Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

my phase 2 > endo > Flashcards

endo Flashcards

1
Q

complications of pituitary tumours

A
  1. press on local structures eg optic chiasm
  2. hypopituitism
  3. hyperpituitism (acromegaly, cushings, prolactinoma)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

anterior pituitary hormones

A

FLAT PeG

GnRH > FSH* + LH* > act on gonads for germ cell development and hormone secretion

CTH > ACTH* > acts on adrenal gland to produce corticosteroids

TRH > TSH* > acts on thyroid to release T3, T4

DA > prolactin* > acts on mammary glands for milk production and breast development

endorphins

GHRH > GH* > stimulates IGF-1 production, growth

(ones with * are the ones released from anterior pituitary)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

functions of cortisol

A

-increases insulin resistance
-suppresses immune response
-upregulates alpha 1 in arterioles to increase BP
-increases osteoclast activity (so osteoporotic)
-increased protein and carb breakdown

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

insulin action

A

biphasic release
insulin increases peripheral glucose uptake (glucose> glycogen)

1.glucose binds to GLUT2 receptors on pancreatic beta cells, stimulating insulin release

2.insulin binds to peripheral insulin receptors which activates intracellular tyrosine kinases and cascade resulting in increased GLUT4 channel expression on CSM (so increased peripheral uptake)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

posterior pituitary hormones

A

oxytocin (paraventricular nucleus)- milk ejection and labour induction

vasopressin (ADH) (supraorbital nucleus)- recruited when decrease in BV, stress, major RAAS player
-increases APO II expression
-vasoconstricts BV
-increases aldosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

which region of the adrenal gland releases which hormone

A

go find rex, make good sex

zona glomerulosa- mineralocorticoids (aldosterone)
zona fasciculata- glucocorticoids (cortisol)
zona reticularis- sex hormones (androgens)

salt, sugar, sex, deeper you go the sweeter in gets (moving inwards, controls production of salt etc)

adrenal medulla- adrenaline and noradrenaline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

when is cortisol released

A

released with chronic stress and increasing blood sugar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Cushing’s disease/syndrome definition

A

hypercortisolaemia
clinical manifestation of prolonged elevated cortisol
Cushing’s syndrome- abnormal high cortisol of any cause
Cushing’s disease- high cortisol due to high ACTH from pituitary adenoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Cushing’s epidemiology (G)

A

obesity, diabetes, older women

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Cushing’s aetiology (G)

A

ACTH dependent- excessive ACTH from the pituitary gland (pituitary adenoma), or ectopic ACTH producing tumour eg small cell lung cancer, or excess ACTH administration

non ACTH dependent- excess glucocorticoid administration (iatrogenic) eg steroids eg prednisolone or adrenal adenomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Cushing’s risk factors (G)

A

pituitary adenoma
adrenal adenoma
corticoid steroids
hypertension
uncontrolled diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Cushing’s presentation

A

big in the middle, thin limbs, signs of stress

-central obesity
-round moon face
-buffalo hump (fat on back of neck)
-abdominal straie
-osteoporosis
-hypertension
-hyperglycaemia
-depression
-easy bruising and poor skin healing
-cardiac hypertrophy
-irregular periods
-erectile dysfunction
-hirsutism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Cushing’s pathophysiology (G)

A

negative feedback:
low blood cortisol > increased CRH from hypothalamus> ACTH from pituitary > increased cortisol from adrenal gland > negative feedback slows ACTH production when cortisol levels are sufficient

released with circadian rhythm- peaks in the mornings, least at night. With Cushing’s this rhythm is lost so unregulated CRH, ACTH, cortisol levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Cushing’s investigations (G)

A

1: random plasma cortisol (midnight), if positive ACTH plasma
urinary free cortisol (24 hours)

gold:
dexamethasone overnigth test
dexamethasone is a glucocorticoid so should trigger negative feedback loop
give 1mg at 11pm and measure control, measure again at 8AM
with Cushings’s: not suppressed, >50nanomol/L
without Cushing’s: suppressed (negative feedback)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Cushing’s management (G)

A

stop taking steroids
-Cushing’s disease: transspheinoidal resection to remove pituitary adenoma
-if adrenal- adrenalectomy
-ectopic ACTH- remove neoplasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Cushing’s complications (G)

A

osteoporosis, type 2 diabetes,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Cushing’s prognosis

A

untreated- 50% mortality in 5 years
treated is good prognosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Acromegaly definition (G)

A

excess secretion of growth hormone from a pituitary tumour or hyperplasia results in bone and soft tissue overgrowth

acromegaly in adults

gigantism in children (before epiphyseal plates fuse)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

acromegaly epidemiology (G)

A

2-13/100000

effects men and women equally

median age of diagnosis: 50s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

acromegaly aetiology (G)

A

Unregulated GH secretion due to anterior pituitary adenoma
rarely ectopic GH from non-endocrine tumour eg lung

21
Q

acromegaly risk factors (G)

A

MEN-1
(multiple endocrine neoplasia)

22
Q

Acromegaly pathophysiology (G)

A

GHRH (released from hypothalamus) > excessive GH (anterior pituitary) > excessive production of IGF-1 (insulin growth factor 1)

IGF-1 stimulates growth of bone and muscle, increased protein synthesis, lipolysis

23
Q

acromegaly presentation (G)

A

-box jaw
-coarse facial features

-spade like hands and feet
-increase in shoe size

-interdental separation
-macroglossia

-snoring
-deep voice
-obstructive sleep apnoea
-sweating

-arthritis
-back pain
-arthralgia
-carpal tunnel

tumour related symptoms:
-visual disturbances (bitemporal hemianopia)
-headaches

24
Q

Acromegaly investigations (G)

A

1st:
serum IGF-1 (raised)
random serum GH (raised, not diagnostic as fluctuates with circadian rhythm)

gold:
oral glucose tolerance test
(failure of glucose to suppress GH)

other:
MRI pituitary

25
Q

acromegaly management (G)

A

1st:
transsphenoidal removal of pituitary tumour

medication:
2nd: somatostatin analogue to block GH release eg octreotide
3rd: dopamine agonist to block GH release eg carbergoline
4th: growth hormone receptor antagonist: pegvisomant

radiotherapy

26
Q

acromegaly monitoring and prognosis (G)

A

-lifelong monitoring of IGF-1 and GH
-prognosis good with surgery

27
Q

acromegaly DD (G)

A

pseudo-acromegaly

28
Q

Acromegaly complications (G)

A

T2DM, sleep apnoea

29
Q

prolactinoma definition (G)

A

benign lactotroph adenoma releases excess prolactin, resulting in hyperprolactinaemia

30
Q

prolactinoma epidemiology (G)

A

more women than men, child bearing years, 20-40, presents earlier in women than men

31
Q

prolactinoma aetiology (G)

A

prolactin is released from the anterior pituitary and is inhibited by dopamine from the hypothalamus

excess prolactin:
pituitary adenoma, other non-functioning tumour compressing the infundibulum

lack of dopamine:
reduced dopamine levels, drug induced: dopamine antagonist or antipsychotics

32
Q

Prolactinoma risk factors (G)

A

women 20-50, pregnant, oestrogen therapy
men 30-60

33
Q

prolactinoma presentation

A

infertility
loss of libido
tumour: visual disturbances, headaches

women:
amenorrhea/ oligomenorrhea
galactorhhea

men:
gynecomastia
hypogonadiam
osteoporosis
erectile dysfunction

34
Q

prolactinoma pathophysiology (G)

A

increased prolactin inhibits GnRH
decreased GnRH > decreased LH + FSH > decreased oestrogen/ progesterone in women, less testosterone in men

prolactin stimulates mammary glands > galactorrhoea

can be micro <10mm or macro

35
Q

prolactinoma investigations (G)

A

1st/gold:
basal serum prolactin (elevated)

other:
pituitary MRI, CT head

36
Q

prolactinoma management

A

dopamine agonist:
1.carbergoline,
2.bromocriptine

transsphenoidal removal of tumour

hormone replacement therapy

radiotherapy

37
Q

prolactinoma complications (G)

A

infertility
sight loss
raised ICP

38
Q

prolactinoma DD (G)

A

drug induced hyperproclactinaemia
primary hypothyroidism
renal insufficiency
pregnancy
PCOS

39
Q

Adrenal insufficiency/ Addison’s disease definition (G)

A

Insufficient production of steroids (mainly cortisol (glucocorticoid), aldosterone (mineralocorticoid) from the adrenal gland. Steroids are essential to life so can be fatal

primary- Addison’s disease. Due to autoimmune destruction of the adrenal gland

secondary- pathology of the pituitary gland results in inadequate ACTH stimulating the adrenal gland

tertiary- pathology of the hypothalamus results in inadequate CRH release

CRH> ACTH> cortisol and aldosterone

40
Q

Adrenal insufficiency/ Addison’s disease epidemiology (G)

A

more women than men
mostly autoimmune
30-50

41
Q

Adrenal insufficiency/ Addison’s disease aetiology (G)

A
  1. -developed world: autoimmune destruction of adrenal antibodies (21-alpha-hydroxylase) results in destruction of adrenal gland
    -developing world: TB
    -adrenal metastases eg liver, lung, breast
    -adrenal haemorrhage (AKA waterhouse-Friderichsen syndrome commonly caused by meningococcol menigitis)
    -antiphospholipid syndrome
  2. pituitary insufficiency due to long term steroid (iatrogenic) use or pituitary adenoma
  3. hypothalamus insufficiency due to long term steroid use or radiotherapy
42
Q

Adrenal insufficiency/ Addison’s disease risk factors (G)

A

female
adrenal haemorrhage
adrenocortical antibodies
other autoimmune conditions

43
Q

Adrenal insufficiency/ Addison’s disease pathophysiology

A
  1. autoimmune destruction of adrenal antibodies (21-alpha-hydroxylase), destruction of adrenal gland so less cortisol/aldosterone production. This results in excess ACTH as lack of negative feedback. Rising ACTH acts on melanocytes to produce melanin resulting in hyperpigmentation
  2. Pituitary/ hypothalamus insufficiency causes HPA axis suppression, causing decreased ACTH so no hyperpigmentation
44
Q

Adrenal insufficiency/ Addison’s disease presentation (G)

A

remember 4Ts- tanned, tired, tearful, thin

-hyperpigmentation (tanned, bronzed, in palmar creases especially)
-vitiligo
-weight loss/ anorexia
-tearful/ depressed
-loss of axillary/ pubic hair in women
-tired
-N+V
-weakness
-abdominal cramps
-postural hypotension
-hypoglycaemia
-headaches

45
Q

Adrenal insufficiency/ Addison’s disease investigations

A

1:
serum electrolytes (Na+ low, K+ high, due to low aldosterone, high glucose)
morning serum cortisol (low)
plasma ACTH (1-high, 2-low)

gold:
ACTH stimulation Short Synacthen test (to test adrenal reserve)
-measure basal cortisol at 9am (highest here, if low, major problem)
-administer synacthen
-measure cortisol 30 and 60 mins after
failure for ACTH to stimulate rise in cortisol (less than double baseline) shows primary adrenal insufficiency <500nmol/l. If over 580 can rule out addisons

other:
renin: aldosterone (renin high in addisons, aldosterone low)
FBC (anaemia)

46
Q

Adrenal insufficiency/ Addison’s disease DD (G)

A

1/2/3 adrenal insufficiency,
adrenal suppression due to glucocorticoid drugs,
hyperthyroidism

47
Q

Adrenal insufficiency/ Addison’s disease management (G)

A

1:
hydrocortisone (glucocorticoid to replace cortisol)
fludrocortisone (mineralocorticoid to replace aldosterone)
-will correct Na K+ and postural hypotension

double steroid use in illness/ trauma/ infection/ stress as cortisol needed in stress respone

patients given steroid card and emergency ID to alert emergency services as dependent on steroids for life

secondary: long term steroids weaned off, treat cause

48
Q

Adrenal insufficiency/ Addison’s disease red flags (G)

A

trauma
infection
dehydration
ending steroid treatment

49
Q

Adrenal insufficiency/ Addison’s disease complications (G)

A

Addisonian/ adrenal crisis:
-severe adrenal insufficiency (esp cortisol),
-presents with shock, reduced consciousness, hypotension, hypoglycaemia, hyponatraemia, hypokalaemia,
-management: immediate IV hydrocortisone, IV fluid resus, correct hypoglycaemia with dextrose

  • shock, coma, death if not treated

my phase 2 (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions