PBL 6 Flashcards

1
Q

what does Sarah have

A

Has clinically non-functioning pituitary tumour.

o Pressing on pituitary stalk = stops blood flow from median eminence to anterior pituitary.

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2
Q

what is hyperprolactineamia

A

 Prolactin secretion = under negative control of dopamine produced by
hypothalamus. Stalk effect = Obstruction causes hyperprolactinaemia

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3
Q

what is the pituitary gland located

A

Sella Turcica – A saddle shaped depression in the
sphenoid bone

The seat of the saddle which holds the pituitary
gland is also known as the hypophyseal fossa

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4
Q

what another name for the posterior lobe

A

neruohypophysis

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5
Q

what does the posterior lobe of the pituitary secrete

A

oxytocin

ADH

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6
Q

what is another word for the anterior pituitary

A

Aden-hypophysis

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7
Q

what hormones does the anterior pituitary secrete

A
GH 
PR
LH
FSH 
ACTH 
TSH
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8
Q

what stimulates and what inhibits pituitary hormones

A

GnRH - causes GH - IGF-1(liver)
THR - TSH - T3 and T4 -
- these are both inhibited by somatostatin
- CRH goes to ACTH - produced in the adrenal cortex
- Dopamine inhibits PRL which goes to the marry gland
- GNRH - causes increase in FSH/LH - goes to the ovaries and testes

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9
Q

what does the growth hormone do

A
  • gluconeogensis - in the liver
  • increases lipolysis in adipocytes
  • protein sparing effect - stimulates protein produce in the muscle
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10
Q

what happens if you have excess growth hormone

A

x

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11
Q

what is the difference between T3 and T4

A
  • thyroid mainly produces T4
  • T4 is less active than T3
  • most T3 is formed from peripheral conversion of T4
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12
Q

what do thyroid hormones do

A

both T3 and T4 increase the basal metabolic rate

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13
Q

what does ACTH do

A

stimulates the Zona fasiculata of the adrenal cortex to release cortisol

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14
Q

what does cortisol do

A

Increase plasma glucose

↑ gluconeogenesis; ↑ glycogenolysis

Suppresses immune system

Increases blood pressure

Decreases bone formation

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15
Q

what does excess cortisol lead to

A

cushings syndrome

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16
Q

what does a deficiency of corstiol lead to

A

hypocortisolism - Addisons

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17
Q

what does prolactin do

A

Development of mammary glands and production
of milk

Decrease oestrogen and testosterone

Maintenance of high levels of prolactin
(post-pregnancy) is responsible for suppressing
ovulation

Tubero-infundibular dopamine pathway

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18
Q

what does LH and FSH do in males

A

maturation of the germ cells

LH stimulates leydig cells to produce testosterone.

FSH stimulates conversion of testosterone into DHT in sertoli
cells. Enzyme: 5α-reductase

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19
Q

what does LH and FSH do in females

A

maturation of the germ cells

LH stimulates theca cells to produce testosterone.

FSH stimulates conversion of testosterone into oestradiol in
granulosa cells. Enzyme: aromatase

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20
Q

what are the causes of hypopituitarism

A

Tumours

Infection

Vascular

  • Sheehan syndrome – post-partum haemorrhage
  • Pituitary apoplexy – infarction of pituitary

Radiation

Trauma/subarachnoid haemorrhage

Congenital

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21
Q

what is a pituitary adenoma

A

Benign adenoma, invasive adenoma, carcinoma

Micro- <10mm ; macro- >10mm

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22
Q

what does a pituitary adenoma consist of

A

Can consist of secretory cells or non-functioning
cells

Tumours disrupt normal secretory activity and can
compress surrounding structures by local invasion

23
Q

what goes through the cavernous sinus

A
OTOM CAT 
O occulomotor
T trochlear
O -opthalmic branch of V 
M - maxillary branch of V 
C internal carotid 
A abdunces 
T trochlear
24
Q

why does she get a bitemporla hemiaponia

A
  • due to the optic chaiasm above the pituitary being pressed on
25
Q

what is transsphenodial adenomectomy

A
  • when you go through the nasal cavity and then through the sphenoid sinus which is hollow and just below the pituitary in order to remove the adenoma
  • only if symptomatic non function pituitary tumour
  • if the tumour is asymptomatic managed by continuous monitoring
26
Q

what are treatments for prolactinoma

A
Dopamine agonist (bromocriptine, cabergoline)
- these can be variable regards to tumour shrinking 
  • should not be used for macro adenoma where there are symptoms of compression and surgery should be undertaken instead
27
Q

what are treatments for acromegaly

A

Somatostatin analogues (octreotide, lanreotide)

GH antagonist (pegvisomont)

28
Q

what is the insulin tolerance test

A

IV insulin 🡪 induced hypoglycaemia below 2.2mol/l

Assess compensatory rise in GH and ACTH
- ACTH will stimulate the adrenal cortex to release cortisol

GH and cortisol are counterregulatory hormones to
insulin therefore the insulin should decrease and GH and ACTH rise

ECG done to ensure there no underlying heart
disease that could be exacerbated

Assesses body’s ability to respond to stress

  • test can be dangerous and cannot be done if the patient has a low cortisol/thyroid hormone levels or history of heart disease, MI, stroke or epilepsy
  • cortisol replacement should be given if it is low
29
Q

What hormones can you replace

A

Prednisone/hydrocortisone - give this first
- Increase dose during stress (e.g. infection)

Levothyroxine

Oestrogen/testosterone

Growth hormone (in children and symptomatic
adults only)
30
Q

what does the anterior pituitary receive stimuli from

A

AP receives stimuli from various nuclei, most importantly from the
arcuate, infundibular and paraventricular nuclei (parvocellar neurons).

31
Q

What does the posterior pituitary receive stimuli from

A

PP receives stimuli via neuronal axons from magnocellar neurons of the
paraventricular and supraoptic nucleus.

32
Q

what is ACTH coded by

A
  • polypeptide conned by POMC gene
33
Q

what is prolactin stimulated by

A
  • stress
  • exercise
  • pregnancy
  • drugs
34
Q

what does the reduced thyroid hormones cause

A
  • lethargy
  • tiredness
  • inability to cocnentrate and skin paleness
35
Q

explain her blood results and symptoms

A

low free T4

  • correlates to just exhausted, miserable and very slowed down
  • pale, her skin is dry and flaky and her hair appears dry and brittle
  • TSH should be rising due to the low T4 but it is down
Low GH 
- impaired brain function, and fatigue 
deficiency 
- insulin resistance 
- lipid metabolism - hyperlipidaemia 
- decreased bone mineral function 
- imparted cardiac function 
  • Low LH and FSH can cause loss of menstural periods - high prolactin in this case can inhibit LH and FSH release

loss of oestrogen - loss of libido

elevated prolactin
- stalk damage - dopamine cannot inhibit prolactin in the pituitary as dopamine is released from the hypothalamus therefore prolactin levels increase

36
Q

High prolactin can inhibit..

A

GnRH

37
Q

what is the secretion of GH modulated by

A

ï‚· Sleep
ï‚· Exercise
ï‚· Nutrition
ï‚· Stress

38
Q

what does GH stimulate

A

GH stimulate the production of SS

- this SS inhibits GH when it gets too high it also inhibits TSH

39
Q

IGF-1 stand for

A

insulin growth factor-1

40
Q

how do you measure IGF-1

A

Because of pulsatile properties hard to measure:
ï‚· Low levels suspected: perform a stimulation test (insulin, glucagon, GHRH and arginine)
ï‚· High levels suspected: perform a suppression test (oral glucose tolerance test).

41
Q

what does GH do

A
  1. Direct effect by binding on target cells.
  2. Indirect effect through stimulation of IGF production in all peripheral tissues as well as in the liver.
    a. There are two IGFs = I and II (resemble proinsulin).
    i. IGF1 = complex IGF-binding protein and ALS (acid labile subunit).
    b. Promote cell replication in muscles connective tissue, cartilage and bones.
42
Q

what is IGF-1 synthesised

A

Main pool of IGF is synthesized in the liver and secreted into the bloodstream under control of GH.
ï‚· IGF-1 is synthesized in peripheral tissues (bone). Controlled by GH and by factors secreted locally.

43
Q

what do GH and IGF do

A

o Exerts a protein sparing effect (diabetogenic property).
o Elevates blood glucose levels by lowering glucose uptake by skeletal muscle and
desensitizing the tissue to the action of insulin.
o Increases gluconeogenesis.
o Promotes lipolysis in adipocytes.

44
Q

what is the main control of adult growth hormone deficiency

A

o Exerts a protein sparing effect (diabetogenic property).
o Elevates blood glucose levels by lowering glucose uptake by skeletal muscle and
desensitizing the tissue to the action of insulin.
o Increases gluconeogenesis.
o Promotes lipolysis in adipocytes.

45
Q

what does cortisol do in the fasted state

A

1, stimulation of glucoengeosis
2, mobilisation of amino acids
3, inhibition of glucose uptake in muscle and adipose tissue
4, stimulation of fat breakdown in the adipose tissue

46
Q

what does loss of ACTH and therefore loss of cortisol result in

A
  • actue onset - hypovalemic shock, vascular collapse, confusion and psychosis
  • in terms of Sarah she has slightly low blood pressure
  • lethargy and exhaustion
  • low sugar
  • abdominal pain
  • weight loss
47
Q

IGF-1 and IGF 2

A
  • both proteins that resemble insulin
48
Q

Growth hormone increase in

A
  • night due to pulsatile
  • stress - hypoglycaemia
  • ??
49
Q

what happens if you have low oestrogen and growth hormone

A
  • can get osteomalacia
50
Q

growth hormone and the kidneys

A

decrease growth hormone decreases GFR leads to hypofiltraiton - look at ADH effect on the renal system
- this low GFR rate could cause activation of the RAAS and thus cause blood pressure to increase

51
Q

order in which things are damaged

A
  • growth hormone
  • LH and FSH
  • TSH
  • then prolactin last
52
Q

why would you do an emergency removal of an adenoma

A
  • acute mass effect due to pituitary adenoma in pregnancy when there is sudden bitemporal hemiapnoati
53
Q

FSH scattered positive cells

A
  • finding cells that are sensitivity to FSH in the adenoma itself or it might be that the adenoma is producing FSH (Not in the PBL)