Biochemistry - Pituitary Function and Pituitary Disease Flashcards Preview

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Flashcards in Biochemistry - Pituitary Function and Pituitary Disease Deck (39):
1

Acidophi

Somatotrophs
Lactotrophs

2

Basophils

Thyrotrophs
Corticotrophs
Gonadotrophs

3

Chromophobe

Prolactin secretion

4

Somatotrophs secrete

Growth Hormone (entire body)

5

LActrotrophs secrete

Prolactin (mammary)

6

Thyrotrophs secrete

TSH (thyroid)

7

Corticotrophs secrete

ACTH (Adrenal)

8

Gonadotrophs secrete

LH/FSH (Testes/Ovaries)

9

Chromophobe secrete

(Prolactin)

10

Corticotrophin releasing factor (CRF)

ACTH

11

Thyrotrophin releasibg factor (TRH)

TSH

12

Luteinising hormone RH (LHRH, GnRH)

LH/FSH

13

Growth Hormon releasing hormone (GHRH)

GH

14

Hypothalamic Peptide:
Releasing Factor

Corticotrophin releasing factor (CRF)
Thyrotrophin releasibg factor (TRH)
Luteinising hormone RH (LHRH, GnRH)
Growth Hormon releasing hormone (GHRH)

15

Inhibiting Factor:

Somatostatin (GH RIF)
Dopamine (Prolactino RIF)

16

Pituitary Tumours

Usually benign/slow growing (rarely metastesis)
Functional/Non-functional (non hormone secreting)
Local Effects
Secondary endocrine effects

17

Hyper-function

Primary/Secondary (prolactinoma)
Usually single hormones involved
Prolactin, GH, ACTH

18

Hypo-function

Usually generalised (al hormones effected)
Occasionally isolated (GH, LH/FSH, ACTH)
Causes: Tumours (primary/secondary). Infarction
Surgery/Irradiation, meningitis

19

Basal Hormone measurements

• Pituitary hormones
• Target hormones

Limitations: diurinal changes

20

Stimulation testing

Checking for deficiency

Individual/combined – give pituitary hormones/[physiological induce (fasting)
• ACTH: hypoglycaemia. CRF
• TSH: TRH
• LH/FSH: LHRH
• GH: Hypoglycaemia

21

Suppression testing

Hormone Excess
ACTH: Dexamethasone (Blocks)
GH : Glucose

22

Investigation of pituitary function:

Basal Hormone measurements

Stimulation testing
Suppression testing

23

Growth Hormone Production – Induction

Stress
Exercise
Amino Acids
Sleep
Ghrelin

24

Growth Hormone Production – Inhibition

Glucose/Somatisation

25

Growth Hormone Production – Assessment of GH

IGF-1
IGF-2 – shows excess production of GH

26

Growth Hormone Production – Deficiency/Excess of GH

Deficiency – short stature
Excess – Gigantism acromegaly

27

Growth Hormone Production – Metabolic effects of GH

Protein Biosynthesis – muscle, cartilage, viscerae
Carbohydrate metabolism – insulin antagonism
Lipid metabolism – Lipolysis
Increased GIT absorption of calcium –(mainly by hydroxylation)

28

Growth Hormone Production – Phenotypic Excess in GH Excess

Facial Changes
Hands and feet enlarge
Height increase in pre-pubertal

29

Diagbosis

Biochemical Confirmation
• Basal GH and IGF1 9not subject to pulsatile and diurnal and therefore wont effect drugs.
• Suppression (GTT)
• Other Anterior Pituitary function

30

GH deficiency

Children:Short Stature
Adults: Significantly less clear

31

Destructive lesions

Tumours, surgery, irradiation, meningitis, head injury

32

Functional: some forms of short stature

Pyschosocial, endocrine abnormalities,
Laron dwarfism (GH receptor defect) – very rare

33

Diagnosis

Inutero development is normal

34

Diagnosis GH

Basal – GH/IGF-1 levels (Some overlap between normal and patho)
Stimulation tests:
• Insulin (Gold standard) – not pleasant for patient and dangerous
• Glucagon (children <5 years) – stimulates GH production
• Arginine +/- GHRH
• Clonidine

Failure of two stimuli required → GH +5 g/l

35

Diagnostic response

1. Flat response – deficient
2. Intermediate = some response

36

Causes of Hyper-prolactinaemia

• Physiological
• Pathological

37

Physiological

• Pregnancy
• Stress
• Drug induced:
→ Dopamnie receptor antagonist phenothiazines
→ Dopamine depleting agents methyl dopa
→ Oestrogens – oral contraceptives/PCOP
• Macroprolactin – high molecular wt prolactin

38

Macroprolactin diagnosis confirmation

Not Cleared therefor not responsive to treatment and so diagnostic

39

Pathological causes

• Pituitary Tumour:
1. Prolactin secreting micro/macro adenoma
2. Acromegaly
3. Functionless pituitary tumour – affects of dopamine transfer
• Lesions hypothalamic/pituitary stalk – lack of dopamine transfer
• Primary hypothyroidism (TRH) – low thyroxine and so high TSH driven by TRH and so also stimulates Prolactin release
• Chronic Renal Failure

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