Biochemistry - Pituitary Function and Pituitary Disease Flashcards

1
Q

Acidophi

A

Somatotrophs

Lactotrophs

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2
Q

Basophils

A

Thyrotrophs
Corticotrophs
Gonadotrophs

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3
Q

Chromophobe

A

Prolactin secretion

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4
Q

Somatotrophs secrete

A

Growth Hormone (entire body)

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5
Q

LActrotrophs secrete

A

Prolactin (mammary)

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6
Q

Thyrotrophs secrete

A

TSH (thyroid)

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7
Q

Corticotrophs secrete

A

ACTH (Adrenal)

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8
Q

Gonadotrophs secrete

A

LH/FSH (Testes/Ovaries)

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9
Q

Chromophobe secrete

A

(Prolactin)

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10
Q

Corticotrophin releasing factor (CRF)

A

ACTH

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11
Q

Thyrotrophin releasibg factor (TRH)

A

TSH

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12
Q

Luteinising hormone RH (LHRH, GnRH)

A

LH/FSH

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13
Q

Growth Hormon releasing hormone (GHRH)

A

GH

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14
Q

Hypothalamic Peptide:

Releasing Factor

A

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

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15
Q

Inhibiting Factor:

A

Somatostatin (GH RIF)

Dopamine (Prolactino RIF)

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16
Q

Pituitary Tumours

A

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

17
Q

Hyper-function

A

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

18
Q

Hypo-function

A

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

19
Q

Basal Hormone measurements

A
  • Pituitary hormones
  • Target hormones

Limitations: diurinal changes

20
Q

Stimulation testing

A

Checking for deficiency

Individual/combined – give pituitary hormones/[physiological induce (fasting)
•	ACTH: hypoglycaemia. CRF
•	TSH: TRH
•	LH/FSH: LHRH
•	GH: Hypoglycaemia
21
Q

Suppression testing

A

Hormone Excess
ACTH: Dexamethasone (Blocks)
GH : Glucose

22
Q

Investigation of pituitary function:

A

Basal Hormone measurements

Stimulation testing
Suppression testing

23
Q

Growth Hormone Production – Induction

A
Stress
Exercise
Amino Acids
Sleep
Ghrelin
24
Q

Growth Hormone Production – Inhibition

A

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