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PRIYA ENDO > pituitary summary > Flashcards

pituitary summary Flashcards

1
Q

what are the 4 roles of cortisol?

A

increases BG levels
increased body fat
defend body against infection
helps body response to stress

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2
Q

how to do synachten test

A
  1. measure corisol @ 0, 30 and 60 minutes
  2. expect cortisol to reach 500 + increase by 150
  3. if not, insufficient
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3
Q

how to do an insulin stress test / prolonged glucagon test?

A
  1. not in epilepsy
  2. cortisol + GH response every 30 mins for 2-3 hours
  3. normal cortisol >500
  4. normal GH >7
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4
Q

how to do a water deprivation test?

A
  1. check serum + urine osmolarities for 8 hours then 4 hours after giving IV DDAVP
  2. if Ur / serum osmolarity ration >1.9 then normal
  3. otherwise its DI
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5
Q

how to treat big pituitary adenoma

A

transsphenoidal surgery + replace hormones

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6
Q

which drug increases PRL

A

metoclopramide - a dopamine antagonist

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7
Q

symptoms of prolactinoma in females

A 
early presentation
ammerhorea 
galactorrhoea (milky nipples) 
menstruation irregularity 
infertility
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8
Q

symptoms of prolactinoma in males

A 
late presentation
impotence
visual field abnormality 
headache
anterior pituitary malfunction
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9
Q

how to treat prolactinoma

A

cabergoline (dostinex) - a dopamine agonist

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10
Q

what are the 2 tests for acromegaly

A

IGF-1 + OGTT

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11
Q

how to do OGTT test?

A

diagnostic
give 75g oral glucose (check GH 0,30,60,90,120)
normally - GH suppresses to <0.4 after glucose
acro - unchanged / no suppression

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12
Q

how to treat acromegaly

A
  1. surgery
  2. somatostatin analogues (octrecitde)
  3. dopamine agonistst (carberholine)
  4. GH antagonists - pegvisomant
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13
Q

what causes cushings syndrome

A

pituitary adenoma

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14
Q

what are the symptmos of cushings

A

protein loss - promixal muscle wasting, OP (fractures), thin skin, bruising
altered carb/lipid metabolism
excess mineral corticoid (hypertension + oedema)
excess androgen (virsulism, hirsulism, acne, oligo/ammenhorea)

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15
Q

what are the 3 screening test for cushings syndrome?

A

overnight 1mg dexamethasone - >130 is abnormal
urine free cortisol - 24 hours urine collection, total <250 = normal
diurinal cortisol cariation (midnight /8am) - in cushigns its constant

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16
Q

what are the 2 diagnostic tests for cushings?

A

low dose dexamethasone test - 2day,2mg/day, cortisol <50 6 hours after last dose = no cushings, cortisol >130 definietly cushings
CRH test - >50% increase in ACTH + >20% increase in cortisol, suggestive of pituitary disease

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17
Q

how to treat cushings?

A

metyrapone
ketoconazole (hepatotoxic)
pasireotide LAR

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18
Q

what are the 3 causes of panhypopituitarism

A

pituitary tumours
granulomatous disease
autoimmune disease

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19
Q

how to replace ADH

A

desmopray

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20
Q

what is the familial cause of cranial DI

A

DIDMOAD

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21
Q

how to diagnose cranial DI

A

water deprivation test

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22
Q

how to treat cranial DI

A

desmospray 10-60mgc daily

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23
Q

what are the 6 steps of thyroid hormone synthesis

A
  1. thyroglobulin synthesis
  2. uptake and concentration of iodine (I-)
  3. oxidation of iodine (I-) to iodine (I)
  4. iodination of thyroglbulin
  5. formation of MIT and DIT
  6. secretion
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24
Q

where does idoine uptake take place

A

follicular cells

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25
Q

which step is inhibited by carbimaozole and PTU

A

iodine attaching to tyrosine residues on thyroglobulin to form MIT and DIT

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26
Q

which is the biologically active thyroid hormone

A

T3

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27
Q

how does T3/4 go from colloid to follicular cells

A

pinocytosis

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28
Q

are thyroid hormones hydrophilic or phobic

A

hydorphic - hence the need to be bound to a carrier protein

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29
Q

what are the 4 roles of thyroid hormones?

A
  1. increase basal metabolic rate
  2. increase thermogenesis
  3. carb metabolism
  4. protein metabolism
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30
Q

what are the outcomes of T3 + T4s sympathomimetic action and what does it mean?

A

they increase responsiveness to adeaenlinaand noradreanline by increasing the number of receptrs - anxiety, sweating, tachycardia -> treateed with proproanolol

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31
Q

where is D1 found

A

liver and kidney

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32
Q

where is D2 found

A

heart, skeletal muscle, CNS, fat, thyroid + pituitary

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33
Q

where is D3 found

A

fetal tissue, placenta, brain (not pituitary)

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34
Q

what is the anterior pituiatry called and where is it derviced from

A

adenohypophysis

rathkes pouch

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35
Q

what is the posterior pituitary celled

A

neurohypophysis

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36
Q

which 3 cells make up the anerior pituitary

A

acidophils (somatotrophs - GH and mamotrophs - PRL)
basophils (corticotrophs - ACTH, thyrotrophs - TSH and gonadotrophs - FSH / LH)
chromophobe

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37
Q

which cells make up the posterior pituitary gland

A

non-myelinated axons of neurosecretory neurones

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38
Q

what is a craniopharyngioma

A

tumour of pituitary gland
derived from remnants of rathkes pouch
5-15 year olds or 6th-7ths decades
growth retardation

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39
Q

what is acute hypofunction of adrenal cortex

A

waterhouse fredrichen (caused by bleeding secdonary to infections, usually N meningitis)

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40
Q

what is chronic hypofcutnion of adreanl cortex

A

addisons

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41
Q

what is prenenolone

A

produces aldosterone, cortisol + Testosterone

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42
Q

what is an adraenocorical adenoma

A

encapsulated lesion
small 2/3cm
yellow
well differentiated, small nuclei, rare mitoses

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43
Q

what is an adraenocortical carcinoma

A 
functional 
mets - haematogenous
large >50g + >20cm
frequet mitoses
lack of clear cells
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44
Q

which bodies are found in conns

A

spironolactone

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45
Q

what casues acute primary adrenocortical insufficiency

A

rapid withdrawal of steroids

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46
Q

what causes chronic primary adrenocrotical infufficiency

A

addisons

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47
Q

what is addisons

A

adreanl cortex destruction by autoimmune reactions leading to a decrease in glucocorticoids (hypoglycaemia)

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48
Q

what is the biochem for addisons

A

decrease in mineralcorticoids
K+ retention
Na+ loss

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49
Q

what is the pigmentation in addisons caused by

A

POMC

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50
Q

what is the histology of the adrenal medulla

A

inervaetd by pre synpatic fibres from sympathetic NS

neuroendocrine / chromaffin cells (secrete catecholamines)

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51
Q

what is a rare cause of secondary hypertension

A

phaeochromocytoma

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52
Q

what are the symptoms of phaeochromocytoma

A

headache, hypertension, sweating

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53
Q

how to diagnose phaeochromocytoma

A

urianry catecholamiens

MRI

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54
Q

what does the 10% tumour mean

A 
bilateral
extra-adrenal
not hypertensive 
malignant
25% familial
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55
Q

how to treat phaeochromocytoma

A

phenoxybenzamine (A)

propranolol (B)

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56
Q

men 2a

A

phaeochromocytoma
MTC
parathyroid hyperplasia

57
Q

men 2b

A 
phaeochromocytoma
MTC
meningioma
ganglioneuroma
marfan old habitus
RET mutation
58
Q

zona glomerulosa produces

A

mineral corticoids eg aldosteron

59
Q

zona fasciculata prodces

A

coritsol, corticosteroids, cortison

60
Q

zona reticularis produces

A

andrognes

61
Q

adreanl medulla produces

A

stress hormoens eg epinephrine

62
Q

what does mineralcorticoids do

A

increased NA+ reabsorption
K+ / H+ excretion
BP regulation
regulation of extracellular volume

63
Q

how to diagnose adrenal insufficiency

A 
decreased Na
increased K+ 
short synacten test 
ACTH levels increased 
adreanl antibodies
64
Q

how to treat adrenal insufficiency

A

hydrocortison (2 doses for diurinal rhythm)

fludrocortisone (replace aldosterone)

65
Q

what is seocndary adreanl insufficiency

A

clincal featuers same as addisons but pale skin (no increased ACTH)

66
Q

how to treat secondary adreanl insufficiency

A

hydrocortison only

67
Q

what is primary aldosteronism

A

autonomous production of aldosterone, independent of its regualtors (ANG2 / K+ )

68
Q

clinical features of primary aldosteronism

A

significant hypertension
hypokalaemia
alkalosis

69
Q

how to diagnose primary aldosteronism

A
  1. confirm aldosterone excess - measure plasma aldoserone + renin + express as ratio
    - if increased, so saline suppression test
    - failure of plasma aldosterone to suppresss by >50 with S2 of normal saline confirms PA
  2. confirm subtype - adrenal CT
70
Q

how to manage adreanal adenoma

A

unilatearl laparoscopic adreanlaectomy

71
Q

how to manage bilateral adrenal hyperplasia

A

MR antagonists eg spironolcatone or epelenone

72
Q

genetics of congenitl adreanl hyperplasia

A

21a hydroxylase deficiency

basal 17-OH progesterone (end product is 21aHD)

73
Q

symptoms of CAH males and females

A

males - adreanl insufficiency, poor weight gain

females - genital ambiguity

74
Q

definition of OP

A

<2.5SD below adult mean

75
Q

oral bisphosphonate example

A

aldendronate

take 30 mins before breakfast with a glass of water

76
Q

when to give drugs for DEXA score for OP

A

T score <2.5

77
Q

what controls water balance and how does it work?

A

ADH

makes you pee less by aborbting water from renal tubules

78
Q

what does decreased ADH mean

A

decreased urine but increased concentration = increased osmolarity

79
Q

what does decreased osmolarity mean

A

increased ADH

increased urine but decreased concentration

80
Q

what control sodium balance

A

steroids eg aldosterone by adrenals

81
Q

what does decreased BP do

A

Na+ retention eg increased Na

82
Q

what sodium follow water or water follow sodium?

A

water follows sodium

83
Q

what are the signs of hypotronaemia

A 
increased pulse
postural hypo
decreased urine output 
decreaed consiousness
decreased skin tugor 
soft / sunken eyeballs
dry mouth
84
Q

signs of hypertronaemia

A 
coughing
tiredness
SOB
pulmonary oedema
pleural effusion
swelling in ankles
85
Q

causes of hypotronaemia

A 
Na loss (adrenal, gut, skin) 
decreased Na+ intake 
decreased H20 excretion (SIADH) 
increased water intake
86
Q

causes of hypertronaemia

A

increased NA+ intake (drowning)
decreased NA+ loss (DI)
decreased H20 intake (give dextrose)

87
Q

how do you describe the volume of ECF

A

half that of ICF

88
Q

symptoms of non-osmotic SIADH

A

hypovolaemia
hypotension
pain
nausea/ vomiting

89
Q

acute hypercalcaemia symtpoms

A

thirst
dehydration
confusion
polyuria

90
Q

chronic hypercalcaemia

A 
muscle cramps
myopathy
muslce weakness
osteopenis
depression
hypertension
pancreatitis 
renal caliculi
91
Q

increased Ca
increased serum PTH
increased Ca urinary output

A

hyercalciaemia

92
Q

increasec Ca
increased serum PTH
decreased Ca urinary output

A

FHH

93
Q

secondary hypercalcaemia biochem

A

decreased Ca

increased PTH

94
Q

malignant hypercalcaemia

A

increased ALK PHOS

95
Q

indications for parathyroidectomy

A

end organ damage eg OP
Ca > 285
<50
eGFR <60

96
Q

what happens in FFH

A

autosomal dominnat

deactivating mutation in the calcium sensing receptor eg increased Ca required before PTH is swithced off

97
Q

signs of hypocalcaemia

A

parasthesia, muscle cramps / weakness, bronchosoasm
choveks sign
trosseau sign

98
Q

what is trosseau sign

A

carpopedal spasm when taking BP

99
Q

hypocalacemia biochem

A

increased PTH

decreased Ca

100
Q

acute treatment of hypocalcaemia

A

IV calcium glyconate 10ml 10% over 10 minutes (in 50ml saline of dextrose)

101
Q

causes of hypoparathyroidism

A

digeorge

autoimmune hypomagnesaemia

102
Q

what causes hypomagesaemia

A

Ca release from cells is dependent of Mg (MG deficiency = intracellular Ca is high, PTH release is inhibited)
alcohol, thizides, PPIs

103
Q

what causes pseydohypoparathyroidism

A

GNAS1 defect causing PTH resistacne rather than failrue to produce PTH

104
Q

pseudohypoparathyroidism biochem

A 
decreased Ca
increased PTH (due to resistance)
105
Q

symptoms of psueohypoparathyroidism

A

bone abnormalities eg mccune albright
obesity
subcutaneous calcification
bracdactyly

106
Q

what is the biochem of pseudopseudohypoparathyroidism

A

no alterataion in PTH - normal Ca

107
Q

phases of menstrual cycle

A

follicular
ovulation
luteal
menstruation

108
Q

increased frequency pulsatility of GnRH

A

LH

109
Q

decreased frequency pulsatility of GnRH

A

FSH

110
Q

what regulates GnRH

A

kisspeptin + GnRH neurones

111
Q

whcih day is ovulation

A

14

112
Q

what does FSH lead to

A

growth of ovarian follicles

113
Q

what does the LH surge do

A

ovulation
reagultion of corpus luteum
progesterone production + Secretion

114
Q

what does the LH surge activate

A

theca cells (convert androgens into oestrogen)

115
Q

functions of oestrogen

A

thickens uterine wall
reagulates LH surge
reduced vaginal Ph through increased lactic acid production
decreased viscosity of cervical mucous to facilitate sperm production

116
Q

functions of progesterone

A

maintains thickness of endometrium
infertile thick mucous (prevents sperm transport)
relaxes myometrium

117
Q

what do leydig cells

A

secrete testoserone in respone to LH

118
Q

what do sertoli cells do

A

support germ cells during their development into spermatozoa

119
Q

what do germ cells do

A

differentiate into spermatozoa

120
Q

symptoms of PCOS

A

worse on weight gain
hiruitism
increased androgens, increased LH, impaired glucose tolerance

121
Q

diagnosis of PCOS

A

2/3 of
chronic anovulation
polycystic ovaries
hyperandrogenism

122
Q

what causes premature ovarian failue adn what are the symptoms?

A

turners 45 XO
hot flushes, night sweats, atrophic vaginitis
increased FSH, LH and low oestridiol

123
Q

what is hydrosalpinx

A

blocked fallopian tube with water fluid

abdo pain, vaginal discharge, painful sex

124
Q

what is endometriosis

A

presence of endometrial glands otuside the uterine cavity

dsmennhorea, painful sex, painfeul defeacation, chronic pelvic pain, chocolate cysts

125
Q

what is non-obstrctive male fertility

A

eg kleinfelters / undescended testes
increaed LH and FSH
dcerased testosterone

126
Q

management of female infertility

A

weight loss
folic acid
10mg of vit d

127
Q

how to treat chamydia

A

doxycyline

128
Q

features of rubella

A

rash
microcephaly
patent ductus arteriosus
cataracts

129
Q

treatment of male infertility

A

sperm analysis

surgery to obstructed vas deferent

130
Q

group 1 ovulatory disorder

A

hypothalamic pituitary failure 10%

stress, exercise, kallmans syndrome, anorexia

131
Q

biochem of group 1

A

decreased FSH
decreased LH
decerased osteogen
normal PRL

132
Q

mangement of group 1

A

bmi >18
pulsatile GnrH
gonadotrophin daily infections

133
Q

group 2

A

hypothalamic pituitary dysfuntion (85% PCOS)

134
Q

managemnet of group 2

A

clomifene citrate

135
Q

diagnosis of group 2

A

2 of oligo/ammerhoea
polycystic ovaries (>12 2-9cm)
signs of hypergonadism

136
Q

group 3

A

ovarian failure

menopause / premature ovarianfalure

137
Q

groupo 3 biochem

A

increased gonadotrophins, decreaeed oestrogen (menoause)

138
Q

lambda sign

A

non identica

139
Q

T sign

A

identical

PRIYA ENDO (8 decks)

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