
Metryrapone = inhibition of 11β-hydroxylase; steroid synthesis in the zona fasciculata [and reticularis] is arrested at the 11-deoxycortisol stage
51
Conns syndrome
benign adrenal corticol tumour = ALDOSTERONE secretions increased
52
which condition increases aldosterone secretion?
Conns | Primary aldosteronism
53
treatment for Conns ?
Competitive Mineralocorticoid antagonists Spironolactone Epleronone blocks aldosterone from binding
54
phaeochromocytoma hyperadrenalism of what? what part of adrenal gland?
XS catecholamines adrenaline/noradrenaline medulla
55
Symptoms | of phaeo?
``` palpitations headache sweating chest pains, nausea, tremor, anxiety, hypertension, pallor, tachycardia, fever, weight loss ``` due to stimulates alpha and beta adrenergic receptors
56
what heart condition can Phaeo lead to?
Hypertension > MI/Stroke ventricular fibrillation = death
57
management of Phaeo
Alpha blockade IV fluids Beta blockade Surgery to remove tumour
58
Hypoadrenalism?
Addisons | Congenital adrenal hyperplasia