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EndocrineJaz > Adrenal and Pituitary > Flashcards

Adrenal and Pituitary Flashcards

1
Q

anterior pituitary is also called the ___

is derived from ____

A

adenohypophysis

Rathke’s pouch

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2
Q

non-trophic hormones produced by anterior pituitary =

A

GH and PRL

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3
Q

posterior pituitary aka ___

is an extension of ____ consisting of ___+___

A

neurohypophysis
neural tissue
modified glial cells
axonal processes

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4
Q

histology of anterior pituitary = __
acidophils =+
basophils =__+__

A

islands, cords of cells ; chromophobe islands
acido = somatotrophs (GH-50%) mammotrophs (PRL 20%)
baso = corticotrophs (ACTH 20%), thyrotrophs (TSH 5%) gonadotrophs (L/FSH 5%)

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5
Q

histology of posterior pituitary

A

non-myelinated axons of neurosecretory neurons

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6
Q

Pituitary adenoma can be associated with __ (__ syndrome)

A

MEN1

Wermer syndrome

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7
Q

3 affects of a prolactinoma

A

infertility
lack of libido
25% have amennorhoea

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8
Q

large pituitary adenoma local affects may be __+__+__

A

visual field defect (bitemporal hemianopia)
P atrophy of surrounding tissue
infarction => panhypopituitarism

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9
Q

ischaemic necrosis of pituitary that causes panhypopituitarism =

A

Sheehan syndrome

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10
Q

granulomatous disease that can cause panhypopituitarism

A

sarcoidosis

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11
Q

craniopharyngioma is derived from _____ = 1-5% of IC tumours

A

Rathke’s pouch remnants

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12
Q

4 features of craniopharyngioma =

can cause ____

A 
slow growing
often cystic
may calcify
most suprasellar some are in sella
=> panhypopituitarism
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13
Q

ages that get craniopharyngiomas

A

5-15 yos or 50-60 yos

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14
Q

_+__ = symptoms of craniopharyngioma

in kids may cause ___

A

visual disturbances and headaches

growth retardation

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15
Q

congenital adrenocortical hyperplasia :
pattern of inheritance =
causes _/__ of steroid enzymes => increased ___

A

auto recessive
lack/deficiency
androgens

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16
Q

nodular adrenocortical hyperplasia is ACTH dep/independent?

A

ACTH independent (diffuse = ACTH driven)

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17
Q

if adrenal cortex tumours in young then consider

A

Li Fraumeni Syndrome

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18
Q

appearance of adrenal cortex adenomas=

A 
well circumscribed
encapsulated
small - 2-3cm
yellow/yellow-brown (lipids)
small nuclei
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19
Q

features of adrenal cortex carcinoma that distinguish it from adenoma

A 
large (>20cm)
haemorrhagic and necrotic
frequent mitoses
atypical mitoses
lack of clear cells
capsular/vascular invasion
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20
Q

primary hyperaldosteronism aka

60% associate with __

A

Conn’s

diffuse/nodular bilateral hyperplasia

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21
Q

Cushings that is ACTH dep = __/___

and leads to ___

A 
pituitary tumour (70%) small cell lung cancer
adrenal hyperplasia
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22
Q

Cushings that is ACTH independent can be caused by __/___

and leads to ___

A 
adrenal adenoma (10%) or carcinoma (5%)
adrenal atrophy
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23
Q

acute primary adrenal insufficiency caused by massive adrenal haemorrhage due to septicaemia =

A

Waterhouse Friederichsen

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24
Q

causes of acute primary adrenal insufficiency =

A

rapid steroid withdrawal
stress on chronic insufficiency
massive adrenal haemorrhage - newborn, anticoagulants, DIC, septicaemia

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25
Q

3 common causes of Addisons

A

AI adrenalitis
infections (tb, HIV etc.)
metastases

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26
Q

chronic primary adrenal insufficiency aka

A

Addisons

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27
Q

signs of Addisons when >90% of adrenal glands are destroyed =

A 
fatigue
anorexia
nausea and vom
wt loss
diarrhoea
pigmentation
increase K+ and decrease Na+ = hypotension
hypoglycaemia
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28
Q

pigmentation in Addisons is caused by

A

ACTH having the same precursor as MSH

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29
Q

zona glomerulosa produces __

A

mineralocorticoids - aldosterone

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30
Q

zona fasciculatis produces ___

A

glucocorticoids - cortisol

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31
Q

zona reticularis produces ___+___

A

glucocorticoids and sex hormones

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32
Q

adrenal medulla is innervated by ___ and chrommafin cells secrete ___

A

pre-synaptic sympathetic fibres

catecholamines

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33
Q

___+___ in neuroblastoma are indicative of a poor outcome

A

amplification of N-myc

expression of telomerase

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34
Q

neuroblastoma is usually diagnosed at age ___

40% from ___ and most of the others are found ___

A

18months
adrenal medulla
along sympathetic chain

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35
Q

neuroblastoma are composed of ___ cells but can show maturation and differentiation towards ___ cells

A

primitive

ganglion

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36
Q

tumour of chromaffin cells in the adrenal medulla =

A

phaeochromocytoma

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37
Q

tumour in adrenal medulla that secretes catecholamines =

leads to secondary =

A

phaeochromocytoma

2ndry hypertension

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38
Q

detect __+___ in urine if have a phaeo

A

catecholamines and metabolites

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39
Q

90% of phaeos are associated with ___ which comes on with +++

A

paroxysmal hbp

stress, palpation of tumour, exercise, posture

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40
Q

if stain phaeo with K2Cr2O7 turns ____ as the catecholamines ____

A

dark brown

oxidise

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41
Q

nests of cells seen in phaeos

A

zellballen

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42
Q

usually phaeos metastasise to ___

A

skeleton

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43
Q

Phaeo is a feature of __ (sipple syndrome )

gene mutation =

A

MEN 2A

gain of function mutation in RET gene on 10q11.2

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44
Q

MEN2B mutation =

tumours associated =

A

activating point mutation in catalytic zone of encoded enzyme
phaeo
MTC, neuromas/ganglioneuromas
marfanoid habitus

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45
Q

tumours ass with MEN2A

A

phaeo in 40%
MTC in 100%
10-20% parathyroid hyperplasia

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46
Q

hormones from hypothalamus > ___ > stimulate the ___ pituitary

A

portal system

anterior

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47
Q

hyphothalamic hormones > ____ >stored in ___ pituitary

A

neuronal tracts

posterior

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48
Q

in synacthen test cortisol should normally rise to ___

A

450-500

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49
Q

dont give a prolonged glucagon test to __/___

A

epileptics or CVDs

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50
Q

insulin stress test =
make bg ___ the measure __+__
normal =

A

<2.2mmol/l
GH and cortisol
both increase so that GH >7microg/l + cortisol >500

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51
Q

water deprivation test - if suspect __
check + for 8hrs and then give ___ and check for 4hrs more
if urine:serum osmolarity >2 (even on random test ) = ___

A

Diabetes Insipidus
serum and urine osmolarities
desmopressin
normal

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52
Q

microadenoma = ___cm

macroadenoma =___cm

A

<=1cm

>1

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53
Q

CN at risk of compression in pituitary pathology

A

CN III, IV and VI

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54
Q

4 physiological causes of raised prolactin

A

Pregnancy
breast feeding
stress
sleep

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55
Q

5 drugs that can cause raised prolactin

A 
D2 antagonist anti-emetics (domperidone +metoclopramide)
phenothiazines
TCA and SSRIs
oestrogens
cocaine
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56
Q

pathological causes of raised prolactin (3)

A

hypothyroidism (raised TSH => raised PRL)
stalk lesions
prolactinoma

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57
Q

Females with raised prolactin tend to present early/late

with ///

A 
early
amenorrhea (most common)
infertility
menstrual irregularity
galactorrhoea
58
Q

Males with raised prolactin tend to present early/late

with ///

A 
late
impotence (decreased testosterone)
visual field abnormality
headache
anterior pituitary malfunction
59
Q

investigations for suspected raised prolactin

A

PRL concn
MRI (prolactinoma, stalk lesion, optic chiasm)
visual fields
pituitary FTs

60
Q

Rx for raised prolactin

effect on tumour size

A

dopamine agonists - usually cabergoline (bromocriptine / quinogolide)
tumour shrinks

61
Q

route that cabergoline is given and how frequently

A

PO

twice a week

62
Q

headache in acromegaly is caused by ___

A

hyperdynamic blood flow

63
Q

signs and symptoms of acromegaly

A 
thickened soft tissues
spade hands
macrognathia
hbp
HF
headache
sleep apnoea
DM
colonic polyps and cancer
visual disturbances
64
Q

2 best Investigations for suspected acromegaly

A

IGF-1 blood test (increased)

OGTT - and check GH response normal = <0.4microg/l

65
Q

first line treatment for acromegaly

A

transspenoidal Sx

66
Q

drug treatment for acromegaly if tumour is unresectable

A

somatostatin analogues - octreotide / lanreotide
D2 agonists - cabergoline
GH receptor antagonists - pegvisomant (last line)

67
Q

D2 agonists are better for the treatment of acromegaly if there is also ___

A

co-secretion of PRL

68
Q

can use SSAs pre op for acromegaly because it __/___

A

relieves headache in 1hr

gives a better outcome

69
Q

side effects of SSAs used for Rx of acromegaly

A

flatulence, diarrhoea (long term)

gallstones (decreased GB contractions)

70
Q

___ = drug that can reduce the size of acromegalic pituitary tumour

A

SSAs - octreotide

re-expands 6wks after stop the drug

71
Q

cancer surveillance for acromegalic patients = __+__

A

colon and tubulo-villous adenoma - every 3 yrs

72
Q

excess cortisol in Cushings causes __ loss, altered __+__ metabolism, __ and central ___

A

protein loss
lipid and carb
DM
obesity

73
Q

proximal myopathy, thin skin, frontal balding (F), chemosis and osteoporosis are characteristics of __

A

Cushing’s

74
Q

chemosis =

A

conjunctival oedema

75
Q

best screening test for Cushing’s =

normal and abnormal limits =

A

overnight 1mg dexamethasone suppression test
normal = <50nmol/l
abnormal =>100

76
Q

2 screening test for Cushing’s =

A

overnight 1mg dexamethasone suppression test

urine free cortisol (24hr urine collection)

77
Q

definitive diagnostic test for Cushing’s =

normal =

A

low dose dexamethasone suppression test
2mg/day for 2 days
normal = <50nmol/l 6 hrs after last dose

78
Q

Cushing’s disease is due to a __

A

pituitary cause

79
Q

ACTH test results for pituitary, adrenal and ectopic causes of Cushing’s

A 
pit = <300
adrenal = <1
ectopic = >300
80
Q

high dose DST result in pituitary, adrenal and ectopic causes of Cushing’s

A

pit = suppress by 50%

adrenal and ectopic = nil

81
Q

treatment for pituitary cushings

A

hypophysectomy (maybe + external radio.)

OR bilateral adrenalectomy

82
Q

treatment for adrenal causes of Cushings

A

adrenalectomy

83
Q

drug treatment for Cushings if Sx fails

A

metyrapone, ketoconazole, pasireotide (SSA)

84
Q

if get normal pituitary hormone levels with low peripheral hormones= _____ = __

A

inappropriately normal

hypopituitarism

85
Q

treatment of hypopituitarism =

A

replacement hormones - give hydrocortisone and then thyroxine then the others

86
Q

testosterone replacements IM = ___, PO = ___

A 
IM = nebido every 10-14wks
PO = restandol (if very mild hypo-testosterone)
87
Q

DIDMOAD aka __
stands for ___
pattern of inheritance =

A

Wolfram Syndrome
Diabetes insipidus, Diabetes mellitus, opti atrophy, deaf
auto recessive

88
Q

test to diagnose DI

A

water deprivation test

89
Q

treatments for DI =

A

desmospray (nasal)

desmopressin PO/IM

90
Q

if a Glucocorticoid receptor dimer is allowed to bind to GRE then steroid causes ___

A

activation of the gene

91
Q

if nGRE only allows a GR monomer to bind then steroid causes ___

A

gene repression

92
Q

steroid effect depends on __ not on __

A

gene sequence

not on the steroid used/the type of receptor

93
Q

steroids also activate the ___ which leads to the adverse effects __+__

A

mineralocorticoid receptor

thin skin and poor wound healing

94
Q

if co-administer a ___ with steroids then can inhibit __+__ as it saturates the __

A

mineralocorticoid
inhibit skin atrophy and increase wound healing
Mineralocorticoid receptor

95
Q

GR activation in the __ of the brain can lead to ___

A

amygdala

alcohol craving

96
Q

Is licensed for acute Cushing’ crisis as it binds to GR and blocks =

A

mifepristone (morning after pill)

97
Q

sign of high androgen levels in CAH for F and M

A 
F = ambiguous genitalia
M = precocious puberty
98
Q

adrenal cortex layers outer to inner =

A

GFR
glomerulosa
fasciculata
reticularis

99
Q

zona glomerulosa is regulated by

A

ATII and extracellular K+

100
Q

zona fasciculata is regulated by

A

ACTH

101
Q

zona reticulatis is regulated by

A

ACTH and others

102
Q

RAS is activated by ___ and it causes __+___

A 
decreased bp
vasoconstriction (ATII)
salt retention (aldosterone)
103
Q

excess cortisol causes osteoporosis because

A

increases osteoclastic activity

decreases serum Ca2+

104
Q

cortisol ___ lipolysis and cause fat to be deposited __

A

increases

centrally

105
Q

effect of cortisol on proteolysis

A

increases it

106
Q

cortisol ___ capillary dilatation and permeability

A

decreases

107
Q

cortisol ___ CO, bp, renal blood flow and GFR

A

increases

108
Q

Ix for diagnosis of Addisons (5)

A 
biochem (Na + bg low, K+ high)
short synACTHen
raised ACTH in blood
raised renin and low aldosterone levels
adrenal autoIgs
109
Q

Rx for addison crisis

A

DON’T delay treatment
hydrocortisone IV immediately
later = fludrocortisone

110
Q

Rx that replaces aldosterone

A

fludrocortisone

111
Q

sick day rules for Rx of Addisons

A

x2 dose if sick
if vomit - retake
if cant keep anything down = IM and go to hospital within 6-8hrs

112
Q

2ndry adrenal insufficiency has same features as primary but __+___

A

no pigmentation (ACTH low) and aldosterone production is intact

113
Q

Rx in secondary adrenal insufficiency

A

just hydrocortisone

no need for fludrocortisone

114
Q

results of long ACTH test in 2ndry adrenal insufficiency -

A

long gradual rise = due to adrenal atrophy

115
Q

purple striae =

A

Cushings

116
Q

gradual withdrawal of steroid therapy is over ___

A

4-6wks

117
Q

Conns (primary hyperaldosteronism) features =__+__
increases number and activity of _____
can lead to __+__

A

hbp and hypokalaemia
Na+ reabsorption channels
LV hypertrophy and atheroma

118
Q

commonest cause of primary hyperaldosteronism (usually older patients) =

A

bilateral adrenal hyperplasia

119
Q

cause of primary hyperaldosteronism (usually in young patients)

A

Conn’s - adrenal adenoma

120
Q

genetic mutations in ___ can cause primary hyperaldosteronism

A

K+ channels

121
Q

to confirm hyperaldosteronism Ix = __

if it is increased then test to confirm primary hyperaldosteronism =

A

plasma aldosterone:renin, plasma K+

saline suppression test (fail to suppress by >50% with 2L = PA)

122
Q

3 Ix to confirm the subtype of primary hyperaldosteronism

A

adrenal CT
adrenal vein sampling (confirms adenoma)
11C metomidate PET-CT

123
Q

if adrenal adenoma is cause of primary hyperaldosteronism Rx =

A

unilateral laparoscopic adrenalectomy

124
Q

if bilateral adrenal hyperplasia is cause of primary hyperaldosteronism Rx =

A

MR antagonists (spironolactone)

125
Q

classical CAH = __+__

non-classical = __

A

salt wasting + virilising

hyperandrogenaemia

126
Q

diagnosis of CAH is dependent on __+__ (Ix)

A

basal/stimulated 17-OH progesterone concn (increased)

gene analysis

127
Q

____ is the stage before 21alpha hydroxylase - a precursor for __>testosterone

A

17-OH progesterone

androstenedione

128
Q

Rx for CAH in paeds =

A

gluco (+maybe mineralo) corticoid replacement

Sx

129
Q

Rx for CAH in adults -

A

control androgen excess
restore fertility
avoid overreplacing steroids

130
Q

__>L-DOPA>___>NA>___

A

tyrosine
dopamine
adrenaline

131
Q

biochemistry of phaeo =

A 
hyperglycaemic
maybe decreased K+
increased Hb
mild hyperCa2+
lactic acidosis
132
Q

Ix to confirm catecholamine excess in phaeo/paragangliomas

A

2x24hr urine fo catecholamines/metanephrins

plasma levels of catecholamines

133
Q

3 diagnostic Ix for phaeo/paraganglioma=

A

MRI
MIBG (meta-iodidbenzylguanidine)
PET (-ve in slow growing/benign)

134
Q

drugs for phaeo/paraganglioma

A 
alpha blocker (phenoxybenzamine 1st line - others = prazosin/doxazosin)
followed by beta blocker (propanolol/metoprolol)
135
Q

malignant phaeos and extraadrenal paragangliomas are less efficient at catecholamine synth and so instead ___ increase

A

precursor levels eg. dopamine

136
Q

ectopic causes of cushings commonly originate in ++_

A

thymus
lungs
pancreas

137
Q

if low dose dex suppression test confirm Cushings then next Ix= ___ to determine if pituitary, adrenal or ectopic

A

high dose dexamethasone suppression test (2mg/6hrs for 2 days)

138
Q

adrenaline acts on ___ receptors in the heart
___ in the vessels
__ in muscles
__ in islet beta cells

A

beta1 heart
alpha 1 vessels
beta2
beta2

139
Q

paragangliomas commonly occur here

A

aortic bifurcation

140
Q

pigmentation in addisons is especially noticable in __+__

A

buccal mucosa

palmar creases

EndocrineJaz (15 decks)

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