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Cardio > Biochemistry - Pituitary Function and Pituitary Disease > Flashcards

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
Q

Growth Hormone Production – Assessment of GH

A

IGF-1

IGF-2 – shows excess production of GH

26
Q

Growth Hormone Production – Deficiency/Excess of GH

A

Deficiency – short stature

Excess – Gigantism acromegaly

27
Q

Growth Hormone Production – Metabolic effects of GH

A

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

28
Q

Growth Hormone Production – Phenotypic Excess in GH Excess

A

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

29
Q

Diagbosis

A

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

30
Q

GH deficiency

A

Children:Short Stature
Adults: Significantly less clear

31
Q

Destructive lesions

A

Tumours, surgery, irradiation, meningitis, head injury

32
Q

Functional: some forms of short stature

A 
Pyschosocial, endocrine abnormalities,
Laron dwarfism (GH receptor defect) – very rare
33
Q

Diagnosis

A

Inutero development is normal

34
Q

Diagnosis GH

A

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
Q

Diagnostic response

A
  1. Flat response – deficient

2. Intermediate = some response

36
Q

Causes of Hyper-prolactinaemia

A
  • Physiological

* Pathological

37
Q

Physiological

A

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

38
Q

Macroprolactin diagnosis confirmation

A

Not Cleared therefor not responsive to treatment and so diagnostic

39
Q

Pathological causes

A

• 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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